Download to read offline
More Related Content
Similar to Bacterial_ocular_infections.pptx
Bacterial_ocular_infections.pptx
- 1. BY / SH I M A A H A S S A N BACTERIAL OCULAR INFECTIONS
- 2. Lecture outlines Ocularbacteriology Bacterial Infections of the orbit Bacterial Infections of the Eyelid Margin and Conjunctiva Bacterial Infections of the Cornea and Sclera Bacterial Uveitis Endophthalmitis
- 3. Bacteria are prokaryotes,organisms in which the genetic material is not separated from the cytoplasm by a nuclear membrane gram-positive gram-negative cocci Staphylococcus species Neisseria spp Streptococcus species Enterococcus species rods Corynebacterium species Pseudomonas species Propionibacterium species Enterobacteriaceae Bacillus species Haemophilus species Bartonella henselae Filaments Mycobacterium species Nocardia species Actinomyces species
- 5. Streptococci inhabit the mucousmembranes of the normal upper respiratory tract and female genital tract
- 6.
- 7.
- 8.
- 9. Bacterial Infections ofthe orbit Cellulitis Bacterial infections of the orbit or periorbital soft tissues originate from 3 primary sources: direct spread from adjacent sinusitis, dacryocystitis, or dacryoadenitis direct inoculation following trauma or skin infection hematologic spread from a distant focus (eg, otitis media, pneumonia)
- 10. Preseptal cellulitis occurs anteriorto the orbital septum. • Eyelid edema, erythema, inflammation may be severe, but the globe is uninvolved • pupillary reaction, vision, and ocular motility are not disturbed • pain on eye movement and chemosis are absen Treattment • In children, oral antibiotics (eg, cephalexin for an anterior etiology, • amoxicillin clavulanate for an infection originating in the sinuses), • frequent warm compresses, • and nasal decongestants (eg, oxymetazoline nasal spray),in cases of associated sinusitis, are typically e_ective therapy;
- 11. Orbital cellulitis Orbital cellulitisinvolves structures posterior to the orbital septum
- 12. Clinical findings • fever,leukocytosis(75% of cases), erythema, proptosis, chemosis, ptosis, and restriction of and pain with ocular movement • Decreased vision, impaired color vision, restricted visual fields • pupillary abnormalities suggest opticneuropathy that demands immediate investigation and aggressive management.
- 13. Microbial Infections ofthe Eyelid Margin and Conjunctiva Staphylococcal Blepharitis This condition is not purely infectious, so antimicrobial therapy is rarely curative because of a significant inflammatory component clinical manifestations • hard, brittle fibrinous scales and hard, matted crusts surrounding individual cilia on the anterior eyelid margin • telangiectasis of the anterior and posterior eyelid margins, (poliosis), (madarosis), and trichiasis may be seen in varying degrees, depending on the severity and duration of the blepharitis
- 17. Phlyctenulosis local cornealand/or conjunctival inflammation that is believed to hypersensitivity response induced by microbial antigens such as the cell wall components of staphylococcus. Phlyctenulosis is frequently associated with S .aureus in developed countries and is classically associated with Mycobacterium tuberculosis in malnourished children
- 18. Hordeolum • inflammatory orinfectious nodules that develop in the eyelid. • Results from inspissation and secondary infection of sebaceous glands. • external hordeola, or styes. occurring on the anterior eyelid in the glands of Zeis or lash follicles • internal hordeola occurring at the posterior eyelid from meibomian gland • Hordeola are generallyself-limited, improving spontaneously over the course of 1-2 weeks. • Internal hordeola occaSionally evolve into chalazia
- 19. Bacterial Conjunctivitis inChildren and Adults 80% of cases of infectious conjunctivitis in adults are viral in origin. While, in children, the number of bacterial conjunctivitis cases is similar to that of viral conjunctivitis cases, The source of infection • direct contact with an infected individual’s secretions • spread of infection from the organisms colonizing the patient’s own nasal and sinus mucosa. • In an adult with unilateral bacterial conjunctivitis, the nasolacrimal system should be examined, as nasolacrimal duct obstruction, dacryocystitis, or canaliculitis may be the underlying cause.
- 21. Acute purulent conjunctivitis acuteinflammatory response with purulent discharge of less than 3 weeks’ duration The most common etiologic pathogens are S pneumoniae, Streptococcus viridans, H .influenzae, and S aureus CLINICAL PRESENTATION Streptococcus pneumoniae conjunctivitis : moderate purulent discharge, eyelid edema, chemosis, conjunctival hemorrhages, and occasional inflammatory membranes on the tarsal conjunctiva. Corneal ulceration occurs in rare instances. H influenzae biotype III conjunctivitis (formerly Haemophilus aegyptius) conjunctival membranes do not develop, and peripheral corneal epithelial ulcers and stromal inflltrates occur more commonly. Staphylococcus aureus may produce an acute blepharoconjunctivitisless purulent than that seen in pneumococcal conjunctivitis, the associated signs are generally less severe
- 23. MANAGEMENT Most casesof acute bacterial conjunctivitis resolve in 2–7 days without treatment. Some prospective studies suggest that delaying treatment until day 3 or 4 would significantly reduce the unnecessary use of antibiotics without affecting outcomes. conjunctivitis is improving on day 4, antibiotics may not be necessary at all . Initiating treatment at this time only for persistent or worsening signs Empiric therapy with polymyxin B-trimethoprim, aminoglycoside or fluoroquinolone drops, or bacitracin or ciprofloxacin ointment can be initiated The dosing schedule is 4–6 times daily for approximately 5–7 days
- 24. Hyperacute gonococcal conjunctivitis explosiveonset and very rapid progression of severe purulent conjunctivitis The organism most commonly responsible for hyperpurulent conjunctivitis is N gonorrhoeae disease resulting from direct transmission of the organism, from the genitalia to the hands and then to the eyes or from the mother to the neonate during vaginal delivery CLINICAL PRESENTATION preauricular lymphadenopathy and the formation of conjunctival membranes. Keratitis . Corneal involvement may consist of diffuse epithelial haze, epithelial defects, marginal infltrates, and ulcerative keratitis that can rapidly progress to perforation
- 26. MANAGEMENT . Currenttreatment regimens for gonococcal conjunctivitis reflect the increasing prevalence of penicillin-resistant N gonorrhoeae (PRNG) in the United States. . Patients withgonococcal conjunctivitis without corneal ulceration may be treated on an outpatient basis with 1 intramuscular (IM) ceftriaxone (1 g) injection patients with corneal ulceration should be admitted to the hospital and treated with intravenous (IV) ceftriaxone (1 g IV every 12 hours) for 3 consecutive days. Erythromycin ointment, bacitracin ointment, gentamicin ointment, and ciprofloxacin solution have been recommended for topical therapy Up to one-third of patients with gonococcal conjunctivitis have been reported to have concurrent chlamydial venereal disease., it is advisable to give patients supplemental oral antibiotics for treatment of chlamydial infection
- 27. Neonatal gonococcal conjunctivitis typicallydevelops 3–5 days post partum. The discharge may be serosanguineous during the first several days, with a copious purulent exudate MANAGEMENT For nondisseminated infections, a single IM or IV ceftriaxone injection (up to 125 mg or a dose of 25–50 mg/kg) or cefotaxime at a single dose of 100 mg/kg IV or IM is recommended combined with hourly saline irrigation of the conjunctiva until discharge is eliminated If corneal involvement is suspected, application of topical erythromycin or gentamicin ointment should be considered
- 28. Chlamydial conjunctivitis The bacteriumC trachomatis is an obligate intracellular pathogen causes several different conjunctivitis syndromes trachoma: serotypes A–C adult and neonatal inclusion conjunctivitis: serotypes D–K lymphogranuloma venereum: serotypes L1, L2, and L3
- 29. Trachoma infectious diseasethat occurs in communities with poor hygiene and inadequate sanitation. Most infections are transmitted from eye to eye. Transmission may also occur by flies and household fomites, which spread other bacteria as well, causing secondary bacterial infections in patients with trachoma CLINICAL PRESENTATION • foreign-body sensation, redness, tearing, and mucopurulent discharge • A severe follicular reaction develops, most prominently in the superior tarsal conjunctiva • Large tarsal follicles in trachoma may become necrotic and eventually heal with significant scarring
- 30. . Arlt line: Linear or stellate scarring of the superior tarsus Herbert pits limbal depressions due to Involution and necrosis of follicles .Corneal findings in trachoma include : Epithelial keratitis, focal and multifocal peripheral and central stromal inflltrates, and a superficial fibrovascular pannus, which is most prominent in the superior third of the cornea but may extend centrally intothe visual axis
- 32. Clinical diagnosis oftrachoma requires at least 2 of the following clinical features: • follicles on the upper tarsal conjunctiva • limbal follicles and their sequelae (Herbert pits) • typical tarsal conjunctival scarring • vascular pannus most marked on the superior limbus • Severe conjunctival and lacrimal gland duct scarring from chronic trachoma can result in aqueous tear deficiency, tear drainage obstruction, trichiasis, and entropion
- 33. MANAGEMENT Current recommendations fortreatment of active trachoma are tetracycline 1% ophthalmic ointment, applied twice daily for 2 months, and oral azithromycin 1000 mg, given as a single dose. Topical erythromycin, given at the same frequency as topical tetracycline, oral tetracycline 1.5–2.0 g daily in divided doses for 3 weeks are also effective
- 34. Adult chlamydial conjunctivitis sexuallytransmitted disease often found in conjunction with chlamydial urethritis or cervicitis Onset of conjunctivitis is typically 1–2 weeks after ocular inoculation CLINICAL PRESENTATION mucopurulent discharge, palpable preauricular adenopathy and a follicular conjunctival response that is most prominent in the lower palpebral conjunctiva conjunctival membranes do not develop in adult chlamydial keratoconjunctivitis Corneal involvement may consist of fine or coarse epithelial infltrates
- 35. MANAGEMENT one of thefollowing oral antibiotic regimens is recommended: azithromycin 1000 mg single dose doxycycline 100 mg twice daily for 7 days tetracycline 250 mg 4 times daily for 7 days erythromycin 500 mg 4 times daily for 7 days
- 36. Bacterial conjunctivitis inneonates the causes of neonatal bacterialconjunctivitis, reflective of the vaginal and nosocomial flora, are as follows: • C trachomatis • S viridans • S aureus • H influenzae • group D Streptococcus • Moraxella catarrhalis • E coli and other gram-negative rods • N gonorrhoeae
- 37. Neonatal chlamydial conjunctivitis Chlamydialconjunctivitis in neonates differs clinically from that in adults in the following ways: 1. There is no follicular response in newborns. 2. The amount of mucopurulent discharge is greater in newborns. 3. Pseudomembranes can develop on the tarsal conjunctiva in newborns. 4. Intracytoplasmic inclusions are seen in a greater percentage of Giemsa-stained conjunctival specimens in newborns. 5. The infection in newborns is more likely to respond to topical medications.
- 38. Parinaud Oculoglandular Syndrome Granulomatousconjunctivitis with regional lymphadenopathy Cat-scratch disease (CSD), causes most cases of the syndrome The primary causative agent is B henselae. Other, infrequent causes include coccidioidomycosis sporotrichosis syphilis tuberculosis tularemia “cat-scratch” disease, infection may be transmitted to humans by a cat bite or lick or by contact with a cats feas
- 39. CLINICAL PRESENTATION &MANAGEMENT Unilateral granulomatous conjunctivitis with one or more raised or flat gelatinous, hyperemic, granulomatous lesions develops on the superior or inferior tarsal conjunctiva . Either concurrently or 1–2 weeks later, ipsilateral regional preauricular and submandibular lymph nodes become firm and tender Mild systemic symptoms of fever, malaise, headache, and anorexia develop in about 10%–30% of patients, Antibodies to B henselae can be detected by indirect fluorescent antibody testing or by enzyme immunoassay. The ideal treatment has not yet been determined. Various antibacterial treatment regimens have reported success doxycycline. Rifampin is often used as an adjuvant
- 40. Microbial Infections ofthe Cornea and Sclera Bacterial keratitis predisposing factors include: contact lens wear trauma contaminated ocular medications impaired defense mechanisms altered structure of the corneal surface
- 42. CLINICAL PRESENTATION pain ,conjunctivalinjection, photophobia, and decreased vision Bacterial corneal ulcers are typically a single inflltrate and show a sharp epithelial demarcation with underlying dense, suppurative stromal inflammation that has indistinct edges and is surrounded by edema P aeruginosa typically causes stromal necrosis with a shaggy surface and adherent mucopurulent exudate
- 43. The American Academyof Ophthalmology practice guidelines continue to recommend that initial culturesbe obtained for inflltrates extending to the middle of the cornea, into deep stroma, across a large area (>2 mm), for patients whose history or clinical features suggest fungal, amebic, MANAGEMENT Initial therapy consists of empiric, broad-spectrum topical antibiotics. In routine corneal ulcers, monotherapy with topical fluoroquinolones . These antibiotics should initially be given every 30–60 minutes and then tapered in frequency according to the clinical response . In severe cases, administration of antibiotics every 5 minutes for 30 minutes as a loading dose can more rapidly achieve therapeutic concentrations in the corneal stroma
- 45. clinical response toantibiotic therapy: • blunting of the perimeter of the stromal infiltrate • decreased density of the stromal infiltrate • reduction of stromal edema and endothelial inflammatory plaque • reduction in anterior chamber inflammation • reepithelialization
- 46. Microbial Scleritis Bacterial andfungal infections of the sclera are very rare possible risk factors; • extension of microbial keratitis involving the peripheral cornea • Trauma • contaminated foreign bodies (including scleral buckles) • sclera damaged by previous pterygium surgerywhen mitomycin has been used
- 47. MANAGEMENT Topical antimicrobial therapyis begun just as for microbial keratitis. Because of the diffculty in controlling microbial scleritis, subconjunctival injections and intravenous antibiotics may also be used. Long-term oral therapy shows promise
- 48. Bacterial Uveitis Syphilis TB LYME DISEASE
- 49. Syphilis • chronic bacterialinfection caused by the spirochete Treponema pallidum • associated with numerous ocular manifestations in both the acquired and congenital forms • Ocular inflammatory signs of congenital syphilis may present at birth or decades later and include uveitis, interstitial keratitis, optic neuritis, glaucoma, and congenital cataract.A multifocalchorioretinitis • Keratouveitis is thought to be an allergic response to T pallidum • The constellation of interstitial keratitis,cranial nerve VIII deafness, and Hutchinson teeth is called the Hutchinson triad.
- 50. Active syphilitic interstitialkeratitis
- 51. Acquired syphilis Uveitis mayoccur in up to 5% of patients whose disease has progressed to tertiary syphilis, it can occur at any stage of infection, including primary disease Patients present with pain, redness, photophobia, blurred vision, and floaters. Intraocular inflammation may be granulomatous or nongranulomatous • Anterior segment findings vascularized papules (iris papulosa), larger red nodules (iris nodosa), and gummata. Interstitial keratitis, posterior synechiae, lens dislocation, and iris atrophy can also occur. • Posterior segment findings of acquired syphilis include vitritis, chorioretinitis, focal retinitis,necrotizing retinitis, retinal vasculitis, exudative retinal detachment, isolated papillitis, and neuroretinitis. A focal or multifocal chorioretinitis,
- 53. Syphilitic posterior placoid chorioretinitis early,irregular hypofluorescence
- 54. late staining atthe level of the pigment epithelium
- 55. The diagnosis ofsyphilitic uveitis is usually made according to the history and clinical presentation Treatment Parenteral penicillin G is the preferred treatment for all stages of syphilis
- 56. Lyme Diseas caused bythe spirochete Borrelia burgdorferi transmitted to humans through the bite of infected ticks, Ixodes scapularis in the northeast Intermediate uveitis is one of the most common intraocular presentations . Vitritis may be severe and accompanied by a granulomatous anterior chamber reaction, papillitis, neuroretinitis, choroiditis, retinal vasculitis, and exudative retinal detachment
- 58. Tuberculosis . Primary ocularTB is defined as TB in which the eye is the primary portal of entry, and it manifests mainly as conjunctival, corneal, and scleral disease. Secondary ocular TB, of which uveitis is the most common manifestation, occurs by virtue of hematogenous dissemination or by contiguous spread from adjacent structures. External ocular and anterior segment findings include scleritis, phlyctenulosis, interstitial keratitis, corneal infiltrates, anterior chamber and iris nodules Tuberculous uveitis is classically a chronic granulomatous disease that may affect the anterior and/or posterior segments; it is replete with mutton-fat KPs, iris nodules, posterior synechiae, and secondary glaucoma,. Patients typically experience a waxing and waning course, with accumulation of vitreous opacities and CME
- 59. disc edema, vasculitis,periphlebitis, and CME multifocal, discrete, yellowish choroidal lesions
- 60. tuberculous choroiditis masqueradingas atypical serpiginous-like choroiditis
- 61. Diagnosis Definitive diagnosis ofTB requires direct evidence of mycobacteria in bodily fluids or tissues. In many cases of ocular TB, this confirmation is not possible, A positive result on a PPD test or an interferon-gamma release assay is indicative of prior exposure to TB but not necessarily of active systemic infection In the United States, an • induration of 5 mm or more, read 48–72 hours after intradermal injection of the standard 5-tuberculinunit is considered a positive result in individuals with HIVinfection • . An induration of 10 mm or more is considered indicative of a positive result for other high-risk individuals(DM/RF..) • . Patients with no known risks for tuberculosis are considered to exhibit a positive test result with an induration of 15 mm ormore
- 62. Treatment 2-month induction courseof INH, rifampin, and pyrazinamide administered daily, followed by a continuation phase of 4–7 months
- 63. Endophthalmitis Infectious endophthalmitis maypresent in an acute form in a more indolent or chronic form The hallmark of endophthalmitis is vitreous inflammation, but other signs include eyelid or periorbital edema, ciliary injection, chemosis, anterior chamber inflammation, hypopyon, decreased visual acuity, corneal edema, and retinal hemorrhages ). Most cases present within 3–10 days of surgery, with a median of 6 days, The most common bacterial causes were gram-positive coagulase-negative Staphylococcus epidermidis (70%), Staphylococcus aureus (9.9%), Streptococcus species (9.0%), other gram-positive bacteria (3.1%), Enterococcus species (2.2%), and gram-negative bacteria (5.9%).
- 64. Chronic Postoperative Endophthalmitis mostcommonly caused by Propionibacterium acnes Other bacteria with limited virulence, such as Staphylococcus epidermidis and Corynebacterium P acnes may sequester itself between an intraocular lens (IOL) implant and the posterior capsule. In this relatively anaerobic The patient may present with slight blurring of vision and a persistent granulomatous inflammation that begins on average 3–4 months after surgery
- 65. • The differentialdiagnosis of chronic postoperative endophthalmitis includes noninfectious causes • such as lens-induced uveitis • intraocular inflammation from iris chafing resulting from IOL malposition, • uveitis-glaucoma-hyphema • syndrome, and intraocular lymphoma masquerade syndrome Pars plana vitrectomy and injection of intravitreal and endocapsular vancomycin is therapeutic in many cases of chronic postoperative bacterial endophthalmitis
- 66. Endogenous Endophthalmitis caused byhematogenous dissemination of bacterial organisms, resulting in intraocular infection there is an extraocular focus in 90% of cases The most common gram-positive organisms are Streptococcus species(endocarditis), Staphylococcus aureus (cutaneous infections), and Bacillus species (from intravenous drug The most common gram-negative organisms are Neisseria meningitidis, Haemophilus influenzae, and enteric organisms such as Escherichia coli and Klebsiella species
- 67. Clinical symptoms acute onsetof pain, photophobia, and blurred vision. Examination • severely reduced visual acuity, • periorbital and eyelid edema, and fibrin in the anteriorchamber; hypopyon may be present • . Small microabscesses in the retina or • subretinal space and white, centered retinal hemorrhages (Roth spots) may also be present antibiotic treatment is sometimes required for several weeks, depending on the organism isolated.