This document discusses various viruses that can cause eye infections or diseases. It provides details on the general properties of viruses, then examines specific viruses like adenovirus, herpes simplex virus, herpes zoster, cytomegalovirus, pox viruses, picornaviruses, paramyxoviruses, measles, rubella and HIV. For each virus, it describes the viral structure, transmission, signs and symptoms of ocular infection, laboratory diagnosis and treatment approaches.
Ocular virology; an Introduction
Lecture delivered by Dr. Iddi Ndyabawe (MMed Ophthalmology, 1st year at Makerere University, Uganda). Modulator: Dr. Lusobya Rebecca (Ophthalmologist)
Ocular virology; an Introduction
Lecture delivered by Dr. Iddi Ndyabawe (MMed Ophthalmology, 1st year at Makerere University, Uganda). Modulator: Dr. Lusobya Rebecca (Ophthalmologist)
Detailed instumentaion and use of manual Lensometer and just a outline of automated lensometer.
I have used the picture of manual lensometer with out the parts describtion because i have explained orally by showing the picture..
Hope u all like it and may help you in learning better. :)
Detailed instumentaion and use of manual Lensometer and just a outline of automated lensometer.
I have used the picture of manual lensometer with out the parts describtion because i have explained orally by showing the picture..
Hope u all like it and may help you in learning better. :)
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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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.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
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.
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.
2. GENERAL PROPERTIES OF VIRUS
Virus is the smallest known micro organism
[10nm-300nm]
It consists of a nucleic acid core(RNA/DNA)
surrounded by a protein coat.
They are metabolically inert and hence requires
living cells to survive and replicate.
The protein coat which is antigenic in nature is
called a ‘Capsid’ and together with the nucleic
acid is termed as ‘Virion’. The capsid is made up
of protein subunits called as ‘Capsomeres’
4. ADENOVIRUS- ADENOVIRAL CONJUNCTIVITIS
Family- Adenoviridae
Double stranded DNA virus without an envelope
70-90nm in diameter, icosahedral symmetry, 252 capsomeres.
Has an affinity for mucous surfaces and hence infect the
conjunctiva, pharynx and small intestine.
Humoral immunity plays a major role in combating adenovirus
infections and aslo a long lasting immunity is conferred against
reinfection.
Mode of transmission- hand to eye transfer, unsterilized instruments,
fomites, water borne(swimming pool)
12. HERPES VIRUS
Family- Alpha herpes virus
Double stranded DNA virus with a capsid and envelope.
150-200nm in diameter, 162 capsomeres
2 subtypes- HSV 1 & HSV 2
It multiplies in the nuclei of infected cells and produces
intracellular inclusion bodies “Lipschutz inclusion bodies”
Virus proliferates in the cells of the stroma and keratocytes and
sets up an inflammatory reaction.
It remains latent in the trigeminal ganglion- recurrent infection.
Primary infection- face, eye, mouth( 6mth-5yrs/newborns through
mother)
Latent infection-reactivation. May not involve the eye
13.
14. CLINICAL FEATURES
Epithelial dendritic/geographic keratitis causing ulcer which stains
well with fluorescein dye.
Ends of the ulcer has terminal buds staining with rose bengal
Decreased corneal sensation. Scarring and vascularization in
prolonged cases. Disciform keratitis, necrotizing stromal
keratitis, neurotrophic ulceration
Keratoconjunctivitis and anterior uveitis
Preauricular lymphadenopathy, vesicular eruptions on the skin.
Fever and malaise
DD:-
Herpes zoster keratitis
Acanthaemoeba keratitis
16. LAB DIAGNOSIS
Direct demonstration by electron microscopy/immunofluorescence.
Corneal scrappings- Giemsa/papanicola stain and intra nuclear
eosinophilic inclusion bodies can be demonstrated.
Cytology of infected tissue for multinuclear giant cells,
polymorphonuclear cells and monocytes.
Conjunctival fluid for virus culture- human embryo lung cells,BHK-
21,MRC-5 cells.
CPE occurs within 24-48hrs which is characterised by rounding of
cells and plaque formation.
ELISA
17. HERPES ZOSTER
Same group as HSV, but antigenically distinct.
It travels in a retrograde manner to the dorsal route and
cranial nerve sensory ganglia, where it remains dormant
for decades and gets reactivated when VZV-specific cell
mediated immunity fades.
HZO describes Shingles involving the dermatome supplied
by trigeminal nerve.
18. FEATURES:
Direct viral invasion- conjunctivitis, epithelial keratitis
Secondary inflammation with episcleritis, scleritis, keratitis,
uveitis, optic neuritis, cranial nerve palsy and cicatrizing
complications of eyelids.
Inflammation and destruction of the peripheral nerves or
central ganglia maybe responsible for post herpetic
neuralgia.
Reactivation causes necrosis and inflammation in the sensory
ganglia, corneal anaesthesia causing neurotrophic keratitis.
Skin vesicles occur which doesn’t cross the midline.
20. TREATMENT
Oral/ointment/topical Acyclovir.
Acyclovir Cream for skin lesions too.
Ganciclovir 0.15% gel
Oral valaciclovir/ famciclovir
Interferon monotherapy
Prostaglandins for IOP control
Topical/ oral steroids
21. CYTOMEGALOVIRUS
Family – Beta Herpes viridae
Double stranded DNA virus with icosahedral capsid and envelope.
Indistinguishable from HSV/VZV by electron microscopy.
Transmission is through placenta, intimate contact, blood
transfusion.
CMV has a profound immunosuppressive effect on the host and
has a tendency to persist in a latent state in the cellular
components of the blood.
Mononuclear phagocytes and natural killer cells play a role in
combating CMV infection.
26. PICORNA VIRUS
RNA virus. A large family
27nm in diameter.
Icosahedral symmetry
Further sub divided
Enterovirus
poliovirus Rhinovirus
coxsachie
echovirus
enterovirus types 68-72
27.
28. OCULAR LESIONS
ACUTE HAEMORRHAGIC CONJUNCTIVITIS-Coxsackie
A24, Enterovirus type 70
Transmission – fomites, faecal oral route, Direct inoculation into
the conjunctiva (contaminated fingers).
Incubation period – 2 days
It multiplies in the conjunctival epithelium and causes
haemorrhagic conjunctivitis.
29. LAB DIAGNOSIS
Virus Isolation: conjunctival swab inoculated into cell lines
like primary monkey kidney cell lines, Vero, HeLa. This
virus produces typical cytopathic effect.
Coxsackie: Isolated by suckling mice inoculation
Serology: Neutralization tests
TREATMENT:
Topical antibiotics
30. POX VIRUS
VARIOLA –
Commonly known as small pox virus. Brick shaped. 230-400nm.
Has an envelope.
Genome is a double stranded DNA and contains DNA dependent
RNA polymerase.
Causes Catarrhal purulent conjunctivitis, lid abscess, corneal pustule
and albinotic spots on the iris.
Lab diagnosis:-
Growth on Chorioallantoic membrane of yolk sac produces pocks.
Cytoplasmic eosinophilic Guarinieri bodies- light microscopy
Complement fixation test
Gutstein’s methyl violet stain
33. VACCINA VIRUS
Used as a small pox vaccine( induces immunity)
Transmission either by contamination or auto innoculation.
Signs :-
Lids – swelling, pustules, Ulcerative blepharitis
Purulent conjunctivitis
Marginal/disciform keratitis. Corneal pustule.
Pseudo retinitis pigmentosa
LAB:-
Growth on cell lines- HeLa, MRC-5
TREATMENT:-
Vidarabine and Iodoxuridine.
Topical and i.m use of vaccina immunoglobulin
34.
35. PARAMYXO VIRUS
RNA virus, spherical in shape, pleomorphic, 150-300nm.
Enveloped virus having a hemagglutin(HN) and fusion(F)
glycoprotein spikes. HN is responsible for the host cell attachment
of the virus and F for fusion of viral envelope with host cell
plasma membrane.
Transmitted by droplet infection, humans being their only host.
Spreads to salivary glands.
Incubation period= 7-25 days
Ocular signs- Dacryoadenitis, optic neuritis, conjunctivitis, unilateral
stromal disciform keratitis.
36. LAB DIAGNOSIS
Immunofluorescence technique
Virus isolation by monkey kidney cell lines- rounding and giant cell
syncytium formation. Confirm by hemadsorption and
hemagglutination inhibition test using mumps virus specific
antiserum and immunofluorescence.
Complement fixation test
Haemagglutination inhibition test
Single radial hemolysis
ELISA
TREATMENT:- Oral supportive therapy
37. MEASLES- RUBEOLA
Enters the host via respiratory route and spreads to the lymph nodes.
Incubation period= 1-3 weeks
Both humoral and cell mediated immunity take part in combating
infection, has a life long immunity.
OCULAR MANIFESTATIONS-Conjunctivitis,
Koplik’s spots, SPK
LAB:-
Virus isolation from conjunctival biopsy
Direct immunofluorescence- microscopy
Culture- Cell lines- primary monkey kidney, human fibroblast cells
Serology- Hemagglutination inhibition test, complement fixation test,
neutralisation test.
38. RUBELLA- GERMAN MEASLES
RNA virus.
Family- Togaviridae.
Genus- Rubivirus
Spherical virus
70nm in diameter
Has a lipid envelope which has virus specific hemagglutinin spikes.
It Causes-
Post natal Rubella
Congenital Rubella syndrome{CRS}
39. CRS
Viremia occuring in pregnant women results in infection of
placenta and the differentiating cells of the foetus.
These children who are born secrete the virus in pharyngeal
secretions, urine and CSF fluid, which is detectable for 12-18
months.
Clinical triad of CRS=
Congenital heart disease+ Total/partial blindness(cataract,
glaucoma, chorioretinitis)+ Neurosensory deafness
Demonstration of IgM rubella antibody in infants is the Diagnostic
of CRS.
40.
41.
42.
43. LAB DIAGNOSIS
Virus isolation from the specimen- Cell lines: Vero, RK-13
derived from rabbit, SRIC. In these cell lines it produces a
non specific cytopathic effect.
The virus can be demonstrated by- immunofluorescence with
specific antibody, interference method(using Coxsachie
antigen as challenge virus)
Serology- Hemagglutination Inhibition test: agglutinates
erythrocytes of 1day old chick, pigeon and sheep.
ELISA for IgG & IgM: Rise in IgG antibody titre should be
demonstrated in 2 serum samples and obtained at an interval
of 10-14 days. Else rubella specific IgM should be
demonstrated in a single specimen.
44. PREVENTION & CONTROL
MMR= Mumps, Measles, Rubella vaccine in a combined
form between 12-18 months of age.
Live attenuated MMR vaccine-
Routine vaccination of children < 12yrs
Immunisation of adolescents and children of child bearing
age.
Screening all pregnant women and immunising them
45. RETRO VIRUS
HIV belongs to the family Retrovirus and the genera Lentivirus.
Etiologic agent of Acquired Immuno Deficiency Syndrome.
It is a linear single stranded RNA virus. It is an enveloped Spherical
virus, 100-140nm in diameter, has a cylindrical bar shaped
nucleoid. Has the enzyme ‘Reverse Transcriptase’
HIV infects the T4 cells, monocytes, macrophages. As the disease
progresses T4 cells are destroyed and leads to reversal of T4:T8
ratio.
There is a decrease in production of Interleukins and Lymphokines,
abnormal activation of B-cells, Decreased natural killer cell activity
and impaired lymphocyte and macrophage functions.
46.
47. PATHOGENESIS
Exposure to HIV
Pt is asymptomatic Symptomatic
Persistent glandular lymphadenopathy
AIDS
Immunosuppression
Opportunistic infection
Lymphoma
Kaposi’s sarcoma
48. ROUTES OF TRANSMISSION
Sexual route
Trans placental route
Contaminated blood and its products
49. HIV AND THE EYELIDS
Kaposi’s sarcoma
Multiple molluscum lesions
Severe herpes zoster ophthalmicus
50.
51.
52. HIV AND THE ORBIT
CELLULITIS:
From contiguous sinus infection
B-CELL LYMPHOMA
53. HIV AND THE CONJUNCTIVA
Kaposi Sarcoma
Squamous Cell Carcinoma
54.
55. HIV AND THE CORNEA
KERATITIS - Due to
Microsporidium
Herpes Simplex
Herpes zoster
56. HIV AND THE EYE -
UVEA AND POSTERIOR SEGMENT
Anterior Uveitis
HIV Retinopathy
Asymptomatic
Multiple cotton wool spots
57.
58. Retinitis - Due to
CMV-Vasculitis, Vitritis, Haemorrhages.
VZV-Progressive outer Retinal necrosis
Toxoplasmosis-Retinitis
61. OCULAR MANIFESTATIONS IN AIDS
Ocular adnexal Kaposi sarcoma
Molluscum contagiosum follicular conjunctivitis
Herpes zoster ophthalmicus
Keratitis due to Microsporidia and HSV
Infectious conjunctival granulomas due to cysticercosis, TB and
fungus
CMV retinitis
Acute retinal necrosis syndrome due to HZV
Toxoplasma chorioretinitis
Syphilitic chorioretinitis
Ocular histoplasmosis
HIV retinopathy
62. DIAGNOSTIC TESTS FOR HIV
Non specific tests to detect immuno compromised state
Leucocyte count< 2000/mm3
Total CD4 count <200/mm3
Reversal of CD4: CD8 ratio
Raised IgG and IgA levels
Decreased platelet counts- thrombocytopenia
Diminished CMI by skin tests
63. Specific Tests:
Antigen detection P24 is the earliest viral marker.
IgM followed by IgG disappears within 4-8weeks.
Virus isolation - Tissue culture in embryonic kidney cells/ MRC-5.
PCR- DNA PCR / RNA PCR
Antibody detection
Screening with ELISA
Western Blot test- Confirmatory
64. TREATMENT
I.V Ganciclovir and Foscarnet are used in the treatment of CMV
retinitis.
Zidovudine and Didanosine are presently available, they block the
enzyme Reverse transcriptase.