This document discusses bacterial keratitis and corneal ulcers. It defines bacterial keratitis as any corneal inflammation caused by bacteria, and a corneal ulcer as bacterial keratitis accompanied by a loss of epithelium. It then lists common bacterial causes and describes characteristics of infections caused by different bacteria. The document provides guidance on diagnosing, treating, and managing bacterial keratitis and corneal ulcers.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
Aphakia and its causes. Correction of Aphakia. Advantages and disadvantages of different corrections. Surgeries and related signs and symptoms of aphakia. Complications related to Aphakia.
Aphakia and its causes. Correction of Aphakia. Advantages and disadvantages of different corrections. Surgeries and related signs and symptoms of aphakia. Complications related to Aphakia.
Myself Dr. Manish Tiwari Tutor Department of microbiology at saraswati medical college and research center( unnao) making presentation is only for MBBS and MD students.
In a healthy animal, the internal tissues, e.g. blood, brain, muscle, etc., are normally free of microorganisms. However, the surface tissues, i.e., skin and mucous membranes, are constantly in contact with environmental organisms and become readily colonized by various microbial species. The mixture of organisms regularly found at any anatomical site is referred to as the normal flora.
occulomycosis- infections of eye and its related structures by various fungal agents.
3 broad category
1.keratomycosis
2.fungal endophthalmitis
3.fungal infections of occular adnexa
Infection- microbiology and pathology in orofacial infectionPunam Nagargoje
INTRODUCTION
Oral and maxillofacial infections are commonly caused by teeth they are referred as odontogenic infections.
The etiological agents may be bacteria viruses or fungi.
The infection may spread directly from the tooth or secondary infections of cyst or tumours or infection of surgical wound or by contaminated needles.
Infection may be defined as invasion and multiplication of microorganisms in body tissues, especially that causing local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response.
Aerobic bacteria
Gram positive cocci –
Streptococcus species
S.Milleri
S.sanguis
S.Salivarius
S.Mutans
Staphylococcus species
Gram negative cocci –
Neisseria spp.
- N. subflava
N. sicca
Gram positive rods-
Dipetheroids
Lactobacillus spp
Gram negative rods-
Moraxella catarrhalis
Actinobacilllus actinomycetemcomitans
Campylobacter spp.
Capnocytophaga spp.
Eikenella corodens
Helicobactor pylori
Anaerobic bacteria
Gram positive cocci –
Peptococcus species
Pepto Streptococcus species
Gram pasitive bacilli –
Actinomycosis spp
Eubacterium spp
Gram negative species-
veillonella spp.
Gram negative bacilli-
Bacteroids
Prevotella species
Porphyromonas species
Fusobacterium
There are three stages in progression of acute odontogenic infections
Stage I – Innoculation
Stage II – Cellulitis
Stage III – Abscess
Stage IV – Space infection
TYPES
Acute stage - 3 forms
1.Abscess
2.cellulitis
3.fulminating infection
FULMINATING INFECTIONS
Here the infection involves secondary spaces involving vital structures.
Chronic stage
C/c fistulous tract or sinus formation
Abscesses neglected for a long time may discharge intraorally or extra orally
Spread of oral infection
Routes of spread
Direct continuity through tissues
By lymphatics to the lymph nodes.From lymph nodes to tissues results in secondary areas of cellulitis or tissue space abscess.
By blood stream-local thrombophlebitis may spread via the veins entering the cranial cavity producing cavernous sinus thrombosis. It may cause septicemia.
Invasion of dental pulp by bacteria after
decay of a tooth
¯
Inflammation, edema & lack of collateral
blood supply
¯
Venous congestion or avascular necrosis
(pulpal tissue death)
¯
Reservoir of bacterial growth(anaerobic)
¯
Periodic egress of bacteria into surrounding
alveolar bone
Factors influencing spread
General factors
Host resistance
Virulance of micro organism
Combination of both
Local factors
Anatomic barriers-
Alveolar bone
Periosteum
IgA preven
Endophthalmitis is an inflammation of the vitreous and the inner coats of the eye. This inflammation leads to infection which is caused by fungi or bacteria.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
How to Give Better Lectures: Some Tips for Doctors
Bacterial corneal ulcer
1. Dr. K. Vasantha M.S., F.R.C.S., Edin
Director RIO Chennai (Rtd)
2. Bacterial keratitis implies any form of corneal
inflammation either superficial, interstitial or
deep caused by bacteriae
When this inflammation is accompanied by a
loss of epithelium, it is termed a Corneal Ulcer.
4. Pseudomonas aeruginosa
Neisseria species
Haemophilus species
Moraxella species
Serratia marcescens
Proteus sp., Acinetobacter sp., Enterobacter sp, E.
coli,
Klebsiella sp., Eikenella sp.
Pasteurella multocida, Xanthomonas sp.,
5. Aerobic, nonfermenting gram negative rods
Achromobacter xylosoxidans and Stenotrophomonas
maltophilia are important causes for contact lens
induced keratitis. These are resistant to fluoroquinolones
and aminoglycosides
Actinomycetes including Nocardia are common in
developing countries
With orthokeratology lenses Pseudomonas, S.aureus,
Acanthamoeba and Stenotrophomonas are found
6. Normally the epithelium protects the cornea from getting infected.
But these bacteriae can penetrate the epithelium
Neisseria gonorrhoeae, Neisseria meningitidis
Corynebacterium diphtheriae
Haemophilus aegypticus
Listeria species
7. Ulcers can occur as secondary infection from the
conjunctival commensals, from the lids or from the sac
when it is inflamed. This will happen when there is an
abrasion. This is the reason why when there is a chronic
dacryocystitis it must be immediately dealt with
Diabetes and immuno suppressives will also predispose
the person to infection
Contact lens wear
8.
9. Watering, pain and redness usually following injury.
Defective vision. More if the ulcer is in the center
Lid edema, muco purulent discharge
Circum corneal congestion, sometimes conjunctival
congestion also. Chemosis if there is severe
inflammation
Opacity in the cornea which will take up fluorescein stain
as the epithelium will be abraded.
10. Pupil will be constricted and sluggishly reactive due to
irritation to the iris.
This toxic reaction can produce hypopyon which will be
sterile in bacterial ulcer.
In fungal ulcer fungal hyphae may be present.
Injury with vegetative matter should make one suspect
fungal etiology
If chronic dacryocystitis is present Pneumococcal
infection must be thought of
11. Stage of progressive infiltration
Stage of active ulceration
Stage of regression
Stage of cicatrization
12. Characteristics
• Suppuration is the hallmark
•Yellow – white, oval, densely opaque ulcer with relatively clear
surrounding cornea with or without hypopyon
•Two types of stromal infiltration:
•- small, discrete, peripheral anterior stromal infiltrates (free of
replicating bacteria)
•- large, severe, central stromal infiltrates (replicating bacteria
present)
•Tissue damage irreversible and leads to permanent scarring
13.
14. Often seen when chronic dacryocystitis is present
Suppuration and cicatrization are seen together. Ulcer
progresses on one side when the other side is healing.
Hypopyon will be present as this causes severe
iridocyclitis
See the sutures made for sac
excision
15.
16.
17. Irregular ulcer with thick greenish mucopurulent
exudate and ground glass appearance of surrounding
cornea (mushy/soupy stroma)
Presence of hypopyon
Rapid course – liquefactive necrosis, Descemetocoele
and perforation in 1 or 2 days
Most common pathogen in bacterial keratitis
associated with contact lens wear
18. This is a commensal organism present on the skin and
conjunctiva
Opportunistic infection
Usually causes secondary infection on HSV keratitis, or
on bullous keratopathy
Here the ulcer is on a
leucoma
19. Usually uniocular, mild, paracentral or perilimbal
Central grey infiltrate – ulcer with grey membranous
base
Second area of infiltration around it in the deep layers
of stroma with clear area in between
Infiltrated margin lacking and remaining cornea
relatively clear
20.
21. Commonest cause is Streptococcus viridans
Other etiologic agents: like
Staph. epidermidis, Pseudomonas, Mycobacteria,
Enterococci , Strep. pneumoniae , Peptostreptococcus
and Haemophilus also can rarely cause crystalline
keratopathy
Serratia marcescens also will give raise to satellite
lesions
22. Corynebacterium also can cause ulcer in preexisting
corneal lesions
Bacillus species will cause a rapidly progressing ulcer.
There will be a ring infiltrate remote from the site of
injury
Enterobacteriaceae will give raise to a shallow ulcer
with grayish white pleomorphic suppuration opaque
stroma and ring infiltrates -> ->
23. When you see an ulcer the following tests must done to
find the causative organism
Smear
KOH suspension
Culture
Detection of antigens, antibodies and endotoxins
Immunoglobulins
PCR
Confocal microscopy – not possible to see bacteriae as
they are only 0.5 microns in size
24. Apply topical anesthetic and wait for 3 – 5 mins for the
anesthetic to drain off
Remove the purulent material with a cotton swab and
discord
Use a Kimura’s spatula or a surgical blade to take the
sample. This is preferably done under a slit lamp. The
spatula can be sterilized with flame or 70% alcohol.
Contamination by eye lashes is avoided by using a
speculum
Immediate transfer needed due to small sample
25. Gram stain: for bacteria, yeasts, cysts of Acanthamoeba.
Can detect 60 – 70% of bacteriae. Fungal hyphae are
Gram negative or faintly stained walls with unstained
protoplasm
Giemsa: viral and Chlamydia inclusion bodies,
polymorphs and mononuclear cells besides the above
microbes
Ziehl-Neilson: Mycobacteria and Nocardia
Acridine orange: bacteria, fungi and Acanthamoeba
cysts
26.
27. Blood agar: for aerobic bacteriae and fungi esp.
Fusarium
Chocolate agar: Haemophilus, Neissaria and Moraxella
Sabouraud’s dextrose agar: fungus
Thioglycollate broth: both aerobic and anaerobic
Non nutrient agar with E. coli – Acanthamoeba
Thayer Martin agar: to isolate Neisseria
Brain heart infusion: filamentous fungi and Yeast
Lowenstein Jenson for Mycobacteria
28. Not satisfactory because of
Small sample
Prior antibiotic use
Many organisms are difficult to grow – Streptococci and
Propionibacterium
Polymicrobial keratitis can occur. It is difficult to
differentiate this from contamination
So while specificity is satisfactory sensitivity is poor
29. Elisa for detecting different antigens
Serological tests for IgG and IgM to detect viruses and
Microsporidia
Limuluslysate test: to detect endotoxins
Eubacterial PCR is done for all bacteriae
30. A DNA sequence determination is coupled with
bioinformatic analysis to detect matches between the
sample and a data base of reference genome sequence.
Rapid and highly accurate identification is possible
31. Aim of the treatment
To reduce the number of organisms as much and as
quickly as possible
To reduce the detrimental changes to the cornea caused
by the inflammation
32. Atropine eye drops are given to cause dilatation and
cycloplegia. This will reduce pain as ciliary spasm which
is the cause for the pain is relieved
Dilatation will break any synechiae and also prevent
further synechiae from forming
Atropine reduces the tear secretion and there by
increases the lysozomal content of the tears
It also separates the corneal lamellae and helps in
penetration of the drops applied
33.
34. If chronic dacryocystitis is present sac excision has to
be done
As diabetes may predispose to infection and delay
healing, this must be checked for
History must be taken regarding use of
immunodepressants and immunosuppression
35. Broad spectrum fortified antibiotic drops like
Gentamycin and Tobramycin for gram negative
organisms
Cefuroxime 500 mg in 2 ml if mixed with 8 ml of tear
substitute will give a fortified i.e. 50 mg in one ml
solution
Loading dose for the first half an hour or so and then
every hour initially
Once healing starts it can be tapered a little but not like
steroids as tapering might cause resistance
36. Has a broad spectrum – even against penicillin and
methicillin resistant bacteriae
Acts against anaerobes and atypical mycobacteriae
Has a higher solubility than the earlier antibiotics
Minimum concentration needed is low
It is bactericidal
Toxicity and allergenicity are low
37. Moxifloxacin is less active against Pseudomonas but
more active against Mycoplasma than Gatifloxacin. It is
less likely to give raise to resistance as two mutations
are needed. Moxifloxacin is self preserved and hence
preservatives are not needed
Since it reaches a higher concentration in the anterior
chamber development of mutation are prevented
Gatifloxacin acts against even Chlamydia and
Mycoplasma
38. Recommended drugs Alternative drugs
No organism Cefuroxime +
Tobramycin
or
Ciprofloxacin
Bacitracin
Gentamicin
Ofloxacin
Gram positive cocci Cefuroxime Bacitracin
Vancomycin +
Tobramycin
Gram negative
cocci
Cefuroxime Ciprofloxacin
Fortified Ceftriaxone
Gram negative
bacilli
Tobramycin
or
Ciprofloxacin
Gentamicin
Ofloxacin
Gram negative
diplobacilli
(Moraxella sp.)
Cefuroxime
or
Ciprofloxacin
Fortified Ceftriaxone
Ofloxacin
43. Symptoms will be less
Congestion will be less
The ulcer will stop progressing
The edges will become rounded
Hypopyon will disappear
The cornea around the ulcer will become clearer as the
edema comes down
44. Compliance must be checked
Change the antibiotics if it is different as per the culture
report
It must be remembered that with the small sample we get
with ulcers the results may not be accurate
Resistance to even fluoroquinolones are developing
Decision regarding therapeutic keratoplasty must be
taken before the ulcer reaches the peripheral cornea
45. Even when an ulcer heals a scar is produced which will
cause defective vision
A small peripheral scar may not affect vision .
If the scar is central mechanical obstruction to vision is
caused.
A nebular opacity or a peripheral opacity especially one
with iris adherence can cause astigmatism and affect
vision
46.
47.
48.
49.
50. An ulcer may perforate as the stroma dissolves due to
infection and by the action of neutrophils
If the perforation is in the periphery the iris plugs the
leak and the ulcer may heal with an adherent leucoma
If the perforation is in the center a fistula will form. When
this ulcer heals an anterior polar cataract may form
Sometimes if a small ulcer perforates it may help in
healing as it acts like a paracentesis
51. Before the ulcer perforates the Descemet’s membrane
will with stand for some time as it is elastic. This will
cause the membrane to bulge forward giving raise to
Descemetocoele
At this stage and for small perforations glue with either
bandage or bandage contact lens can be used to seal the
perforation
Glue has a mild antibiotic activity
It also blocks the neutrophils which causes further
necrosis
52.
53. If the ulcer progresses further it will become a total ulcer.
A therapeutic keratoplasty must be done if the ulcer is
progressing fast. A rim of normal cornea will give a
better result. So TKP should be done before the ulcer
progresses to involve the peripheral cornea
Since the eye is inflamed the chances for getting a clear
graft is poor. There is a danger of the infection occurring
in the graft also
Since large grafts will be needed rejection and glaucoma
are more common
54. If the infection involves all the layers of the eye it is
called panophthalmitis. Once this happens the eye may
have to be eviscerated. If the infection is controlled at
this stage the eye will become phthisical.