a presentation on infective bacterial keratitis.pptx

presentation on cornea.. bacterial keratitis

1. INFECTIVE KERATITIS

2. BACTERIAL KERATITIS CAUSATIVE ORGANISM Exogenous cause, due to pyogenic bacteria: Pseudomonas, Staphylococcus aureus, Pneumococcus, Neisseria gonorrhoeae, E. coli. Mode and Source of Infection Break in the corneal epithelium Diminished resistance of the epithelium, Necrosis or desquamation of the epithelium

3. B acterial corneal ulcers may manifest as: i . Purulent corneal ulcer without hypopyon ii. Hypopyon corneal ulcer.

4. SYMPTOMS 1 Pain and foreign body sensation due to mechanical effects of lids and chemical effects of toxins on the exposed nerve endings. 2 Watering Reflex hyperlacrimation . 3 Photophobia intolerance to light results from stimulation of nerve endings. 4 Blurred vision corneal haze 5 Redness of eyes congestion of circumcorneal vessels.

5. SIGNS: 1. Lids are swollen. 2. Marked blepharospasm. 3. Conjunctiva is chemosed and shows conjunctival hyperaemia and ciliary congestion. 4. Corneal ulcer usually starts as an epithelial defect associated with greyish-white circumscribed infiltrate

6. Hypopyon corneal ulcer Etiopathogenesis Causative organisms. Many pyogenic organisms (staphylococci, streptococci, gonococci, Moraxella) may produce hypopyon, but by far the most dangerous are pseudomonas pyocyanea and pneumococcus. T erm 'hypopyon corneal ulcer' caused by pneumococcus ( ulcus serpens ) Term 'corneal ulcer with hypopyon' for the ulcers associated with hypopyon due to other causes. Source of infection for pneumococcal infection is usually the chronic dacryocystitis.

7. Hypopyon ulcers are much more common in old debilitated or alcoholic subjects.

8. MECHANISM OF DEVELOPMENT OF HYPOPYON.

9. Pseudomonas keratitis associated with extended wear soft contact lens. A paracentral corneal infiltrate with surrounding corneal edema and hypopyon. A Streptococcus pneumoniae corneal ulcer in an immunocompromised patient with deep stromal infiltrates and dense hypopyon.

10. Complications of corneal ulcer 1. Toxic iridocyclitis. It is usually associated with cases of purulent corneal ulcer 2. Secondary glaucoma. It occurs due to fibrinous exudates blocking the angle of anterior chamber (inflammatory glaucoma). 3. Descemetocele. Descemet's membrane herniates as a transparent vesicle called the descemetocele or keratocele. This is a sign of impending perforation and is usually associated with severe pain. 4. Perforation of corneal ulcer.

11. Sequelae of corneal perforation

12. Management of a case of corneal ulcer

13. TREATMENT EMPIRICAL APPROACH: This approach is based on the pre-existing culture and sensitivity data without specifically obtaining corneal specimens from the patients. Fortified antibiotics such as cefazolin or vancomycin for Gram-positive organisms and tobramycin or ceftazidime for Gram negative organisms are used. F luoroquinolone antibiotics, have shown by clinical trials to have an efficacy for common ocular pathogens equivalent to that of the fortified antibiotics.

14. P rolonged and nonelective use of fortified antibiotics is not preferred because 1. Expensive 2. poor compliance 3. ocular discomfort and epithelial toxicity. 4. none

15. HERPES VIRUS Are ubiquitous human pathogen capable of causing both asymptomatic infection and active disease Humans are natural reservoir of HSV 2 types – HSV 1- oropharynx HSV 2 – genital area Ocular disease typically caused by type 1 Causes primary infection in children and neonates MODE OF INFECTION: IP – 3- 9 days HSV 1 – close contact HSV 2 – venereal – birth canal

16. MECHANISM OF ACTION HSV ( epitheliotropic & cytolytic ) binds to one or more cellular receptor – heparin sulphate Virus fuses with cell membrane Enters the cell and nucleus where the transcription of viral DNA occurs – protein

17. TG is the most common source of recurrent HSV infection. Primary infection may subsequently reactivate by travelling via ophthalmic division of 5 th CN to the eye.

18. CLASSIFICATION OF OCULAR DISEASE 1.Congenital & Neonatal 2 . Primary infection 3. Recurrent infection

19. CONGENITAL AND NEONATAL OCULAR HERPES May be acquired by one of the three periods : Intrauterine (5%) Peripartum(10%) Postpartum (85%) Intrauterine infection occurs in 1/300,000 births, with features of microophthalmia, retinal dysplasia, optic atrophy and chorioretinitis.

20. CONGENITAL AND NEONATAL OCULAR HERPES HSV infections in latter two periods are further classified as skin, eyes, or mouth (SEM) with or without the other involvement seen in intrauterine infections. Ocular herpes include one or all: conjunctivitis, epithelial keratitis, stromal immune reaction, cataract, necrotizing chrioretinitis. Because most congenital cases are acquired in conjunction with genital herpes in the mother and during parturition, HSV-2 accounts for 80% of cases. Because of the potentially serious complications of congenital and neonatal ocular HSV disease, prompt medical treatment is mandated in conjunction with amblyopia therapy.

21. Primary infection (first attack) involves a nonimmune person. B etween 6 months (because the passive immunity has diminished by then) and 5 years of age and in teenagers. By the age of 5 years, nearly 60% of the population has been infected with HSV. Clinical features 1. Skin lesions. Vesicular lesions may occur involving skin of lids, periorbital region and the lid margin (vesicular blepharitis).

22. VIRAL KERATITIS DIAGNOSIS?? Primary HSV presenting as bilateral blepharitis.

23. PRIMARY INFECTION Acute follicular conjunctivitis with regional lymphadenitis is the usual and sometimes the only manifestation of the primary infection. Keratoconjuctivitis with non- suppurative lymphadenopathy Diffuse punctate keratitis – that evolves into multiple scattered micro dendrite figures. As a rule confined to epithelium clinically – d/t lack of previous immunologic stimulus Treatment-Topical antivirals supported by antibiotics & cycloplegics

24. R ECURRENT OCULAR HERPES Factors for reactivation – UV rays Trauma Heat, abnormal body temperature Other infectious disease Emotional disease Menstrual stress Steroids, immunosuppresant , PGs

25. CLINICAL FEATURES Suspicion of viral keratitis arises if there is Associated skin lesions, recurrences of these lesions Stress-induced recurrence Immuno compromised status History of contact Symptomatic eye ( Pain ,Photophobia ,Blurred vision, Tearing ,Redness) with minimal conjunctival and corneal signs Superficial dendrites with loss of corneal sensation

26. R ECURRENT OCULAR HERPES

27. R ECURRENT OCULAR HERPES Blepharitis V esicular lesion involving a focal area of the eyelid with surrounding erythema Conjunctivitis Primary infection with HSV can present as a follicular conjunctivitis. Conjunctivitis with lid lesions was the most common form of recurrence of HSV and accounts for 83% of recurrences.

28. RECURRENT INFECTION Patients with recurrent herpes have both cellular and humoral immunity against the virus. corneal vesicles dendritic ulcer geographic ulcer(amoeboid) D isciform keratitis

29. Herpes simplex epithelial keratitis Dendritic ulcer with terminal bulbs Stains with fluorescein May enlarge to become geographic Aciclovir 3% ointment x 5 daily Ganciclovir ophthalmic gel 0.15% - 5 times daily Supported by antibiotics and cycloplegics Debridement if non-compliant Treatment I n herpes, corneal sensation is reduced in approx 70 % of the patient. MC PRESENTATION 2-3wks

30. D/D OF DENDRITIC KERATITIS • Herpes zoster dendritic keratitis ( pseudodendrites ) • Acanthamoeba keratitis • Contact lens keratopathy • Antiviral toxicity

31. STROMAL KERATITIS

32. Pathogenesis of Disciform keratitis

33. Herpes simplex disciform keratitis Central epithelial and stromal oedema Folds in Descemet membrane Small keratic precipitates Occasionally surrounded by Wessely ring Signs Associations

34. Sign s of Disciform keratitis Focal disc-shaped patch of stromal oedema without necrosis, Folds in Descemet's membrane, Keratic precipitates, Ring of stromal infilterate ( Wessley immune ring) may be present surrounding the stromal oedema. It signifies the junction between viral antigen and host antibody. Corneal sensations are diminished. Intraocular pressure (IOP) may be raised despite only mild anterior uveitis.

35. TREATMENT T opical steroids (pred 1% or dexa 0.1%) + with antiviral cover(Acyclovir 3%) Oral (in immunodeficient or children) :: Acyclovir 400 mg PO 5t/d * 14 days, or :: Famcyclovir 500 mg PO twice daily for 14 days, or :: Valacyclovir 500 mg PO twice daily for 14 days, or

36. Diffuse stromal necrotic keratitis . Pathogenesis: direct viral invasion of the corneal stroma Symptoms : Pain, photophobia and redness Signs. It presents as necrotic, blotchy, cheesy white infiltrates that lie under the epithelial ulcer. Mild iritis and keratic precipitates. After several weeks of smouldering inflammation, stromal vascularization may occur.

37. Treatment: high-dose antiinflammatory and antiviral medications. refractory to treatment Keratoplasty should be deferred until the eye has been quiet with little or no steroidal treatment for several monthsbecause there are high chances of recurrence in a new graft.

38. Neurotrophic keratopathy ( Metaherpetic ) Damage to gasserian ganglion Impaired corneal innervations Decreased tear secretion Excess use of antivirals Signs – Irregular cornea with loss of corneal lustre Characterized by persistent epithelial defect Oval in shape with gray, thickened smooth borders Rx- Stop all unnecessary medications Gentle debridement of boggy epithelium Artificial tears Mild steroid :If active stromal keratitis + ve Therapeutic soft CL Doxycycline 100mg PO once daily to inhibit collagenase Cycloplegics : if iritis is + ve Tarsorrhaphy to treat chronic exposure Cyanoacrylate glue – if perforation occurs

39. VARICELLA ZOSTER VIRUS Incidence & epidemiology: Spread by saliva droplets, or direct contact with infected rash. The maculopapular rash appears in successive crops, lesions of various stages present simultaneously. Contagious period approx 1 day before rash & continues approx 1 week after app of each crop of lesion or until the cutaneous sores crust over. IP: 12- 17 days after contact.

40. CLINICAL DISEASE Congenital varicella syndrome If mother contracts varicella during first or second trimester of pregnancy. Ocular findings ~ chorioretinits , optic nerve atrophy or hypoplasia , congenital cataract and Horner Syndrome. No specific treatment. Vaccinate all women with no history of previous varicella .

41. HZO First described by Hutchinson in 1865 MC involves ophthalmic division of 5 th nerve Frontal branch is MC involved Nasociliary involvement – 76% ocular involvement Hutchinson’s sign – vesicles at the side & tip of nose precedes HZO HZO lies dormant in TG

42. Herpes zoster keratitis Develops in about 50% within 2 days of rash Small, fine, dendritic or stellate epithelial lesions Tapered ends without bulbs Resolves within a few days Develops in about 30% within 10 days of rash Multiple, fine, granular deposits just beneath Bowman membrane Halo of stromal haze Nummular keratitis Acute epithelial keratitis May become chronic

43. OPHTHALMIC COMPLICATIONS Ramsay Hunt syndrome 7 th nerve palsy + loss of taste over ant 2/3 rd tongue + earpain + vesicles in external auditory canal or pinna

44. DIAGNOSIS Diagnosis based on acute or recent history of systemic disease with ocular or periocular involvement with vesicles. INVESTIGATIONS- vesicular fluid for PCR, immunomicroscopy

45. TREATMENT   ACTIVE DISEASE Antivirals ( treat for 7 days , starting within 72 hrs) Famcyciclovir 500mg PO TDS Valacyclovir 1 g PO TDS Acyclovir 800mg PO 5t/d Lesions of lid, conjunctiva or cornea ( dendritic or rarely geographical keratitis) – topical Antiviral (trifluridine applied 9t/d * 7-10 days) plus an topical Antibiotic. 3. Pain prevention- TCA’s( eg nortryptyline , desipramine ) 25-75 mg PO * 3months Non narcotic or short term narcotic analgesic . 4. Immunocompromised patients with any zoster – I.V Acyclovir 15 – 20 mg/kg/day

46. 3. Irrespective of the etiology of a corneal ulcer, the drug always indicated is: a. Corticosteroids b. Cycloplegics c. Antibiotics d. Antifungals B

47. 4. Dense scar of cornea with incarceration of iris is known as: a. Adherent Leucoma b. Dense leucoma c. Ciliary staphyloma d. Iris bombe A

48. 5. Corneal sensations are diminished in: a. Herpes simplex b. Conjunctivitis c. Fungal infections d. Marginal keratitis A

49. 9. Which of the following organism can penetrate intact corneal epithelium? A. Strept pyogenes B. Staph aureus C. Pseudomonas pyocyanaea D. Corynebacterium diphtheriae D

50. The effective treatment of dendritic ulcer of the cornea is: a. Surface anesthesia b. Local corticosteroids c. Systemic corticosteroids d. Acyclovir ointment D

51. 6. The color of fluorescein staining in corneal ulcer is: a. Yellow b. Blue c. Green d. Royal blue C

52. Thank you