Ophthalmology

1. BY / S H I M A A H A S S A N
BACTERIAL OCULAR
INFECTIONS

2. Lecture outlines
 Ocular bacteriology
 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 mucous membranes of the normal upper
respiratory tract and female genital tract

6. Gram-negative Cocci
Neisseria

7. Gram-positive Rods
Propionibacterium acne

8. Gram-negative Rods
Pseudomonas aeruginosa

9. Bacterial Infections of the 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 anterior to 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 cellulitis involves 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 of the 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 corneal and/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 or infectious 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 in Children 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
acute inflammatory 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 cases of 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
explosive onset 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
 . Current treatment 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
typically develops 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 bacterium C 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 disease that 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 of trachoma 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 for treatment 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
sexually transmitted 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 the following 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 in neonates
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
Chlamydial conjunctivitis 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
Granulomatous conjunctivitis 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 of the 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 ,conjunctival injection, 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 Academy of 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 to antibiotic 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 and fungal 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 therapy is 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 bacterial infection 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 interstitial keratitis

51. Acquired syphilis
Uveitis may occur 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 at the level of the pigment
epithelium

55. The diagnosis of syphilitic 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 by the 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 ocular TB 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 masquerading as
atypical serpiginous-like choroiditis

61. Diagnosis
Definitive diagnosis of TB 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 course of INH, rifampin, and pyrazinamide administered
daily, followed by a continuation phase of 4–7 months

63. Endophthalmitis
Infectious endophthalmitis may present 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
most commonly 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 differential diagnosis 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 by hematogenous 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 onset of 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.