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IMMUNOLOGY: Definitions
-Name some characteristics of innate immunity
-What are the main stimuli for innate immune reactions?
-Is there molecular variation in the receptors for innate immunity?
Definitions
-Innate immunity: antigen-independent, stereotyped/preprogrammed response to stimuli, nonspecific effector cells recruited, stimuli removed in nonspecific ways (phagocytosis, enzyme degradation)
-Main stimuli: molecular motifs on triggering stimuli
-Receptors of innate immunity are identical within all individuals of a species
IMMUNOLOGY: Definitions
-Name similarities and differences between the innate and adaptive immune responses
Definitions
-BOTH: use WBC receptors to recognize offending stimuli (but different types of receptors used by each), trigger inflammation, use nonspecific effector cells to carry out functions
-DIFFERENCES: triggers (adaptive - antigen; innate - toxins, cell debris of bacteria); recognition receptors, time of onset (adaptive is delayed, innate is fast), memory & specificity (only in adaptive immunity)
IMMUNOLOGY: Definitions
-What cells are increased in number in vernal keratoconjunctivitis?
-What are the 3 main functions of monocytes/macrophages?
Definitions
-Mast cells: increased number in conj of pts w/ VKC
-Macrophages (tissue)/monocytes (blood): scavengers, APCs for T cells, inflammatory effector cells
IMMUNOLOGY: Definitions
-What are dendritic cells?
-What are Langerhans cells?
Definitions
-Dendritic cells: mononuclear cells distinct from monocytes/macrophages; involved in antigen presentation --> initiate responses in quiescent lymphocytes
-Langerhans cells: subset of dendritic cells in conj & limbus --> the only cells in these areas to express MHC II
IMMUNOLOGY: Definitions
-Where do B & T cells mature, respectively?
-What are 2 important lymphoid structures in the adaptive immune response?
Definitions:
-B cells: mature in Bone marrow
-T cells: mature in Thymus
-Spleen & lymph nodes: important in adaptive immunity
IMMUNOLOGY: Definitions
-Describe the process by which an APC presents stimuli to T cells
-What is the relationship b/w type of HLA molecule and different antigens
Definitions
-APC phagocytoze antigen --> carry it to lymph node --> present Ag fragments within groove of HLA molecule on cell surface to T cells --> stimulation of T cells
-Different HLA molecules are capable of binding to different antigen types (therefore the HLA type determines the repertoire of antigens capable of being presented to a T cell by an APC)
-Note: this is why APCs from 1 individual cannot present to T cells from another individuals UNLESS the 2 individuals share HLA haplotype
IMMUNOLOGY: Definitions
-What cells carry class II MHC molecules? What cells are stimulated by class II cells?
-What cells carry class I MHC molecules? What cells are stimulated by class I cells?
Definitions:
-Class II MHC: present on macrophages, dendritic cells --> recognized by CD4 T cells
-Class I MHC: present on all nucleated cells --> recognized by CD8 T cells
IMMUNOLOGY: Definitions
-What Ig's do naive B cells have on surface? What is the function of these Ig's?
-Do B cells require Ag processing by APCs?
-What is the difference b/w a naive and an activated B cell? What regulates the activities of active B cells?
Definitions
-Naive B cells: have IgM & IgD on surface --> these serve at Ag receptors for the B cell
-B cells DO NOT require Ag processing by APCs
-Active B cells have ability to switch from IgM to another class --> this is regulated by cytokines released by CD4 cells
IMMUNOLOGY: Definitions
-What are the 2 antigen-specific effectors of adaptive immunity?
-Describe the 2 exposures required for effector cells
Definitions
-Ag-specific effectors of adaptive immunity: T cells, B cells + their Abs
-2 exposures needed for these effector cells: 1) initial exposure --> priming/activation within lymph node; 2) second exposure --> restimulation in the peripheral tissue where initial Ag found
IMMUNOLOGY: Definitions
-What are differences b/w primary and secondary immune responses?
-Why is the secondary immune response shorter?
Definitions:
-Primary response: Ag must find the rare B/T cells specific to it --> these cells are then stimulated from a resting/naive state
-Secondary response: B/T cells active during primary response are re-activated within 12-24 hours of repeat Ag exposure; more B/T cells specific for the Ag are present due to previous exposure (these cells may migrate to other sites of Ag encounter); low levels of Ag may persist in node/site so chronic low grade Ag stimulation may continually occur --> this is why secondary response is faster
IMMUNOLOGY: Ocular immunology
-What are immunologic features of the conjunctiva?
Ocular immunology
-Immunologic features of conjunctiva: drainage to preauricular/submandibular nodes, APCs, foliclles, mast cells, IgE mediated degranulation of mast cells, IgA (most abundant Ab in tear film)
IMMUNOLOGY: Ocular immunology
-What is MALT (mucosa-associated lymphoid tissue)?
-What are its immunologic features?
Ocular immunology
-MALT: mucosal sites (GI/GU tracts, respiratory tract, ocular surface/adnexae) that are connected by specific immunologic features
-Features: 1) rich in APCs, 2) specialized structures for localized Ag processing, 3) unique effector cells (i.e., mast cells)
-Effector B & T cells have universal response to ALL MALT sites in response to immunization at one site
-TH2 responses favored --> predominantly IgA & IgE antibodies produced
IMMUNOLOGY: Ocular immunology
-Since the eye does not contain lymphatics, how is particulate matter cleared?
-What structures in the anterior segment contain APCs?
-Where does immune processing by the APCs occur?
-What are unique features of the vitreous compared to aqueous?
Ocular immunology
-Clearance of particulate matter from inner eye depends on aqueous humor outflow channels, endocytosis by TM macrophages and endothelial cells
-Immune processing does NOT occur locally --> APCs travel to spleen --> TH2 response favored
-Vitreous: gel can bind charged proteins --> may serve as antigen depot for leukocyte adhesion
IMMUNOLOGY: Ocular immunology
-What is anterior chamber-associated immune deviation (ACAID)? What are its specific features?
Ocular immunology
-ACAID: "deviant" immune response in AC --> robust systemic Ab response to an Ag but lack of delayed hypersensitivity response to that Ag
-Features: decreased effectivity of TH1 DH cells, CD8/NK cells and complement in anterior uvea compared to elsewhere, presence of Fas ligand on iris/corneal endohtelium (induces lymphocyte apoptosis)
IMMUNOLOGY: Ocular immunology
-What are 5 factors that contribute to corneal graft rejection in experimental models?
Ocular immunology: K graft rejection
-Central corneal vascularization
-Stromal MHC molecule expression (usually very low)
-Graft contamination w/ donor-derived APCs
-MHC disparity b/w donor & recipient
-Pre-immunization of recipient to donor transplantation Ags
IMMUNOLOGY: Innate effectors
-What is another name for endotoxin? Which component is responsible for most of the inflammatory effects of endotoxin?
-What types of molecules are exotoxins? Examples?
Innate effectors
-Endotoxin (LPS): component of gram negative bacterial cell walls --> lipid A is most important mediator of inflammation
-Exotoxins: enzymes that cause tissue damage --> leads to inflammation (ex: streptolysin O, C. perfringens toxin, collagenases)
IMMUNOLOGY: Innate effectors
-Name 3 other triggers/modulators of innate immunity
-What are the 2 most important receptors for phagocytosis of pathogens?
Innate effectors
-3 other nonspecific modulators: complement, acute phase reactants, enzymes in tear film
-Phagocytosis: mediated by antibody Fc receptors & complement receptors (pathogens complex w/ Abs or complement --> ingested by cell displaying one of these receptors)
IMMUNOLOGY: Innate effectors
-What are the functions of resting, primed, stimulated & activated macrophages (respectively)?
Innate effectors: Macrophages
-Resting: scavengers
-Primed: Ag-presentation (express MHC class II)
-Stimulated: wound repair, angiogenesis, mild inflammation (incompletely activated)
-Activated: severe inflammation, tumoricidal, bactericidal --> epitheliod cells & giant cells are terminally differentiated forms
IMMUNOLOGY: Adaptive effectors
-What is an immune hypersensitivity reaction?
-In an immunoglobulin, what part defines the specific isotype?
-What is the name for the Ag-recognition part of the Ig molecule?
-What is the name for the effector cell-binding part of the Ig molecule?
Adaptive effectors
-Immune hypersensitivity reaction: inflammation due to adaptive immune response
-Heavy chain: defines specific Ab isotype
-Fab region (hypervariable region): contains Ag-recognition domain
-Fc region: attachment site for effector cells
IMMUNOLOGY: Adaptive effectors
-What are idiotopes and epitopes on an antibody molecule?
-Distinguish b/w a monoclonal and polyclonal antibody response
Adaptive effectors
-Idiotope: region of antibody itself that is antigenic (idiotypes are antibodies to idiotopes)
-Epitope: antigenic site on foreign molecule
-Polyclonal: population of all ag-specific Abs to various epitopes (Abs are derived from different B cell clones)
-Monoclonal: products of 1 specific B cell (i.e. myeloma)
IMMUNOLOGY: Adaptive effectors
-What are functions of Ag-Ab complexes in the intravascular space?
-What is the classic clinical setting in which immune complexes cause disease?
Adaptive effectors
-Intravascular Ag-Ab complexes: 1) neutralization of pathogen ability to bind cells; 2) opsonization (facilitates clearance of pathogen); 3) agglutinization (complex precipitates out of solution); 4) cytolysis via complement activation
-Classic example: serum sickness
IMMUNOLOGY: Adaptive effectors
-What are the features of Ag-Ab complexes in peripheral tissues?
-Which Ig subclass can passively leak into peripheral tissues?
Adaptive effectors
-Ag-Ab complexes in peripheral tissues: complement-mediated cell lysis via MAC, production of anaphylotoxins (complement fragments) in Arthus reaction, stimulation of target cells (Graves disease)
-IgG subclass can passively leak into peripheral tissues
IMMUNOLOGY: Adaptive effectors
-How is an Arthus reaction different from intravascular Ag-Ab complexes?
-What is a chronic Arthus reaction?
Adaptive effectors
-Arthus reaction caused by LOCALLY formed Ag-Ab complexes (not formed in blood)
-Chronic Arthus reaction: lymphocytes, plasma cells, granulomatous features --> caused by persistence of Ag within the site
IMMUNOLOGY: Adaptive effectors
-What disease states are produced by TH1 reactions?
-What disease states are produced by TH2 reactions?
Adaptive effectors
-TH1: classic delayed hypersensitivity reaction (i.e., PPD), intracellular infection, fungal infection, transplant rejection, most severe forms of inflammation
-TH2: atopic disease, parasitic infections
IMMUNOLOGY: Adaptive effectors
-What disease states are associated with CD8 T cells?
-What is the ideal CD8 T cell antigen?
-What cell assists in differentiation of CD8 T cells?
Adaptive effectors
-Involved in tumors, viruses, graft rejection
-Ideal antigen: intracellular protein
-Requires CD4 T cells to fully differentiate
IMMUNOLOGY: Adaptive effectors
-What are the 2 mechanisms by which CD8 T cells kill cells?
-What is one similarity and one difference b/w NK cells and CD8 T cells?
Adaptive effectors
-CD8 killing mechanisms: 1) assassination (lysis of target cell w/ perforin); 2) suicide induction (apoptosis of target cell w/ Fas ligand)
-NK cells: kill using same mechanisms as CD8 cells but do not have a specific Ag receptor (unlike CD8 cells)
IMMUNOLOGY: Adaptive effectors
-What are lymphokine-activated T cells?
Adaptive effectors
-Lymphokine-activated T cells: T cells that are nonspecifically activated by iatrogenic administration of immune cytokines (i.e., IL-2)
IMMUNOLOGY: Amplifiers of immune response
-By which pathway is complement activated in active and innate immunity, respectively?
-What are the 4 basic functions of complement?
-What are the principal complement-derived mediators?
Amplifiers of immune response
-Complement activated by classic pathway in adaptive immunity, alternative pathway in innate immunity
-4 functions: 1) enhance phagocytosis, 2) promote cell membrane lysis; 3) recruit neutrophils, induce inflammation; 4) modulates Ag-specific immune responses
-Principal complement-derived mediators: anaphylotoxins (induce chemotaxis and change in cell adhesiveness)
IMMUNOLOGY: Amplifiers of immune response
-What are the effects of kinins? What is the best known kinin?
-What are the effects of fibrin? What is fibrin deposition a clinical sign of?
-What are the effects of vasoactive amines? What are the sources of each type?
Amplifiers of immune response
-Kinins: vasodilation, pain, increased vascular permeability, Arachidonic acid metabolism stimulation (bradykinin = best known kinin)
-Fibrin: hemostasis, fibrosis, angiogenesis, leukocyte adhesion (clinical sign of delayed hypersensitivity)
-Vasoactive amines (serotonin and histamine): increase vascular permeability and blood flow, mediate allergic reactions
-Serotonin: found in platelets
-Histamine: mast cell, basophil granules
IMMUNOLOGY: Tolerance
-What are mechanisms of immunologic tolerance?
-What is a mechanism of autoimmunity?
Tolerance
-Mechanisms of tolerance: CLONAL DELETION (destruction of self-reactive T cells by thymus), ANERGY (Ag-specific B/T cells rendered incapable of mounting inflammatory response), REGULATION (regulatory T cells to balance population of inflammatory T cells), NON COMPLEMENT-FIXATING ABS (anti-self Abs that are unable to fix complement so do not cause inflammatory response)
-Mechanism of autoimmunity: molecular mimicry (immunologic cross-reaction b/w epitopes of unrelated foreign Ag and self-epitopes w/ similar structures)
IMMUNOLOGY: HLA
-What are HLA molecules and what is their function?
HLA
-HLA molecules are major histocompatibility complex proteins (MHC) expressed on surface of APCs
-Type of HLA haplotype determines repertoire of Ags to which individual can respond (not all HLA molecules can bind all Ags) --> some HLA haplotypes will be unable to mount a T cell response response to certain Ags if unable to bind these Ags
IMMUNOLOGY: HLA
-What % of pts w/ acute anterior uveitis have HLA-B27 haplotype?
-What is the proposed pathophysiology of HLA-B27 associated uveitis?
HLA
-50% of pts w/ anterior uveitis are HLA-B27+ (pathogenesis unknown)
-HLA-B27 assoc uveitis: individuals w/ specific HLA molecule type are predisposed to processing certain Ags that also cross-react w/ certain self Ags --> uveitis occurs
UVEITIS: Classification
-What is the etiology of most types of anterior uveitis? posterior uveitis?
-What is intermediate uveitis?
Classification
-Anterior uveitis --> mostly sterile, inflammatory reactions
-Posterior uveitis --> usually infectious
-Intermediate uveitis --> inflamm of posterior ciliary body, pars plana (floaters, CME, cataract may occur)
UVEITIS: Classification
-What are the most common causes of panuveitis?
Classification
-Panuveitis: Tb, syphilis, Lyme, sarcoidosis, sympathetic ophthalmia, Bechet's, VKH
UVEITIS: Symptoms
-What are consequences of chronic uveitis?
-What is the definition of recurrent uveitis?
-What is the most common cause of eye pain in uveitis?
Symptoms
-Chronic uveitis: complicated by cyclitic membrane (w/ secondary CB detachment, hypotony), calcific band keratopathy, cataract, CME --> decreased vision
-Recurrent uveitis: periods of inactivity for >3 months off all meds, followed by return of sx
-Pain in uveitis is secondary to iris inflammation, secondary glaucoma or ciliary spasm --> may radiate over trigeminal nerve (V) distribution
UVEITIS: Signs
-What is the predominant intraocular inflammatory cell in uveitis?
-What are signs of anterior uveitis?
-Name 3 types of iris nodules and their location
Signs
-Lymphocyte = predominant inflammatory cell in uveitis
-Signs of anterior uveitis: KP, cells, flare, fibrin, hypopyon, pigment dispersion, iris nodules, miosis
-3 types of iris nodules: Koeppe (pupillary border), Busacca (mid-iris), Berlin (iris angle)
UVEITIS: Signs
-What are 4 types of AC reaction and what are the predominant cell types in each?
Signs
-Serous (aqueous flare, protein influx)
-Purulent (PMNs, necrotic debris, hypopyon)
-Fibrinous (plasmoid)
-Sanguinoid (inflammation + RBCs)
UVEITIS: Signs
-How are AC cells and flare graded?
Signs
-AC cells graded by looking at # of cells in 1x1mm slit beam: if < 15 (0-1+), 15-50 (2-3+), > 50 (4+)
-AC flare graded by visibility of iris/lens detail: if details clear (0-2+), if hazy (3+), if fibrin or plasmoid aqueous (4+)
UVEITIS: Signs
-What is the mechanism for low and high IOP in uveitis?
Signs
-Low IOP (more common): decreased aqueous production or increased alternative outflow
-High IOP: inflammatory cells/debris clog TM or trabeculitis (inflammation of TM itself)
UVEITIS: Testing
-What are the differences b/w type I and type 2 patterns on ICG?
Testing - ICG
-Type 1 pattern: early and late multifocal areas of hypofluorescence (MEWDS)
-Type 2 pattern: early hypofluorescence, late hyperfluorescence (sarcoid, SO, birdshot, VKH)
UVEITIS: Medical mgmt
-Why are mydriatics and cycloplegic agents used in uveitis?
-What is the utility of topical NSAIDS? Side effects?
Medical mgmt
-Mydriatics/cycloplegics: prevent posterior synechiae formation, relieve photophobia associated w/ ciliary spasm
-NSAIDs: reduce prostaglandin synthesis in inflammation; useful for postop inflammation/CME but unclear utility for endogenous anterior uveitis
-Side effects of NSAIDs: GI bleeding/ulceration, hepatotoxicity, nephrotoxicity
UVEITIS: Medical mgmt
-How should steroid tx be initiated?
-What are indications for periocular steroids?
-When should periocular steroids be avoided?
Medical mgmt
-Initiation of steroids: start high dose --> taper as inflammation subsides
-Periocular steroid indications: need for more posterior effect than that provided by topicals, poor response to topical/systemic steroids
-Avoid periocular steroids in necrotizing scleritis or infectious uveitis
UVEITIS: Medical mgmt
-What are indications for systemic steroids?
-What are indications for starting immunomodulatory therapy?
Medical mgmt
-Systemic steroid indications: vision threatening chronic uveitis w/ insufficient control w/ topical meds, need for treatment of systemic disease
-Immunomodulatory therapy indications: pt requires dose of steroids > 10 mg/day for chronic treatment, if pt needs steroids > 3 months, failed tx w/ steroids, contraindicated steroids, reversible disease
UVEITIS: Medical mgmt
-What are indications for the sustained release fluocinolone implant? What are the most common side effects?
Medical mgmt
-Sustained release fluocinolone implant: for chronic noninfectious posterior uveitis --> releases drug for median of 30 months
-side effects: cataract (seen in nearly all phakic pts), glaucoma (60% of pts)
UVEITIS: Medical mgmt
Name drugs in each category...
-Antimetabolites
-Inhibitors of T-cell signaling
-Alkylating agents
-Biologics
Medical mgmt
-Antimetabolites: MTX, azathioprine, mycophenolate mofetil
-T cell signaling inhibitors: cyclosporine, tacrolimus, sirolimus
-Alkylating agents: cyclophosphamide, chlorambucil
-Biologics (cytokine inhibitors): etanercept, infliximab, daclizumab, etc
UVEITIS: Medical mgmt
-What is the first line drug of choice in immunomodulation with children? Which disease has been studied for this?
-What drug category is used only if other drugs fail? For which disease are these drugs first line?
Medical mgmt
-Methotrexate: first line immunomodulatory agent in children (long success record in JIA/JRA)
-Alkylating agents (cyclophosphamide, chlorambucil) are used only if other drugs fail --> increased risk of malignancy
**Note: alklyating agents are 1st line tx for necrotizing scleritis assoc w/ systemic vasculitides
AUTOIMMUNE: Anterior uveitis
-What are the 2 most common patterns of acute anterior uveitis?
-What are the seronegative spondyloarthropathies associated with HLA-B27 uveitis?
Anterior uveitis
-2 patterns: 1) acute, unilateral, recurrent in either eye; 2) acute, bilateral, assoc w/ tubulointerstitial nephritis
-HLA-B27 associated uveitis: assoc w/ spondyloarthropathies (ankylosing spondylitis, Reiter syndrome/reactive arthritis, psoriatic arthritis, IBD)
AUTOIMMUNE: Anterior uveitis
-What are the typical symptoms of ankylosing spondylitis? Xray findings?
-Mainstay of treatment?
-Drug that reduces ocular recurrences?
-What % of pts have +HLA-B27?
Anterior uveitis
-AS: low back pain/stiffness after inactivity
-Xray: sclerosis, narrowing of joint space, fusion of vertebrae on sacroiliac views
-NSAIDS = mainstay of tx
-Sulfasalazine: may reduce frequency of iritis recurrences
-HLA-B27+ in 90% of pts
AUTOIMMUNE: Anterior uveitis
-What is the triad of Reiter syndrome?
-What 2 other conditions are considered major diagnostic criteria?
Anterior uveitis
-Reiter syndrome triad: urethritis, polyarthritis, conjunctivitis + iritis
-Other important conditions: 1) keratoderma blennorrhagicum (scaly eruptions on palms/soles); 2) circinate balanitis (circumferential rash of distal penis)
AUTOIMMUNE: Anterior uveitis
-What % of pts w/ Reiter syndrome have +HLA-B27?
-What are organisms assoc w/ triggering infections?
-Most common population of pts w/ disease?
-Most common eye finding in Reiter's syndrome?
Anterior uveitis
-85-95% have +HLA-B27
-Triggering infections: Shigella, Salmonella, Yersinia, Chlamydia, Ureaplasma
-Epi: young adult males
-Most common ocular finding: mucupurulent, papillary conjunctivitis (nongranulomatous iritis in 5-10% of pts)
AUTOIMMUNE: Anterior uveitis
-What % of pts w/ IBD have HLA-B27+?
-What are features of psoriasis-assoc uveitis? (compared to other forms of HLA-B27 assoc uveitis)
-Clinical features of psoriasis?
Anterior uveitis
-60% of pts w/ IBD have HLA-B27+
-Psoriasis-assoc uveitis: older mean age of onset, bilateral, more chronic, requires PO NSAIDs
-Psoriasis features: sausage digits, erythematous hyperkeratotic rash, nailbed pitting, subungual hyperkeratosis
AUTOIMMUNE: Anterior uveitis
-What population gets tubulointerstitial nephritis uveitis (TINU)?
-Diagnostic criteria?
-Mgmt?
Anterior uveitis - TINU
-Adolescent girls (11-120), women (early 30s)
-Diagnosis: 1) abnl serum Cr or decreased Cr clearance; 2) abnormal U/A; 3) systemic illness (constitutional sx, abnl LFTs, etc)
-Mgmt: high dose PO steroids
AUTOIMMUNE: Anterior uveitis
-What is the clinical presentation of Poser-Schlossman syndrome? What meds should be used and avoided in mgmt?
Anterior uveitis - Posner-Schlossman
-Presentation: unilateral, mild acute iritis w/ markedly elevated IOP, K edema, fine KP, low grade cell/flare
-Mgmt: topical steroids & IOP lowering meds --> avoid Pilo (may exacerbate ciliary spasm)
AUTOIMMUNE: Anterior uveitis
-How does lens-associated uveitis occur?
-How does the uveitis present?
-Histologic appearance?
-Mgmt?
Anterior uveitis - Lens-associated uveitis
-Pathophysiology: altered tolerance to lens proteins --> immune reaction to lens material released via leakage from capsule in hypermature cataract OR following trauma to capsule
-Uveitis: KPs present; may be granulomatous OR nongranulomatous, no fundus lesions
-Mgmt: surgical removal of all lens material (curative)
AUTOIMMUNE: Anterior uveitis
-Pathophysiology of phacolytic glaucoma?
-Are KPs present? Other features of the uveitis?
Anterior uveitis - Phacolytic glaucoma
-Pathophysiology: leakage of lens protein thru capsule in hypermature cataracts --> TM clogging by lens material & engorged macrophages --> acute IOP rise
-Uveitis: NO KPs, no synechiae, presence of refractile bodies in AC (lipid laden macrophages)
AUTOIMMUNE: Anterior uveitis
-What are mechanisms of IOL-associated uveitis?
-What is the most severe form of IOL-assocaited uveitis called?
Anterior uveitis - IOL-associated uveitis
-Mechanisms: retained lens material, effect of surgery itself, iris chafing by IOL, K touch by IOL --> endothel decompensation & inflammation
-UGH = most severe form of IOL-associated uveitis
AUTOIMMUNE: Anterior uveitis
-Name some medications that are associated w/ uveitis
Anterior uveitis - Drug-associated
-Rifabutin
-Bisphosphonates
-Sulfonamides
-OCPs
-Diethylcarbamazine (anti-filarial)
-Topicals: prostaglandin analogs, anticholinesterase inhibitors, metipranol (beta blocker)
AUTOIMMUNE: Anterior uveitis
-What is the most common systemic disease assoc w/ anterior uveitis in children?
-What are the 3 subtypes of this disease? Risk of uveitis w/ each type?
Anterior uveitis - JIA/JRA associated
-JIA/JRA = most common systemic disease assoc w/ iritis in pediatric age group
-Definition: arthritis beginning before age 16, lasting at least 6 weeks
1) Systemic (Still disease): <5 yo, systemic sx w/ minimal joint inflammation initially, rarely assoc w/ uveitis
2) Polyarticular: > 4 joints involved, 7-14% get uveitis, if +RF --> no uveitis
3) Pauciarticular: < 4 joints, account for 80-90% of JIA pts w/ uveitis, type 1 (females, <5yo, ANA +), type 2 (males, older, 75% HLA-B27+)
AUTOIMMUNE: Anterior uveitis
-What is the correlation b/w joint and ocular inflammation in JIA?
-What is the average age of onset of uveitis in JIA?
-What are major risk factors for development of uveitis in JIA?
Anterior uveitis
-No correlation b/w ocular & joint inflammation in JIA-uveitis
-Risk factors: female, pauciarticular, ANA+, RF negative
-Average age of onset of uveitis = 6 yo
AUTOIMMUNE: Anterior uveitis
-What is the recommended screening schedule for uveitis in JIA pts? (i.e., screening schedule for <7 yo and >7yo)
-When should steroids be initiated?
-What is the most commonly used steroid-sparing agent?
Anterior uveitis - JIA-associated
-Screening for <7 yo: q3-4 mo (if ANA+), q6 mo (if ANA neg)
-Screening for >7yo: q6 months for all except Still's disease
-Still disease: q12 months
-Indications for steroids: active cellular reaction (do not use in pts w/ chronic flare but no cell)
-MTX (weekly, low dose): most commonly used steroid-sparing drug
AUTOIMMUNE: Anterior uveitis
-What are complications of cataract surgery in pts w/ JIA uveitis who develop cataract?
-What are some guidelines to follow in considering cataract surgery in JIA pts?
Anterior uveitis - JIA-associated
-Cataract surgery in JIA pts complicated by aggressive post-op inflammation
-Guidelines for cataract surgery: inflamm should be well controlled for at least 3 months, use only acrylic lenses, low threshold for explantation of IOL, close follow up, long term immunomodulatory tx before and after surgery
AUTOIMMUNE: Anterior uveitis
-What is the clinical presentation of Fuch's heterochromic iridocyclitis?
-When does the lighter colored iris indicate the involved eye?
-What are characteristics of abnormal vessels within the angle in this disease?
-What is a major cause of visual disability?
-Prognosis?
Anterior uveitis - Fuch's heterochromic iridocyclitis
-Presentation: unilateral, diffuse iris stromal atrophy, diffuse stellate KPs, AC and vitreous cells
-Typically DO NOT see synechiae, fundus lesions
-Complicated by glaucoma, cataract
-AC angle shows abnormal vessels bridging the angle --> can bleed during surgery --> postop hyphema
-Visual disability may result from vitreous opacification, even after uncomplicated CE/IOL
-Good prognosis, but inflamm may persist for decades
AUTOIMMUNE: Intermediate uveitis
-Int uveitis accounts for what % of all cases of uveitis?
-What is the most common form of intermediate uveitis?
Intermediate uveitis
-Accounts for 15% of all cases of uveitis
-Pars planitis = snowbanks, snowballs w/o associated infection/systemic disease --> most common form of intermediate uveitis
AUTOIMMUNE: Intermediate uveitis - Pars planitis
-Age distribution?
-HLA associations?
-Laterality?
-What % of cases develop CME, neovasc, RD?
Intermediate uveitis - Pars planitis
-Bimodal age distribution (5-15 yo, 20-40 yo)
-HLA-DR15 & DR51 (DR15 also assoc w/ MS)
-80% bilateral
-CME, neovasc & RD develop in 10% of pts
AUTOIMMUNE: Intermediate uveitis - Pars planitis
-What other causes of intermediate uveitis must be ruled out before dx of pars planitis is made?
-What dx should be considered in presence of vitritis w/o any other ocular features?
-Histology?
Intermediate uveitis - Pars planitis
-Other causes of intermediate uveitis: syphilis, Lyme, Tb, toxocariasis, MS, sarcoid
-Consider primary CNS lymphoma if vitritis seen w/o other ocular disease features
-Histology: vitreous condensation & cellular infiltration at vitreous base --> macrophages, lymphoctes, plasma cells
AUTOIMMUNE: Intermediate uveitis - Pars planitis
-Prognosis?
-Indications for treatment?
-Steps 1, 2, 3 & 4 of treatment approach?
Intermediate uveitis - Pars planitis
-Prognosis: 10% self-limited, 30% smoldering, 60% prolonged course w/o exacerbations (disease may burn out after 5-15 yrs)
-Indications for treatment: VA affected, symptoms present, CME/retinal vasculitis present (may not need tx if mild cases w/ no CME)
-Step 1: periocular steroids (1st line) --> systemic steroids --> intravitreal steroids
-Step 2: laser/cryo to peripheral retina (do not directly treat snowbanks)
-Step 3: PPV, peripheral laser (use if systemic immunomodulatory tx is contraindicated)
-Step 4: systemic immunomodulation (if all else fails) --> MTX and cyclosporine preferred
AUTOIMMUNE: Intermediate uveitis - Pars planitis
-What are the most common complications and their incidence?
Intermediate uveitis - Pars planitis
-Complications: cataract (15-60%), glaucoma (10%), CME (50% --> hallmark of pars planitis), neovasc (5-15%)
AUTOIMMUNE: Intermediate uveitis - MS
-What is the incidence of uveitis in MS?
-Laterality?
-HLA association?
-Severity of illness compared to pars planitis?
Intermediate uveitis - MS
-1% incidence of uveitis in MS (10x more common in MS pts than in general population)
-95% of cases bilateral
-HLA-DR15 association
-Tends to be milder disease than in pars planitis
AUTOIMMUNE: Posterior uveitis
-What are the most common races affected by SLE?
-Pathophysiology?
-Antibodies associated?
-What % of cases have ocular involvement?
Posterior uveitis - SLE
-African Americans & Hispanics most commonly affected
-Pathophys: polyclonal B cell activation --> hypergammaglobulinemia, autoantibodies, immune complex deposition
-Antibodies: Anti-ssdNA/dsDNA, anti-Sm/Ro/La, antiphospholipid, ANA
-Ocular manifestations in 50% of pts
AUTOIMMUNE: Posterior uveitis
-Which ocular manifestation of SLE is considered an important marker of systemic disease activity?
-How does this ocular disease present?
Posterior uveitis - SLE
-Lupus retinopathy = important marker of systemic disease activity
-Manifestations: cotton wool spots +/- retinal hemorrhages, retinal vascular occlusive disease (arterial/venous thrombosis --> ischemia, neovasc, hemorrhage --> seen w/ antiphospholipid Ab), choroidopathy (ischemia, CNV)
AUTOIMMUNE: Posterior uveitis
-What is polyarteritis nodosa (PAN)?
-Pathogenesis?
-Associations (gender, systemic disease)?
-Antibody?
Posterior uveitis - PAN
-Definition: focal, episodic, necrotizing vasculitis of small/medium sized muscular arteries
-Assoc w/ men, Hep B positivity
-Pathogenesis: immune complex deposition
-p-ANCA positive suggestive of diagnosis
AUTOIMMUNE: Posterior uveitis - PAN
-What is the most common symptom?
-What % of pts have ocular involvement?
-Name some manifestations of ocular disease in PAN
Posterior uveitis - PAN
-Most common symptom: mononeuritis multiplex
-Suspect PAN in any pt w/ retinal vasculitis + multiple systemic complaints concerning for necrotizing vasculitis
-Ocular disease: choroidal infarction, Elschnig spots, neuro-oph disease, PUK, scleritis
AUTOIMMUNE: Posterior scleritis - Wegener's
-Classic triad?
-Most characteristic clinical feature?
-What % of pts have ocular/orbital involvement?
-What % of pts have uveitis?
-Antibody?
Posterior scleritis - Wegener's
-Classic triad: necrotizing granulomatous inflammation of upper and lower respiratory tracts, focal segmental glomerulonephritis, necrotizing vasculitis of small arteries/veins
-Characteristic clinical feature: involvement of paranasal sinuses
-15% have eye involvement at presentation (29% during course of illness)
-10% have uveitis
-c-ANCA positive
AUTOIMMUNE: White dot syndromes - Birdshot
-Epidemiology?
-HLA association?
-Distribution of lesions?
-Mgmt and clinical course?
-ICG?
White dot syndromes - Birdshot retinochoroidopathy
-Epi: Caucasian females, northern European, 4th decade
-HLA-A29+ in 90%
-Lesions concentrated nasally, spread radially (follow underlying choroidal vessels)
-ICG: multiple hypofluorescent spots (more numerous than seen on exam)
-Mgmt: multiple exacerbations/remissions --> give systemic steroids f/b early initaition of steroid-sparing tx
AUTOIMMUNE: White dot syndromes - APMPPE
-Laterality?
-Clinical features?
-IVFA?
-HLA association?
-ICG?
-Mgmt/prognosis?
White dot syndromes - APMPPE
-Bilateral (one eye first --> then other eye)
-50% w/ flulike prodrome
-50% have vitritis
-Large lesions (1-2 disc areas in size)
-IVFA: block early --> stain late in area w/ lesions
-ICG: hypofluorescence of lesions
-HLA-B7 & DR2
-Good prognosis (resolves over weeks, no recurrence); no treatment (steroids do not benefit)
AUTOIMMUNE: White dot syndromes - Serpiginous choroidopathy
-Pathophysiology?
-Genetic/Ag associations?
-Clinical features?
-Laterality?
-IVFA? ICG?
-Mgmt?
White dot syndromes - Serpiginous choroidopathy
-Immune-mediated occlusive vasculitis
-HLA-B7 & retinal S-Ag associations
-Clinical: no vitritis, pseudopodial/geographic lesions starting at disc
-Bilateral
-IVFA: Block early --> late staining of active edge of lesion
-ICG: early hypofluorescence --> late stain
-Recurrent, progressive --> unclear optimal mgmt (steroids alone = ineffective)
AUTOIMMUNE: White dot syndromes - MCP
-Epidemiology?
-Clinical?
-Complications & frequencies of each?
-IVFA? ICG?
-Prognosis/mgmt?
White dot syndromes - MCP
-Epi: young, myopic females
-Clinical: punched-out, white-yellow spots (like PIC & OHS), +vitritis in all cases (unlike PIC & OHS) --> dots evolve to atrophic scars
-Complications: CNV (33%), macular edema (14-41%)
-IVFA: block early --> stain late
-ICG: multiple hypofluorescent spots in mid-phase
-Prognosis: dx of exclusion, poor prognosis --> chronic, recurrent
-Steroids/immunosuppressive therapy
AUTOIMMUNE: White dot syndromes - PIC
-Epidemiology?
-Clinical?
-IVFA?
-ICG?
-Mgmt?
White dot syndromes - PIC
-Epi: young, myopic females
-Clinical: lesions rarely extend to midperiphery (unlike MCP), no vitritis, progress to atrophic scars, CNV is common
-IVFA: early HYPERfluorescence w/ late staining (unlike MCP)
-ICG: midphase hypofluorescence in peripapillary distribution (same as MCP)
-Favorable prognosis if CNV does not occur; mgmt includes periocular/systemic steroids
AUTOIMMUNE: White dot syndromes - SFU
-Epidemiology?
-Clinical?
-IVFA?
White dot syndromes - Subretinal fibrosis & uveitis syndrome
-Epi: young, myopic females
-Clinical: vitritis is present
-Chronic, recurrent
-IVFA: blocked areas & hyperfluorescence early --> late staining w/o leakage
AUTOIMMUNE: White dot syndromes - MEWDS
-Epidemiology?
-Clinical?
-VF defect?
-IVFA?
-ERG?
-Mgmt?
White dot syndromes - MEWDS
-Epi: young, myopic females
-Clinical: 80% unilateral, flulike prodrome, transitory lesions --> leave granular pigment changes (pathognomonic)
-VF: enlarged blind spot
-IVFA: wreath-like configuration of lesions around fovea, stain late
-ERG: decreased A wave and ERP amplitudes
-No treatment --> good prognosis
AUTOIMMUNE: White dot syndromes - ARPE
-Epidemiology?
-Clinical?
-IVFA?
-VF?
-ERG/EOG?
-Prognosis?
White dot syndromes - Acute retinal pigment epitheliitis (Krill disease)
-Epi: Healthy young adults
-Clinical: unilateral, small hyperpigmented lesions with yellow halo in posterior pole
-Central scotoma
-IVFA: early hyperfluorescence of dots and surrounding hyperfluorescent halo w/ late staining
-Normal ERG, abnormal EOG
-Prognosis: benign, self limited
AUTOIMMUNE: White dot syndromes - AZOOR
-Epidemiology?
-Clinical?
-ERG/EOG?
-Differential diagnosis?
White dot syndromes - Acute zonal occult outer retinopathy (AZOOR)
-Epi: young, myopic females
-Clinical: initial subtle RPE changes w/ depigmentation in areas of visual loss --> later, vessel attenuation, pigment migration, focal perivenous sheathing
-Bilatearl, recurrent in 1/3 of cases
-50% have vitritis
-ERG: delayed 30-Hz flicker
-EOG: reduced light rise
-DDx: CAR, RP
AUTOIMMUNE: Panuveitis
-What % of pts w/ sarcoidosis have eye involvement?
-What is the most frequent ocular manifestation?
-Epidemiology?
-HLA association?
Panuveitis - Sarcoidosis
-15-50% of pts have eye involvement
-Uveitis = most frequent ocular manifestation (occurs in 2/3 of pts w/ ocular sarcoidosis)
-Epi: African Americans, F>M, pediatric disease rare
-HLA-DRB1 association
AUTOIMMUNE: Panuveitis
-What does a sarcoid tubercle contain (histologically)?
-What are Schaumann/lamellar bodies & asteroid bodies?
Panuveitis - Sarcoid
-Sarcoid tubercle: noncaseating granuloma --> epitheliod cells, multinucleated giant cells, thin rim of lymphocytes
-Schaumann/lamellar bodies: ovoid, basophilic, calcific bodies containing iron in cytoplasm of giant cells
-Asteroid bodies: star-shaped acidophilic bodies within cytoplasm of giant cells
AUTOIMMUNE: Panuveitis
-What is Lofgren syndrome?
-What is Heerfoldt syndrome?
Panuveitis - Sarcoidosis
-Lofgren syndrome: erythema nodosum, febrile arthropathy, hilar adenopathy, acute iritis
-Heerfordt syndrome: parotiditis, fever, facial nerve palsy, uveitis
AUTOIMMUNE: Panuveitis
-Name some ocular manifestations of sarcoidosis
Panuveitis - Sarcoidosis
-Granulomas (orbid, lids, etc)
-KCS
-Anterior uveitis
-Cornea, posterior disease
AUTOIMMUNE: Panuveitis
-What is the best screening test?
-What is the most sensitive imaging test?
-What combo of tests is most specific for the diagnosis in pts w/ active disease?
-Whihc lab tests reflect total body granuloma content?
-Definitive dx?
Panuveitis - Sarcoidosis
-CXR = best screening test
-Spiral CT = most sensitive screening test
-ACE + gallium scan = specific for dx in pts w/ active disease
-ACE, lysozyme = not diagnostic or specific, reflects total body granuloma content
-Histopathologic = definitive method of dx
AUTOIMMUNE: Panuveitis
-What is the most common precipitating event for sympathetic opththalmia?
-Clinical presentation?
-IVFA during acute stage?
-ICG?
Panuveitis - SO
-Ocular surgery (esp vitreoretinal) = most common precipitating factor for SO
-Clinical: bilateral diffuse granulomatous non-necrotizing uveitis; worse in exciting eye; Dalen-Fuchs nodules
-IVFA: multiple hyperfluorescent sites of leakage at RPE --> persists in late phase; dye pooling beneath exudative RD
-Dalen-Fuchs nodules appear hypofluorescent early (or have block early --> stain late pattern like APMPPE)
-ICG: numerous h ypofluorescent foci
AUTOIMMUNE: Panuveitis
-What does B scan show in sympathetic ophthalmia?
-What areas of the retina are involved in SO?
-What is the significance of Dalen-Fuchs nodules in SO?
-Are the immunogenetics of SO and VKH similar or different? How to distinguish b/w SO and VKH?
Panuveitis - SO
-B scan: choroidal thickening
-In SO, choroid primarily involved (no inflammation of choriocapillaris or retina)
-Dalen Fuchs nodules: present in 1/3 of pts w/ SO, not pathognomonic
-Immunogenetics of VKH & SO are identical (same associations found in both)
-How to distinguish: no history of trauma and presence of systemic sx in VKH
AUTOIMMUNE: Panuveitis
-Epidemiology of VKH?
-Pathophysiology?
-HLA assoc in Japanese?
Panuveitis - VKH
-Epi: darkly pigmented ethnic groups (but rare among African Americans); F>M in Japanese population
-Pathophys: T-cells directed against self-Ags assoc w/ melanocytes
-Target Ags on melanocytes: Tyrosinase/tyrosinase-related proteins, S-100 protein
-HLA-DR4 assoc in Japanese
AUTOIMMUNE: Panuveitis
-Describe the 4 stages of VKH
1) prodromal (systemic sx)?
2) acute (eye findings)?
3) convalescent (eye and systemic findings)?
4) chronic/recurrent
Panuveitis - VKH
-Prodromal stage: flulike sx, auditory problems (75%), meningismus, CSF lymphocytosis (80%)
-Acute uveitic stage: 1-2 days after CNS signs, cloverleaf shaped serous RD, nonnecrotizing granulomatous inflammation concentrated in peripapillary choroid, Dalen Fuchs nodules
-Convalescent stage: resolution of exudative RD, depigmentation of fundus (sunset glow fundus), depigmented Dalen Fuchs nodules, perilimbal vitiligo (Sugiura sign) in 85% of Japanese, alopecia, poliosis
-Chronic recurrent stage: if inadequately treated in stages 2 and 3
AUTOIMMUNE: Panuveitis
-What are essential features for diagnosis of VKH (to differentiate from SO)?
-IVFA?
-ICG?
-B-scan?
Panuveitis - VKH
-Essential for diagnosis: bilateral disease, no hx of trauma, no other ocular/systemic disease
-IVFA (acute): punctate hyperfluorescent lesionsat RPE --> pooling of dye in areas of exudative RD
-IVFA (chronic): multiple window defects 2/2 RPE loss/atrophy
-ICG: delay in choriocapillaris/choroidal vessel perfusion, multiple hypofluorescent spots
-Ultrasound: thickening of posterior choroid, most in peripapillary area --> extends to equator
AUTOIMMUNE: Panuveitis
-What is the management of acute and chronic VKH, respectively?
Panuveitis - VKH
-Acute: early, aggressive topical/periocular/systemic steroids & cycloplegia
-Chronic: recurrent episodes increasingly steroid resistant --> need immunomodulatory drugs
AUTOIMMUNE: Panuveitis
-Epidemiology of Bechet's?
-Pathophysiology?
-4 major diagnostic criteria?
Panuveitis - Bechet's
-Epi: eastern Mediterranean, eastern Asia; M>F
-Pathophys: lack of T-cell hypofunction, hyperactive B cells, no HLA association (sporadic), chronic relapsing occlusive vascuilitis
-4 diagnostic criteria: recurrent oral aphthous ulcers, skin lesions (i.e., erythema nodosum), recurrent genital ulcers, uveitis
AUTOIMMUNE: Panuveitis
-Describe the nature of uveitis in Bechet's disease
Panuveitis - Bechet's
-Explosive onset anterior uveitis (develops over hours)
-Posterior uveitis: essential retinal finding is an obliterative, necrotizing retinal vasculitis
-Optic nerve affected in 25%
AUTOIMMUNE: Panuveitis
-What are principles of mgmt of Bechet's disease? (i.e., meds used)
-Which immunomodulatory agent is most effective?
Panuveitis - Bechet's
-Steroids used initially, but most pts become resistant to corticosteroids --> eventually need immunomodulatory drugs
-Azthioprine, cyclophosphamide & chlorambucil used in Bechet's disease
-Chlorambucil may be the most effective of all immunomodulatory agents
INFECTIONS: Herpesvirus uveitis
-What organism should be considered in Ddx of chronic unilateral anterior uveitis?
-What conditions cause stellate KPs?
-What condition is a frequent complication and diagnostic hallmark of herpesvirus uveitis?
-What is the mechanism of this condition?
Herpesvirus uveitis
-Consider VZV in Ddx of chronic unilateral ant uveitis
-Stellate KP: seen in herpesvirus uveitis & Fuch's heterochromic iridocyclitis
-Glaucoma = frequent complication of herpetic uveitis & diagnostic hallmark (as uveitis usually causes low IOP)
-Mechanisms of glaucoma: trabeculiitis, TM obstruction by inflammatory cells
INFECTIONS: Herpesvirus uveitis
-What is varicella zoster sine herpete?
-What is the umbrella aterm for ARN/PORN type disease?
-What is the constellation of findings diagnostic of ARN?
Herpesvirus uveitis
-Varicella zoster sine herpete: development of ocular VZV disease w/o cutaneous component
-Necrotizing herpetic retinopathy: umbrella term for ARN, PORN
-Clinical findings for ARN: 1) occlusive retinal arteriolitis, 2) multifocal yellow-white peripheral retinitis, 3) vitritis, 4) significant AC reaction
INFECTIONS: Herpesvirus uveitis
-What is the mechanism of RD in pts w/ ARN?
-What etiologic agent of ARN is assoc w/ encephalitis?
-Name 2 diagnostic tests for ARN
Herpesvirus uveitis
-RD in ARN: 2/2 multiple retinal breaks, PVR --> can do prophylactic laser to uninvolved areas
-HSV-1 ARN assoc w/ HSV encephalitis
-Diagnosis of ARN: goldmann-witmer coefficient (if >4 indicates high intraocular Ab production, diagnostic); PCR (most sensitive, specific & rapid)
INFECTIONS: Herpesvirus uveitis
-What is the most common etiologic agent for ARN?
-What is the mgmt of ARN?
-What is PORN (pt population, most common organism, how to differentiate from ARN, prognosis, mgmt)?
Herpesvirus uveitis
-VZV = most common etiology of ARN
-Mgmt of ARN: IV acyclovir, f/b long term PO antivirals
-PORN (progressive outer retinal necrosis): advanced AIDS, immunosuppressed pts
-VZV = most common cause of PORN
-In contrast to ARN: post pole involved early, NO vitritis, minimal initial vasculitis
-Poor prognosis
-Mgmt: combo IV & intravitreal antivirals
INFECTIONS: Herpesvirus uveitis
-What are featues of non-necrotizing herpetic retinitis? (laterality, mgmt, clinical findings)
Herpesvirus uveitis
-Non-necrotizing herpetic retinitis: bilateral, systemic antivirals used for tx, can cause CME & birdshot-like appearance
INFECTIONS: Herpesvirus uveitis
-What is the most common congenital viral infection?
-Is it nessary to follow pts w/ presumed congenital infection even without ocular disease?
-What are the 3 forms of congenital infection?
Herpesvirus uveitis
-CMV = most common congenital viral infection
-Must follow pts w/ congenital CMV even w/o eye findings --> can develop later
-3 forms: fulminant (prominent hemorrhage, necrosis, post pole, assoc w/ vessels), granular (peripheral, minimal edema/heme/vascualr sheathing), perivascular (frosted branch angiitis)
INFECTIONS: Herpesvirus uveitis
-What is the most common ophthalmic manifestation of congenital CMV & HIV/AIDS-assoc CMV?
-How does CMV spread to the eye?
-What is the association b/w CMV retinitis and mortality in HIV/AIDS?
Herpesvirus uveitis
-CMV retinitis = most common ophthalmic manifestation of congen CMV & HIV/AIDS-assoc CMV
-Spreads hematogenously to eye --> infects retinal vascular endothelial cells
-CMV retinitis assoc w/ 1.6x increased mortality in HIV/AIDS --> treatment of CMV retinitis is assoc w/ decreased mortality (independent of other factors)
INFECTIONS: Herpesvirus uveitis
-What are histologic features of CMV retinitis?
Herpesvirus uveitis
-Histology of CMV retinitis: full thickness coagulative necrosis of retina w/ secondary diffuse choroiditis
-Eosinophilic intranclear inclusions
-Basophilic cytoplasmic inclusions
INFECTIONS: Herpesvirus uveitis
-Which herpesvirus has a tropism for B cells and is assoc w/ Burkitt lymphoma?
-What is the most common ocular manifestation of this condition?
-What is the name of the systemic infection associated with this virus?
Herpesvirus uveitis
-EBV has tropism for B cells, assoc w/ Burkitt lymphoma
-Follicular conjunctivitis (self limited) = most common ocular manifestation
-Infecious mononucleosis = systemic condition caused by EBV
INFECTIONS: Herpesvirus uveitis
-What are the antibodies that appear during acute mononucleosis?
-What antibody titers rise with the onset of clinical disease?
-Which antibody rises slowly and then persists for life?
-What antibodies are associated with chronic infection?
Herpesvirus uveitis
-IM: acute infection --> IgM and then IgG to viral capsid antigen appear
-Early antibody (EA) rises with onset of clinical disease (becomes undetectable 6-12 mo after resolution)
-Nuclear antibody (NA) rises slowly, persists for life
-Chronic disease: IgM for VCA and EA chronically elevated
INFECTIONS: Rubella
-What are the most common clinical findings assoc w/ congenital rubella syndrome?
-What are some systemic manifestations?
-DIagnostic criteria?
-Mgmt?
Rubella - Congenital
-Salt-and-pepper pigmentary retinopathy is most common ocular manifestation (25-50% of pts) --> assoc w/ nl vision, vessels & optic nerve
-Other findings: cataracts (15%), glaucoma (10%)
-Systemic: cardiac disease, deafness
-Diagnosis: need to see 4x increased IgG and new IgM Ab
-Supportive treatment
INFECTIONS: Rubella
-What are the most common ocular manifestations of acquired rubella infection?
-What are systemic features?
-Mgmt?
Rubella - Acquired
-Conjunctivitis is most common ocular manifestation (70%)
-Other eye disease: epithelial kerititis, multifocal chorioretinitis
-Systemic: rash spreading from face --> trunk; prodromal constitutional sx
-Supportive mgmt (can give steroids for retinitis)
INFECTIONS: Lymphocytic choriomeningitis virus
-What animal is the reservoir for this virus?
-What is the genetic material of this virus?
-Clinical findings? How to differentiate from congenital toxoplasmosis?
LCMV
-RNA virus
-Rodents = reservoir
-Similar findings to congenital toxo (chorioretinal scars, intracranial calcifications) --> note that in toxo, calcifications are diffuse; in LCMV, calcifications are periventricular
INFECTIONS: Measles
-What are the most common ocular complications of measles?
-Is measles retinopathy more common in congenital or acquired disease?
-What are ERG findings in measles retinopathy?
-Mgmt of systemic and ocular measles?
-Mgmt of measles retinopathy?
Measles
-Keratitis & mild papillary nonpurulent conjunctivitis = most common ocular manifestations
-Measles retinopathy: more common in acquired measles; ERG extinguished
-Mgmt of ocular and systemic measles: symptomatic (self limited disease)
-Steroids can be used for measles retinopathy
INFECTIONS: Measles
-What % of patients with subacute sclerosing panencephalitis have ocular findings?
-What is the most consistent ocular finding?
-Diagnosis of SSPE?
Measles
-10-50% of pts w/ SSPE have ocular findings
-Maculopathy (focal retinitis, RPE changes) = most consistent eye finding
-Dx of SSPE: clinical sx, periodic EEG discharges, IgG measles titer
INFECTIONS: West Nile Virus
-What are presenting ocular symptoms/signs of west nile virus?
-Mgmt?
-Diagnosis?
-IVFA?
West Nile Virus
-Eye findings: pain, photophobia, conj injection, blurry vision, multifocal chorioretinitis, nongranulomatous inflammation --> follows course of choroidal vessels
-Mgmt: self-limited in majority of pts --> VA returns to baseline in months (no proven treatment)
-Dx: IgM Ab to virus
-IVFA: central hypofluorescent & peripheral hyperfluorescence of lesions
INFECTIONS: Ocular histoplasmosis
-Clinical findings?
-Pathogenesis?
-What is the 3 yr risk of maculopathy if macular histo spots present? if no macular histo spots present?
Ocular histoplasmosis
-Clinical: 1) histo spots; 2) peripapillary pigment changes; 3) no vitritis; 4) CNV
-Pathogenesis: focal choroidal inflammation at time of initial systemic infection --> may resolve w/ atrophy OR cause Bruch's disruption & CNV
-Macular histo spots --> 25% risk of maculopathy in 3 yrs
-If no macular histo spots --> 2% risk of retinopathy
INFECTIONS: Ocular histoplasmosis
-IVFA of active disease vs CNV?
-Definition of clinically significant CNV? Mgmt of each type?
-Why is submacular surgery not advocated for mgmt of CNV?
Ocular histoplasmosis
-IVFA (active disease lesion): block early --> hyperfluorescence late
-IVFA (CNV): hyperfluorescence early --> leakage late
-Clinically significant CNV: 1) extrafoveal - 20-200 um from center; 2) juxtafoveal - 1-199 um from center; 3) subfoveal
-Mgmt of extrafoveal/juxtafoveal: thermal laser (Macular Photocoagulation Study)
-Mgmt of subfoveal: PDT (Visudyne in OHS study), intravitreal VEGF/steroids
-Submacular surgery trials (SST) showed high rate of recurrent CNV s/p submacular surgery --> not useful treatment
INFECTIONS: Measles
-What % of patients with subacute sclerosing panencephalitis have ocular findings?
-What is the most consistent ocular finding?
-Diagnosis of SSPE?
Measles
-10-50% of pts w/ SSPE have ocular findings
-Maculopathy (focal retinitis, RPE changes) = most consistent eye finding
-Dx of SSPE: clinical sx, periodic EEG discharges, IgG measles titer
INFECTIONS: West Nile Virus
-What are presenting ocular symptoms/signs of west nile virus?
-Mgmt?
-Diagnosis?
-IVFA?
West Nile Virus
-Eye findings: pain, photophobia, conj injection, blurry vision, multifocal chorioretinitis, nongranulomatous inflammation --> follows course of choroidal vessels
-Mgmt: self-limited in majority of pts --> VA returns to baseline in months (no proven treatment)
-Dx: IgM Ab to virus
-IVFA: central hypofluorescent & peripheral hyperfluorescence of lesions
INFECTIONS: Ocular histoplasmosis
-Clinical findings?
-Pathogenesis?
-What is the 3 yr risk of maculopathy if macular histo spots present? if no macular histo spots present?
Ocular histoplasmosis
-Clinical: 1) histo spots; 2) peripapillary pigment changes; 3) no vitritis; 4) CNV
-Pathogenesis: focal choroidal inflammation at time of initial systemic infection --> may resolve w/ atrophy OR cause Bruch's disruption & CNV
-Macular histo spots --> 25% risk of maculopathy in 3 yrs
-If no macular histo spots --> 2% risk of retinopathy
INFECTIONS: Ocular histoplasmosis
-IVFA of active disease vs CNV?
-Definition of clinically significant CNV? Mgmt of each type?
-Why is submacular surgery not advocated for mgmt of CNV?
Ocular histoplasmosis
-IVFA (active disease lesion): block early --> hyperfluorescence late
-IVFA (CNV): hyperfluorescence early --> leakage late
-Clinically significant CNV: 1) extrafoveal - 20-200 um from center; 2) juxtafoveal - 1-199 um from center; 3) subfoveal
-Mgmt of extrafoveal/juxtafoveal: thermal laser (Macular Photocoagulation Study)
-Mgmt of subfoveal: PDT (Visudyne in OHS study), intravitreal VEGF/steroids
-Submacular surgery trials (SST) showed high rate of recurrent CNV s/p submacular surgery --> not useful treatment
INFECTIONS: Candidiasis
-Predisposing conditions?
-Clinical appearance?
-Pathophysiology?
-Follow up?
Candidiasis
-most common fungus causing endogenous retinal, choroid and vitreous infection
-Predisposing factors: recent major GI surgery, bacterial sepsis, hyperalimentation, systemic abx, indwelling catheters, prolonged neutropenia, organ transplantation, debilitating disease (i.e., diabetes)
-Clinical: multifocal, bilateral, white lesions < 1 mm diameter assoc w/ overyling vitritis
-Pathophys: budding yeast w/ pseudohyphae, hematogenous dissemination to choroid --> breaks through Bruch's & infects retina
-Follow up: all pts w/ candidemia have baseline DFE, followed for at least 2 weeks for development of ocular candidiasis
INFECTIONS: Candidiasis
-What is the mgmt of candidal lesions not yet involving vitreous vs those involving vitreous?
Candidiasis
-Lesions not yet involving vitreous: PO fluconazole or voriconazole
-Lesions involving vitreous: intravitreal ampho/voriconazole w/ PPV
INFECTIONS: Aspergillosis
-Risk factors?
-Clinical appearance?
-Histologic appearance of fungus?
-Mgmt?
Aspergillosis
-Risk factors: IVDA, cancer, chronic pulmonary infection, endocarditis
-Clinical: bilateral vitritis, fluffy exudates (similar to candida) often in post pole/macula, hemorrhagic, broad areas of infarction, rapid progression
-Histo: septate, dichotomously branching hyphae in vitreous fluid; difficult to culture from blood
-Mgmt: systemic + intraocular antifungals, PPV
INFECTIONS: Cryptococcosis
-What organ system does this have a predilection for?
-What disease entity is this the most common cause of?
-Clinical?
-Definitive dx?
-Mgmt?
Cryptococcosis
-Most common cause of fungal meningitis & most frequent fungal eye infection in HIV/AIDS
-Predilection for CNS
-Found in pidgeon feces
-Clinical: multifocal chorioretinitis w/ yellow-white lesions in post pole
-Definitive dx: demonstration of organism w/ India Ink staining or CSF culture
-Mgmt: IV ampho B & PO flucytosine
INFECTIONS: Coccidiomycosis
-Endemic areas?
-How common is ocular involvement?
-Stain used to identify fungus?
-What type of inflammation is present within the eye?
-Mgmt?
Coccidiomycosis
-Endemic areas: Southwestern US, central/south America, San Joaquin Valley in CA
-Ocular involvement is uncommon even w/ disseminated disease --> various forms of eye disease including granulomatous iritis, granuloma formation
-Papanicolaou stain used to identify fungus
-Granulomatous inflammation --> consider in DDx of any pt w/ idiopathic granulomatous iritis who has lived/traveled through endemic areas
-Mgmt: Ampho B = most effective for active infection (can also use PO azoles)
INFECTIONS: Toxoplasmosis
-How common is this condition?
-Definitive hosts?
-3 major forms?
-Which population of pts gets Type I strain & which gets Type II strain?
Toxoplasmosis
-Most common cause of infectious retinochoroiditis in both adults & children!
-Cats = definitive host
-3 forms: 1) oocyst (soil); 2) tachyzoite (infectious); 3) tissue cyst (latent)
-Type I strains: immunocompetent pts
-Type II strains: HIV/AIDS pts, congenital infections
INFECTIONS: Toxoplasmosis
-Principle modes of transmission?
-When during pregnancy is the risk of congenital infection the highest?
-Presentation of congenital toxo?
-Standard of care for congenital toxo?
Toxoplasmosis
-Transmission: undercooked, infected meat; cat feces exposure; unpasteurized goat milk or contaminated fruit/veg; contact w/ infected blood (transfusion, organ transplant), transplacental
-40% of primary maternal infections result in congenital infection (highest rate of transmission in 3rd trimester)
-Presentation: chorioretinitis, hydrocephalus, intracranial califications
-Newborns w/ toxo should be treated for at least 1 year to prevent ocular involvement
INFECTIONS: Toxoplasmosis
-Ocular presentation?
-What is Kyrieleis arteriolitis?
-What is PORT?
Toxoplasmosis
-Ocular presentation: focal white retinal lesion w/ overlying vitritis ("headlight in fog") adjacent to old chorioretinal scar --> usually in posterior pole
-Kyrieleis arteriolitis: perivasculitis in vicinity of active lesion (sheathing of vessels)
-PORT (punctate outer retinal toxo): small multifocal deep retinal lesions assoc w/ scant overlying vitritis
INFECTIONS: Toxoplasmosis
-What are patterns of antibody titers in toxo?
-Indications for treatment?
Toxoplasmosis
-Antibodies: IgG remain positive for life, appear 2 weeks after infection; IgM start early in acute phase, positive for < 1 yr, do not cross placenta
-Presence of IgM in newborns confirms congenital infection
-Indications for tx: lesions near optic nerve/fovea, dec VA, mod to severe vitritis, lesions > 1 DD size, persistence > 1 month, multiple active lesions
INFECTIONS: Toxoplasmosis
-Disease course in immunocompetent vs immunocompromised pts?
-What drugs should NOT be used?
-Classic tx regimen?
-What drug can be used if sulfa allergic?
-What labs should be monitored?
-Are steroids useful?
-What is an alternative treatment to the classic regimen?
Toxoplasmosis
-Disease may be self limited in immunocompetent; always treat in immunocompromised
-Classic triple therapy: pyrimethamine, sulfadiazine & folinic acid
-Clindamycin used if sulfa allergic
-Monitor WBC & plts weekly
-Use systemic steroids at time of tx or within 48 hrs in immunocompetent pts --> DO NOT use long acting periocular or intraocular steroids!
-Alternative tx: Bactrim (same efficacy as triple tx)
INFECTIONS: Toxoplasmosis
-What is the mgmt of toxoplasmosis in pregnant pts?
-How are newborns w/ congenital toxo treated?
-What has long term intermittent bactrim shown to be useful for?
Toxoplasmosis
-Pregnant pts: use spiramycin; alternatives: azithromycin, clinda & atovaquone
-Newborns: pyrimethamine & sulfonamides x 1 yr (w/ peds ID specialist)
-HIV/AIDS - extended systemic tx needed
-Long term intermittent Bactrim decreases risk of reactivation in recurrent toxo chorioretinitis
INFECTIONS: Toxocariasis
-What type of worm is toxocara canis?
-Name of systemic disease?
-Pt population?
Toxocariasis
-Roundworm
-Caucasians most commonly affected
-Visceral larvae migrans = systemic disease
INFECTIONS: Toxocariasis
-What are the 3 recognizable posterior ocular syndromes?
-Symptoms?
-Laterality?
Toxocariasis
-Usually unilateral (bilateral disease rare)
-Posterior segment: 1) luekocoria 2/2 vitritis mimicking endophthalmitis (25%); 2) localized macular granuloma (25%); 3) peripheral granuloma (50%)
INFECTIONS: Toxocariasis
-Laboratory testing?
-Most important consideration for differential diagnosis? How to differentiate b/w this condition and toxocariasis?
-Mgmt?
Toxocariasis
-Labs: serum ELISA 1:8 (90% sensitive & specific for prior exposure) --> but if negative, does not rule out diagnosis!
-Retinoblastoma: most important DDx consideration --> B scan & CT will NOT show calcification in toxocariasis (will see in Rb)
-No uniformly satisfactory tx
-Can use systemic/periocular steroids
INFECTIONS: Cysticercosis
-Type of worm?
-Risk factors for infection?
-Most common intraocular location for infection?
-First sign of cerebral cysticercosis?
Cysticercosis
-Tapeworm
-Risk factors: poor hygeine (acquired via ingestion of eggs/worm)
-Most common intraocular location: subretinal space --> eye is more commonly affected than any other organ in this disease
-Neurocysticercosis: epileptiform seizures = first sign
INFECTIONS: Cysticercosis
-Clinical findings?
-Pathognomonic finding?
-What % of pts have +Abs?
-Mgmt?
Cysticercosis
-Clinical: white cyst w/ head/scolex that undulates in response to examining light within vitreous/subretinal space --> motile anterior chamber, intravitreal or subretinal worm is pathognomonic
-Abs+ in 80% w/ neural cysticercosis & 50% w/ ocular cysticercosis
-Mgmt: antihelminthic drugs not effective for eye disease --> need systemic steroids also & surgical removal of larva from vitreous
INFECTIONS: DUSN
-Pt population?
-Causative organisms?
-Workup & Mgmt?
Diffuse Unilateral Subacute Neuroretinitis
-Healthy, young pts
-Organisms: ancylostoma canium (smaller), Baylisascaris procyonis (larger)
-Systemic/lab workup usually negative
-Mgmt: direct laser of subretinal worm, albendazole
INFECTIONS: DUSN
-Clinical presentation and findings?
Diffuse Unilateral Subacute Neuroretinitis
-Unilateral vision loss 2/2 recurrent inflammation of retina/RPE/nerve
-Multiple, focal, gray white lesions that are evanescent --> looks like white dot syndrome
-Later: abnl EEG, RPE atrophy, optic atrophy
INFECTIONS: Onchocerciasis
-Endemic areas?
-Transmitting insect?
-Name for eye disease?
-How do the microfilariae reach the eye? (3 routes)
Onchocerciasis: "River blindness"
-Endemic areas: Sub-Saharan Africa, Central/South America
-Transmitted by blackfly
-3 routes of spread to eye: direct invasion of cornea from conj; scleral penetration (direct or thru vessels), hematogenous spread
INFECTIONS: Onchocerciasis
-Manifestations of eye disease?
-Treatment of choice & dosing?
-What is a Mazzotti reaction?
Onchocerciasis
-Eye disease: severe anterior uveitis, chorioretinal changes, optic atrophy --> confirm dx by seeing organism in eye or skin bx
-Mgmt: Ivermectin (kills microfilariae but does not kill adult worm) ---> singly monthly dose for 10 yrs needed
-Slows progression of vision loss & optic atrophy
-Mazzotti reaction: caused by massive worm kill when treatment was diethylcarbamazine --> no longer used now
INFECTION: Syphilis
-What are the systemic findings of early and late congenital syphilis?
-What are the most common ocular findings in early and late congenital syphilis?
Syphilis - congenital
-Early systemic: long bone changes, skin rash, hepatosplenomegaly
-Late systemic: Hutchinson teeth, mulberry molars, CN VIII deafness, saber shins, abnl facies
-Early ocular: salt-and-pepper pigmentary retinopathy (nonprogressive, nl vision --> like rubella); retinal vasculitis & chorioretinitis may precede the pigmentary retinopathy
-Late ocular: Nonulcerative stromal interstitial keratitis + anterior uveitis
INFECTIONS: Syphilis
-What is the Hutchinson Triad?
Syphilis - congenital
-Hutchinson triad: interstitial keratitis + CN VIII deafness + Hutchinson teeth
INFECTIONS: Syphilis
-Describe clinical maniefstations of primary, secondary and tertiary syphilis
-During which stage does syphilis uveitis occur?
-What is the most common posterior segment manifestation?
Syphilis - acquired
-Primary: painless chancre at site of inoculation
-Secondary: lymphadenopathy, generalized rash
-Tertiary: gummas, cardiovascular syphilis, neurosyphilis
-Uveitis can occur in ANY stage of syphilis
-Posterior segment: focal, multifocal chorioretinitis assoc w/ vitritis; neuroretinitis also possible
INFECTIONS: Syphilis
-What are the nontreponemal antigen tests for syphilis?
-What are the treponemal antigen tests?
-When do treponemal antigen tests become positive and how are they useful?
-Which tests should be used in the setting of uveitis?
Syphilis
-Nontreponemal tests: RPR, VDRL
-Treponemal tests: FTA-ABS, MHA-TP
-Treponemal tests correlate w/ disease activity, used for monitoring tx for systemic & ocular disease
-FTA-ABS becomes positive during secondary stage, remains positive for life
-In uveitis: need BOTH treponemal & nontreponemal tests (do not skip treponemal test if nontreponemal tests negative) --> treponemal tests have higher predictive value in uveitis!
INFECTIONS: Syphilis
-What test is warranted in all cases of syphilitic uveitis?
-What other disease should be tested for in pts w/ syphilis?
-What diagnostic tests are always positive in congenital syphilis?
-What is the most important test for serodiagnosis of congenital syphilis?
Syphilis
-All syphilis pts should be tested for HIV
-All pts w/ syphilis uveitis should have LP for neurosyphilis
-Congenital syphilis: all newborns are + VDRL & FTA-ABS (due to passive transfer of maternal IgG across placenta)
-Need IgM FTA-ABS for serodiagnosis of congenital syphilis --> presence indicates that infection originated within infant (as IgM does not cross placenta)
INFECTIONS: Syphilis
-What is the preferred tx for all stages of syphilis?
-What dosing regimen should be used for syphilitic uveitis?
-What is the mgmt of congenital syphilis?
Syphilis
-IV PCN G is preferred for all stages of disease
-Syphilitic uveitis should be considered a form of neurosyphilis --> use neuro dosing (18-24 mil units aqueous crystalline PCN G/day x 10-14 days)
-Congenital syphilis: crystalline PCN G x 10 days
INFECTIONS: Syphilis
-What alternatives are available for PCN-allergic pts?
-What is the Jarisch-Herxheimer reaction?
-What other disease is assoc w/ Jarsich-Herxheimer reaction?
Syphilis
-If PCN allergic --> need desensitization and then tx w/ PCN *no other alternatives available)
-Jarisch-Herxheimer reaction: host hypersensitivity response to treponemal Ags released in large numbers are spirochetes killed --> occurs in 1st 24 hrs --> concomitant increase in ocular inflamamtion (may need steroids)
-Lyme can also cause Jarisch-Herxheimer reaction when treated
INFECTIONS: Lyme
-Epidemiology?
-Describe systemic features of stage 1, 2 and 3 disease?
Lyme
-Epi: M>F (53%), May-August
-Stage 1: erythema migrans (target rash at site of inoculation) & constitutional sx
-Stage 2: disseminated disease --> erythema chronicum (sites remote from inoculation), joint disease, neurologic disease
-Stage 3: episodic arthritis, acrodermatitis chronica atrophicans (bluish red lesion on extremities), fibrous bands/nodules
INFECTIONS: Lyme
-Most common ocular manifestations of stage 1, 2 and 3 disease (respectively)?
-2 step protocol for diagnosis?
-Mgmt of eye disease?
Lyme
-Stage 1: follicular conjunctivitis
-Stage 2: intermediate uveitis
-Stage 3: immune stromal keratitis (responds to steroids)
-2 step protocol for diagnosis: 1) IFA or ELISA for IgM & IgG; 2) confirmatory Western blot
-Mgmt: route/duration of abx not established; need LP for neuro eval if eye disease present; give steroids for anterior segment inflammation after abx started
INFECTIONS: Leptospirosis
-Epi?
-Systemic features?
-What is Weil disease?
Leptospirosis
-Tropical/subtropical regions, water sports
-Systemic features: constitutional and GI sx (abrupt onset) --> 85-90% of pts have self limited anicteric illness; 10-15% develop severe septicemia/Weil disease
-Weil disease: renal and hepatocellular dysfunction --> 15-30% mortality rate
INFECTIONS: Leptospirosis
-Ocular findings? --> which is pathognomonic?
-Visual prognosis?
-Diagnostic testing?
-Mgmt?
Leptospirosis
-Ocular findings: circumcorneal conjunctival hyperemia (pathognomonic), anterior/diffuse uveitis --> more vision threatening
-Good prognosis for vision despite severe panuveal inflammation
-Diagnosis: MAT (microagglutination test) = gold standard; can also do ELISA, complement-fixation for IgM detection
-May see false + FTA-ABS or RPR w/ this disease
-Mgmt: IV PCN G x 1 week or PO doxy for 1 week (if milder disease)
INFECTIONS: Nocardiosis
-Systemic disease features?
-Ocular findings?
-Mgmt?
Nocardiosis
-Systemic disease: pneumonia, disseminated abscesses
-Ocular: choroidal abscesses (spreads hematogenously to eye)
-Mgmt: systemic sulfonamide x 6 weeks (immunocompetent) or 1 yr (immunosuppressed)
INFECTIONS: Tuberculosis
-Features of the organism?
-Most common organs infected?
-What % of pts develop pulmonary and extrapulmonary Tb (respectively)?
-What is primary ocular Tb and its manifestations?
Tuberculosis
-Organism: acid-fast, obligate aerobe --> found most commonly in apices of lung and choroid (highest blood flow rate in body)
-Pulmonary Tb occursi n 80% of pts (extrapulmonary Tb occurs in 20% --> half of these pts have normal CXR)
-Primary ocular Tb = eye is primary port of entry --> conj, corneal & scleral disease
INFECTIONS: Tuberculosis
-What is secondary ocular Tb and its manifestations?
-Characteristic lesions of choroiditis?
-IVFA findings?
Tuberculosis
-Secondary ocular Tb: uveitis (disseminated choroiditis) is most common presentation --> granulomatous disease
-Choroiditis --> classic lesions are tubercles or tuberculoma (single large elevated choroidal mass)
-IVFA: active lesions show early hyperfluorescence & late leakage; cicatrical lesions show early blocekd fluorescence w/ late staining
INFECTIONS: Tuberculosis
-What is Eales disease?
-When should PPD testing be used for diagnosis?
-Mgmt of eye disease?
Tuberculosis
-Eales disease: peripheral retinal perivasculitis w/ recurrent unilateral vitreous/retinal heme --> subsequently involves other eye, healthy young men
-PPD: use selectively for pts w/ high index of suspicion for disease (not for routine screening)
-Mgmt: systemic tx of uveitis --> 4 drug therapy; can use steroids in conjunction
INFECTIONS: Ocular Bartonellosis
-Epidemiology?
-Systemic manifestations?
-Ocular disease features?
-Most well known posterior segment manifestation of disease?
Ocular Bartonellosis
-Epi: fall and winter; southern states (CA, Hawaii)
-Systemic features: flu-like illness, regional adenopathy, erythematous papule at primary site
-Ocular disease (5-10% of pts): Parinaud oculoglandular syndrome --> unilateral granulomatous conjunctivitis & regional adenopathy
-Neuroretinitis = most common posterior segment manifestation of B. henslae infection (caused by B. henslae in 2/3 of cases)
-Clinical features of neuroretinitis: abrupt vision loss, unilateral disc swelling, macular star
INFECTIONS: Ocular Bartonellosis
-Diagnostic testing?
-Prognosis?
-Mgmt?
Ocular Bartonellosis
-Diagnosis: single positive IFA or EIA (enzyme immunoassay) titer for IgG or IgM is sufficient to confirm dx
-Prognosis: self-limited, good systemic & visual prognosis
-Mgmt: doxy 100 bid x 2-4 weeks (in peds pts, azithromycin can be used)
-
INFECTIONS: Whipple disease
-Organism?
-Clinical syndrome?
-Eye disease?
-Gold standard for diagnosis?
-Mgmt?
Whipple disease
-Tropheryma whippelii
-Syndrome: middle-aged Caucasian males w/ diarrhea, weight loss, migratory arthritis (protein loss causes pitting edema)
-Eye disease is rare --> bilateral panuveitis & retinal vasculitis; granular deposits on iris, capsule and IOL
-Gold standard for dx: duodenal biopsy --> PAS+ macrophages within intestinal villa
-Mgmt: systemic Bactrim x 1-3 months (relapses occur in 30% of cases)
ENDOPHTHALMITIS: Exogenous
-What are the 3 types of exogenous endophthalmitis?
-Are clear corneal incisions associated with lower or higher risk of endophthalmitis?
-What is the rate of endophthalmitis after PPV?
-What are the primary sources of infection in postoperative endophthalmitis? What organisms?
Exogenous
-3 types of exogenous endophthalmitis: postoperative, post-traumatic and bleb-associated
-CCI associated w/ higher risk of endophthalmitis
-PPV: has low (0.05%) rate of endophthalmitis
-Eyelids & conjunctiva = primary infection source in postop endophthalmitis
ENDOPHTHALMITIS: Exogenous
-What are specific sources of contamination in postoperative endophthalmitis?
-Which IOL material is associated w/ positive bacterial cultures?
Exogenous
-Sources contamination in postop endophthalmitis: secondary infection (i.e., from lacrimal system), blepharitis, contaminated gtts, breach in sterility, contaminated fluids
-IOL material assoc w/ positive bacterial cultures: polypropylene (in haptics)
ENDOPHTHALMITIS: Acute postoperative
-Timeline?
-Difference b/w mild and severe cases (causative organism, VA, time of onset)?
Acute postoperative endophthalmitis
-Up to 6 weeks after surgery
-Mild: VA > 20/400, less painful, 3-14 days postop, coag negative staph
-Severe: VA < 20/400, severe pain and vitritis, 1-4 days postop, S. aureus, Strep spp., gram negative bugs
ENDOPHTHALMITIS: Chronic postoperative
-Timeline?
-Name a characteristic organism and type of infection
-What is the most important fungal cause of chronic postop endophthalmitis?
Chronic postoperative endophthalmitis
-Timeline: 6 wks - years after surgery
-P. acnes: granulomatous KP, white plaque in capsular bag (contains residual lens material, bacteria)
-Candida = most important fungal cause of chronic postop endophthalmitis
ENDOPHTHALMITIS: Post-traumatic
-What factors are related to increased incidence?
-Organism responsible for most fulminant infection?
Post-traumatic
-Highest incidence in rural settings and when intraocular foreign body present
-Bacillus = most fulminant cause of endophthalmitis
ENDOPHTHALMITIS: Bleb-associated
-Risk factors?
-Does this occur in intact or leaking blebs?
Bleb-associated endophthalmitis
-Risk factors: diabetes, use of antimetabolites, inferior bleb, h/o previous resolved blebitis
-Can occur in intact OR leaking blebs
ENDOPHTHALMITIS: Endogenous
-Risk factors?
-Most common bacterial organisms?
Endogenous
-Risk factors: chronic illness (DM, renal failure), immunosuppression, IVDA, indwelling catheters, immediate postop or postpartum
-Bacteria: strep (endocarditis), staph (cutaneous), bacillus (IVDA), gram negatives (i.e., klebsiella - klebsiella endophthalmitis is most common type of endogenous infection in Asia, due to liver abscesses)
ENDOPHTHALMITIS: Endogenous fungal
-Which part of the eye is initially affected?
-Most common organisms?
Endogenous fungal endophthalmitis
-Choroid initially affected --> overlying vitritis
-Candida (most common) & aspergillus (second most common)
ENDOPHTHALMITIS: Endogenous fungal - Candida
-Risk factors?
-% of pts w/ endophthalmitis who are on tx vs those not on tx?
-Diagnosis?
-Follow up?
-Mgmt?
Endogenous fungal - Candida
-Risk factors: immunosuppression, hyperalimentation, IVDA
-Occurs in 10-37% of those not on antifungals; occurs in 3% of those on antifungals
-Diagnosis: blood cultures, intraocular fluid PCR
-Newly diagnosed cases of candidemia should have DFE initially and again 1-2 weeks apart
-Mgmt: voriconazole, caspofungin, ampho B, ketoconazole
ENDOPHTHALMITIS: Endogenous fungal - Aspergillus
-Risk factors?
-Clinical findings?
Endogenous fungal - Aspergillus
-Risk factors: severe chronic pulmonary disease, severe immunocompromise, IVDA, orthotopic liver transplant
-Clinical: subretinal/subhyaloid hypopyon, hemorrhage in all layers, vitreous abscesses, angiocentric inflammation
ENDOPHTHALMITIS: Endogenous fungal - Aspergillus
-How to differentiate Candidal and Aspergillus endophthalmitis?
-Mgmt of aspergillus endophthalmitis? Prognosis?
Endogenous fungal - Aspergillus
-Candida vs aspergillus: primary focus of inflammation is vitreous in Candida but retinal/choroidal vessels and subretinal space in Aspergillus
-Mgmt of aspergillus: PPV + intravitreal ampho B/voriconazole + intravitreal steroids
-Poor prognosis (often involves macula)
ENDOPHTHALMITIS: Prophylaxis
-What measures are proven to reduce endophthalmitis after cataract surgery?
-What is the utility of PO moxifloxacin in prophylaxis of postop endophthalmitis?
Prophylaxis
-Preventative measures for cataract surgery: 1) preop 5% iodine antisepsis (including prep of lids/conj); 2) preop topical, broad spectrum abx; 3) careful isolation of lids/lashes from surgical field
-PO moxi does reach inhibitory concentrations in aqueous & vitreous but is not used routinely for postop prophylaxis
ENDOPHTHALMITIS: DIagnosis
-What is TASS?
-Why is it important to obtain vitreous cultures in addition to aqueous cultures?
-Which method is better to obtain positive culture results: needle tap of intraocular fluid vs mechanized biopsy?
Diagnosis
-Toxic anterior segment syndrome: caused by introduction of unknown toxic substances by surgery via instruments, fluids, IOLs
-Important to obtain vitreous in addition to aqueous cultures because may have + vitreous culture even when aqueous culture is negative
-Equivalent utility of needle tap and mechanized biopsy in obtaining + cultures and in terms of complication rates
ENDOPHTHALMITIS: Treatment
-Criteria for surgical mgmt (PPV)
-Most effective antimicrobial agents?
-What is the utility of systemic abx?
-What is the utility of subconj, topical abx?
-What % of traumatic endophthalmitis cases have VA 20/400 or better after treatment?
Treatment
-If VA is HM or better, do tap/inject instead of PPV (per endophthalmitis vitrectomy study)
-Most effective drugs: vanco (gram positives), aminoglycosides (gram negatives), ceftazidime (not as complete gram negative rod coverage)
-Systemic abx are controversial --> good ocular penetration and broad coverage w/ PO fluoroquinolones
-Subconj/topical abx have little benefit after intravitreal abx given
-Only 10% of pts w/ posttraumatic endophthalmitis have VA > 20/400 after treatment
MASQUERADES: Non-neoplastic
-What is a masquerade syndrome?
-What are some non-neoplastic masquerade syndromes?
-What is Schwartz syndrome?
Non-neoplastic
-Masquerade syndrome: cells in AC but not of immune origin
-RP: nyctalopia, ERG depression, bilateral, +FHx, pigmentary fundus changes w/ vascular attenuation and optic atrophy
-Ocular ischemic syndrome: hypoperfusion 2/2 carotid artery obstruction (>75%); neovascularization, flare>cell, clear vitreous, tortuous vessels and heme
-Chronic peripheral RRD
-Schwartz syndrome: RRD liberates photoreceptor outer segments --> phagocytosed by TM endothelial cells --> secondary open angle glaucoma
-IOFB
-Pigment dispersion
MASQUERADES: Neoplastic
-What is the most common non-neoplastic masquerade syndrome?
-How does it manifest?
Neoplastic
-Primary CNS lymphoma: most common neoplastic masquerade syndrome
-Non-Hodgkin B cell lymphoma, 5-7th decades
-25% of PCNSL have ocular disease; 15% have only ocular disease
-Clinical: decreased vision, floaters, vitritis w/ spillover AC cells, creamy subretinal infiltrates
MASQUERADES: Neoplastic
-Mgmt of primary CNS lymphoma?
-CNS manifestations?
-what is GUN syndrome?
-IVFA?
Neoplastic
-Mgmt: becomes resistant to steroid tx --> PPV to diagnose, chemo, radiation
-CNS: behavioral changes, periventricular lesions on imaging
-GUN syndrome: uveitis, glaucoma & neurologic sx
-IVFA: hypofluorescence due to blockage from subretinal tumor; hyperfluorescence due to window defect from RPE atrophy
MASQUERADES: Non-neoplastic
-What is the best method of diagnosis of primary CNS lymphoma?
-What does cytokine analysis show?
-Prognosis?
Non-neoplastic
-Best method of diagnosis: tissue diagnosis w/ vitreous bx
-Consider vitreous bx if vitreous cells of unidentifiable cause present in pt over 65 yo
-Cytokine analysis: IL-10 elevated in lymphoma (produced by malignant B cells); IL-6 elevated in pts w/ inflammatory uveitis (therefore, increased ratio of IL-10:IL-6 suggests lymphoma)
-Poor overall prognosis
MASQUERADES: Metastatic tumors
-What are the most common primary tumors that metastasize to the eye?
-What % of pts w/ uveal melanoma present w/ uveal melanoma?
Metastatic tumors
-Most common metastatic tumors to eye: breast, lung, cutaneous melanoma
-5% of uveal melanomas present w/ ocular inflammation
COMPLICATIONS: Cataracts
-What type of IOL should be avoided in uveitic eyes?
-Where should IOLs not be placed in uveitic eyes?
Cataracts
-Avoid foldable silicone IOLs --> associated w/ greater post op inflammation and because future vitreoretinal surgery may be necessary
-Do not place IOL in ciliary sulcus and anterior chamber!
COMPLICATIONS: Glaucoma
-What is uveitic glaucoma vs uveitic ocular HTN?
-What IOP elevation increases the risk of glaucoma?
-When does steroid-induced ocular HTN occur?
Glaucoma
-Uveitic ocular HTN: IOP >/= 10 mm Hg above baseline without glaucomatous cupping
-Uveitic glaucoma: elevated IOP w/ progression of cupping and glaucomatous VF defects
-IOP elevation to >24 mm Hg increases risk of glaucoma
-Steroid-induced OHTN rarely occurs before 3 weeks of tx
COMPLICATIONS: Glaucoma
-Describe the types of secondary angle closure uveitic glaucoma (mechanisms, most common causes)
Glaucoma
-Acute secondary angle closure: choroidal inflammation --> forward movement of lens-iris diaphragm (SO, VKH) --> need aggressive steroids to control inflammation; PI doesn't help as underlying cause is choroidal inflammation
-Subacute secondary angle closure: posterior synechiae, pupillary block, iris bombe (sarcoid, VKH) --> need multiple, large PI (laser if light iris, surgical if dark iris)
-Chronic secondary angle closure: PAS formation; may also be due to chronic steroids --> may need surgery
COMPLICATIONS: Glaucoma
-Name types of secondary open angle uveitic glaucoma (mechanisms, most common causes)
Glaucoma
-Acute secondary open angle: blockage of TM by inflammatory cells/debris (toxoplasmosis, ARN, herpetic uveitis)
-Chronic secondary open angle: PAS, direct injury to TM --> need CAIs, beta blockers, alpha agonists (AVOID parasympathomimetics and prostaglandins) --> often also need surgery (tubes better than trabs)
COMPLICATIONS: Hypotony
-Mechanisms of hypotony?
-Mgmt of hypotony early in course of disease?
-Mgmt of chronic hypotony?
Hypotony
-Mechanisms: decreased aqueous production due to acute CB inflammation or chronic CB damage
-Early: intensive steroids, cycloplegics
-Late: topical ibopamine (nonselective dopaminergic agonist, not in US --> increases aqueous production 3-4x)
COMPLICATIONS: Others
-Most common diseases assoc w/ CME?
-Permanent vitreous opacification?
-Retinal/choroidal neovasc?
Others
-CME: assoc w/ pars planitis, birdshot, retinal vasculitis
-Permanent vitreous opacification: toxoplasmosis, pars planitis
-Retinal/choroidal neovasc: pars planitis, sarcoid, retinal vasculitis (does not always require PRP - may resolve w/ resolution of disease)