Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
204 Cards in this Set
- Front
- Back
|
- Capsules: made up of what?
Name an unusual capsule |
mostly are polysaccharide
- Stretococcus pneumoniae capsule is made up of polysaccharide. -Bacillus anthracis capsule is made up of polypeptide consisting of D-glutamic acid. |
|
|
M protein in cell wall
|
of group A streptococci is antiphagocytic (leads to strep throat). This not a capsule!!
|
|
|
The cell wall will be complete removed forms -->
|
a protoplast. The cell wall has been completely removed.
|
|
|
L-forms
|
are produced when bacteria are grown in the presence of penicillin, can occur with certain infections. These were produced in Lister laboratories. Penicillin works on peptidoglycans of cell wall, prevents bacteria from producing cell wall.
|
|
|
Mycoplasma-
|
only naturally occurring bacteria without a cell wall. Has a special cell membrane to keep the cell intact. These contain sterols (the one prokaryotic group that contains sterols so that the cell does not lyse). These have not been treated with any kind of antibiotic
|
|
|
Is the cell membrane a virulence factor?
|
The Cell Membrane
- Is not a virulence factor |
|
|
-Transformation
|
DNA from donor cells leaks out into solution and enters competent recipient cell
o Small piece of DNA leaks out to environment and gets picked up by another bacteria. o Not all cells are able to do this, those that can are known as “competent”. o Can also get transformation from a plasmid. A plasmid can be incorporated into the genome and may bring about resitance. o Bacteria known to be capable of transformation: Gram positive bacteria Steptococcus pneumoniae, streptococcus sansu, Bacillis Gram negative bacteria -> Nesseria honorroeae, moraxella osloensis, haemmophilius infleunzae, pseudonas stuzert, mycoplasma urethlis. |
|
|
Transductions
|
involves a bacterial virus --> bacteriaphage.
- A virus attaches to the cell and incculates its DNA into the cell and the cell will then replicate the viruses’ DNA. - If bacteriaphages undertake the lytic cycle of infection upon entering a bacterium, the virus will take control of the cell’s machinery for use in replicating its own viral DNA. |
|
|
3 ways bacteria can spread resistance
|
Conjugation, transformation, transduction
|
|
|
Lytic or virulent phages
|
are phages which can only multiply on bacteria and kill the cell by lysis at the end of the life cycle.
|
|
|
Lysogenic conversion -
|
When a cell becomes lysogenized, occasionally extra genes carried by the phage get expressed in the cell. These genes can change the properties of the bacterial cell. This process is called lysogenic or phage conversion.
|
|
|
Most common normal flora found in Conjunctiva
|
Staph. Epidermidis is most common (75-90% found in people
|
|
|
- Medically Important Staph Species
|
Staphyloccus aureus- pathogen
STaph. Epidermis- opportunist (is not necessarily pathogenic) Staph. Saprophyticus- free living, opportunist |
|
|
Staph Aureus
a. Eye diseases |
a. Blepharitis- infection of the eyelid
b. Dacrocystiis- infection of lacrimal sac c. Conjunctivitis- infection of the conjunctiva d. Keratitis- infection of the cornea e. Keratoconjunctivits- infection of the conj. And cornea ******************** f. Endophthalmitis- infection of the aqueous or vitreous humor extremely severe. Do not see unless someone is very ill or immunocompromised. |
|
|
Staph Aureus Facts
|
- Gram +
- Grapelike cluster - Major components of the normal flora of skin and nose. - Catalase + - Coagulase + - Facultative - Beta hemolysis on blood agar, we see lyse blood cells- see a clear colony - Responsible for: Food poisoning. Produces enterotoxin. - Golden pigmented (aureus)- often - Protein A- protects organism from phagocytosis. Binds to Fc portion of IgA and may protect proganism from phagocytosis. |
|
|
Staph Aureus Diseases
|
CASE OF I
Carbuncle Abscesses Scalded-skin syndrome Endocarditis Osteomyelitis food posioning Impetigo |
|
|
What is the true pathogen of staphylococci?
|
Staphloccous Auerus
|
|
|
Staphylococcus epidermis Facts
|
- Most common flora of the Conjunctiva
- Non-hemolytic on blood agar - Gram + - Grape like cluster - Catalase + - Coagulase-negative. - Non pathogenic - Found on skin of 75-90% of people - Are opportunists - Are nonsocomial --> infections at hospital - Iatrogenic- caused by physicians and other hopsital personnel |
|
|
Staphyloccus saprophyticus Facts:
- |
Opportunistic
- Urinary tact infection - In young, sexually active woman - Normal flora of genitourinary tact - Spreads via poor hygiene, especially related to sexual activity |
|
|
Staphylococci Treatment:
|
can produce a phage-coded penicillinase that degrades beta lactam antibiotics. Some strains also have modified penicillin binding proteins. Thus beta lactam antibiotics (including methicillin) are often ineffective.
Vancomycin is thus the drug of choice. |
|
|
The Streptococci
|
A. “streptococci” = “chains of spheres” because of the way they divide
B. found in chains which can be short or long (chains are mostly seen from broth cultures) Most streptococci won’t grow on mediums without blood – they produce hemolysins *** Are catalase - (distiniguishing them from Staph!!) |
|
|
Lancefield Group A
|
a) Streptococcus pyogenes
b) Found in humans (oropharynx) c) Pyogenic (pus-producing) d) Causes strep throat and scarlet fever |
|
|
Lancefield Group B
|
S. agalactiae
b) human newborns (babies are infected when born because this organism is part of the normal flora of the female genital area) c) animals CAN CAUSE MENINGITIS |
|
|
Lancefield Group C
|
b) Humans—not important/rare
c) Animals (like horses and cattle) |
|
|
Lancefield Group D
|
a) Enterococcus faecalis & others
b) Normal GI flora (large intestine) - bound in the intestinal tract; involved with fecal material c) Humans d) Animals e) Mainly opportunistic |
|
|
Strep. Organisms without the C carbohydrate: not beta-hemolytic
|
1. Viridans streptococci
a) S. sanguis b) S. salivarius c) S. mutans d)Normal flora of oropharynx e)Cause cavities if you eat a lot of candy/sugar 2.Streptococcus pneumoniae |
|
|
Only Strep that causes: Periorbital cellulitis
|
S. Pyogenes
|
|
|
Only Strep that causes:
Dacrocystitis |
S. Pnuemoniae
|
|
|
The main streptococci that cause eye diseases:
|
S. pneumoniae and S. pyogenes
|
|
|
Erythrogenic toxin:
|
a) Involved in scarlet fever
(1) *Strep with erythrogenic toxin will cause scarlet fever, but those without it will only cause a sore throat |
|
|
S. pyogenes facts
|
- Gram +
- in chains or pairs - Facultative anaerobes (aerobic or anaerobic) - The M protein binds fibrinogen from serum and blocks the binding of complement to the underlying peptidoglycan. This allows survival of the organism by inhibiting phagocytosis. - Catalase - - B hemolysis - Taxo A treated --> bacitracin |
|
|
S pyogene diseases:
|
Erysipelas
Cellulitis Acute Pharyngitis (tonsilitis)-- --------Strep Throat Impetigo Scarlet Fever Fascilitis Sepsis |
|
|
Post-streptococcal diseases:
|
Referred to as “sequelae” of group A Strep infection
b) Rheumatic Fever (about 3 weeks after initial infection) c) Acute glomerulonephritis |
|
|
Streptococcus pneumoniae Facts
|
- Gram +
- Catals - - Alpha hemolysis - lancet-shaped, diplococci - polysaccharide capsule - Cause pneumococcal pneumonia and pneumococcal meningitis*** - Sensitivity to optochin (Taxo P) - Quellung test + – capsular swelling test. |
|
|
Bacillus anthracis Facts
|
- Gram +
- Rod shaped - Aerobic - Capsule: (1)Antiphagocytic (2)D-glutamic acid polymer (polypeptide). An unusual capsule.********** - Has endospore - Entry of spores into host – 3 types of anthrax (1) Skin = cutaneous anthrax (ex. touching the wool of a sheep) (2) Inhalation = Woolsorter’s Disease (pulmonary) (3) Ingestion = gastrointestinal |
|
|
Clostridium Facts
|
- Anaerobic rods
- Gram + - Form spores |
|
|
Clostridium botulinum
|
a. Causes food poisoning, which can be fatal
b. Usually from improper canning procedures home canning c. Early symptom of double vision |
|
|
Clostridium tetani
|
Causes lock jaw
|
|
|
Clostridium perfringens
|
Causes mild food poisoning and gas gangrene
Must amputate affected limbs Follows prolonged antibiotic treatment. |
|
|
Clostridium difficile
|
Causes pseudomembranous colitis (follows prolonged antibiotic treat, several weeks to a month. The antibodies destroy normal body flora, as well. Difficule then can produce a collitis)
(1) Normally kept under control in our GI tracts (2) Treatment with antibiotics can kill off other normal flora and allow this one to take over and produce toxins and pseudomembranous colitis |
|
|
Neisseria Facts
|
- Gram -
- Kidney bean/coffee bean shape. - Aerobic, BUT they actually prefer to grow in an environment with added carbon dioxide (10%). Oxidase positive + a) These organisms have cytochrome oxidase, and when reagent is added to the colony, it turns pink, then slowly black |
|
|
Neisseria meningitidis –
|
- referred to as “meningococcus”, causes meningitis
|
|
|
Neisseria gonorrhea
|
– referred to as “gonococcus” or as “GC”
- Grows on Chocolate Agar, 10% CO2 needed - Will not grow on blood agar - Colony types = T1 – T4 a) T1& T2 are virulent (have pili) and will thus cause gonorrhea. Pili used to attach to mucosal cells b) T3 & T4 will not cause gonorrhea - a) Culture purulent exudates on Thayer-Martin or Martin-Lewis plates |
|
|
Diseases of N. Gonorrhea
|
Conjunctivitis
Keratitis Keratoconjunctivitis ************Ophthalmia neonatorum (1) Conjunctivitis of the newborn (2) Can be caused by any organism that is capable of infecting the newborn (3) Signs appear 2-5 days after birth -Genital itis-es -Bacteremia - Septic Arthritis |
|
|
Neisseria meningitis
|
- One of the most frequent causes of meningitis
- Does not cause an eye disease - Gram-negative diplococcus – looks exactly like N. gonorrhoeae - Contain pili – virulence factor - Attach to nasopharyngeal mucosa - Contains a polysaccharide capsule - 90% are caused by serogroups A, B, & C - Transmission occurs by inhaling respiratory droplets from a carrier or a patient in the early stages of the disease - c) Organism makes an IgA protease, which cleaves IgA and helps to avoid this antibody - Oxidase + -Organisms can be found in CSF and skin - Cannot automatically treat with pencillin. |
|
|
*** there are three organisms that cause meningitis in the young:
|
Neisseria meningitidis, Haemophilus influenzae, and Lancefield group B
|
|
|
Haemophilus Facts
|
- Gram -
- pleomorphic (has many shapes), cocco-bacilli (rounded bacillus) - Can be part of the normal flora found in the mouth - Contains a capsule = virulence factor - Can lead to meningitis - Haemophilus Influenzae type B leads to meningitis - Quellung reaction test + |
|
|
Haemophilus Diseases
|
Conjunctivitis
Keratitis Keratoconjunctivitis Pharyngitis Pneumonia Otis media Cellulitis Sinusitis Epiglottitis Septic Arthritis |
|
|
The Mycobacteria Facts
|
-Acid-Fast
1.cell wall contains 60% lipid (mycolic acid), which makes it lipophilic - Slender rods - Gram-positive - Intracellular parasites – grow inside WBC and kill them - facultative glycolysis - Aerobic - Slow growing |
|
|
Mycobacterium tuberculosis
|
Aquired via Inhalation --> alveoli
- Multiply in pulmonary epithelium or in macrophages. Within 2-4 weeks, many are destroyed by the immune system - No toxins are produced by the organism - Able to grow in macrophages; the macrophage is destroyed and 100s of mycobacteria are released – once organisms are in host cells, the immune system can’t get to them -Immunity – both humoral & cell-mediated responses are stimulated - Detected: The presence of acid fast bacteria in sputum is a rapid presumptive test for tuberculosis (link to method). Subsequently, when cultured, M. tuberculosis will grow very slowly producing distinct non-pigmented colonies after several weeks. M. tuberculosis can be differentiated from most other mycobacteria by the production of niacin. - Tubercle formation – a productive, granulomatous lesion. If lesion arrests, tubercle undergoes fibrosis and calcification - Tuberculin reaction: a) Delayed-type hypersensitivity (DTH) to protein antigens of M. tuberculosis *********Mantoux Test/ PPD test - Tine Test |
|
|
mycobacterium tuberculosis treatment:
|
*Multiple drug therapy* to prevent resistance (KNOW!!!!) Can’t only use one drug, due to resistance
Takes atleast 6 months -Vaccine – BCG (Bacille Calmette-Guerin) |
|
|
Mycobacterium avium-intracellular Complex (MAC)
|
a) “avium” = associated with birds
b) Nonchromogenic c) Found in soil and water d) Opportunists (usually not harmful) e) But can cause disseminated miliary disease in AIDS patients f) Resistant to chemotherapy g) Use four or more drugs at one time h) More resistant than tuberculosis!! i) These are opportunists j) Cord-like, tend to stick together k) Acid-fast |
|
|
Mycobacterium leprae
|
a) Leprosy or Hansen’s Disease
b) Transmitted from human to human c) Prolonged contact between skin of individuals d) Two types (1) Tuberculoid (2) Lepromatous—more serious form of leprosy – affects extremities where body temp is lower – results in deformations – “Leonine appearance”….. ( just like the Thundercats…:P) |
|
|
M. kansasii
|
a) Photochromogens:Produce yellow to orange pigments if exposed to light
- Causes disease similar to TB |
|
|
M. scrofolaceum
|
b) Scotochromogens—
Produce pigment under any conditions |
|
|
Pseudomonas Facts
|
- Can be found in water, soil, plants, on skin & animals
- Gram - rod - Oxidase + - Mainly opportunist - Motile—can swim (they have polar flagella) - Many strains are encapsulated; some are not - Obligate aerobe - Extracellular proteases (elastase, alkaline protease)—break down proteins - Cytotoxin—kills cells - Hemolysins—lyse RBCs - Endotoxins - Exotoxin A and Exotoxin S - Localized infections Resistant to many antibiotics – must do susceptibility testing. Must use a combination of drugs!! |
|
|
The two bacteria to worry about after being burnt?
|
P. aeruginosa and Staphylococcus aureus are the two to worry about with burn victims. Two most common! These are found on the skin, and after being burnt, person does not have that defense mechanism
|
|
|
Pseudomonas eye diseases
|
1. Endophthalmitis—gets into the interior structure of the eye
2. Conjunctivitis 3. Keratitis a) Most infections are in contact lens wearers |
|
|
Pseuodonomas systemic diseases
|
a) Bacteremia—organism in the blood
b) Secondary pneumonia (because it is a 2 invader) c) Bone and joint infections d) Endocarditis—affects the lining of the heart valves e) CNS f) Skin and soft tissue |
|
|
Moraxella lacunata Facts
|
- Gram-negative, coccobacillary (a rod that can look round), usually paired end to end (“diplobacilli”)
- Some require blood or chocolate agar - Oxidase positive - Eye Diseases (1) Usually produces an angular blepharitis (at the lateral canthus; lots of purulent material) (2) May cause follicular conjunctivitis and keratitis |
|
|
3 Oxidase + Bacteria
|
Nisceria, Pseudomonas and Moraxella are all oxidase positive
|
|
|
Enterobacteriaceae
|
1. Large family of Gram-negative rods
2. Normal flora of the colon and female genital tract 3. Transient colonizers of the skin—they are not always present on the skin 4. Opportunists a)E. coli b)Klebsiella pneumoniae c)Proteus species d)Serratia marcescens 5. Pathogens a)Salmonella species b)Shigella species c)Yersinia species d)Some strains of E. coli - Can lead to a) Endophthalmitis -Cell wall polysaccharide = “O” antigens - Endotoxin - Capsular layer -Flagellar antigens = “H” antigens |
|
|
Pathogenic E.coli
|
d) Some strains of E. coli—the “bad boys” of E. coli
(1) Enterotoxigenic (ETEC) - Traveler’s diarrhea (a) Aka “Montezuma’s Revenge” (b) Do not drink unbottled water or eat salad in Mexico; people who live in that country develop resistance, but we have to be careful when we go there (2) Enteropathogenic (EPEC) - Diarrhea in infants (3) Enterohemorrhagic (EHEC) - Hemolytic uremic syndrome |
|
|
Lab Testing for Enterics
|
(1) api system
(a)20 different cupules of biological tests (b)Look at color to differentiate organisms (c)Results are read by a computer to yield the name of the organism (2) EMB plate (Eosin Methylin Blue) - inhibits gram + organisms (a)Purple colored agar. 2 Dyes used. (b)Allows gram (-) to grow (c)Differential and selective media. Gram + will not grow! Those that ferment sugar lactose will give you a colored colony, which helps to identify which organism is present. (d)E. coli gives off a metallic sheen. (e)If organism ferments lactose, will yield a colored colony (f)If not, yields a colony without color (3) Meconky’s agar (a)If organism ferments lactose, will yield a red colony (b)If not, will give a white colony (4)Enterotube system (a)Each chamber is filled with a different substrate (in agar) (b)Insert a colony into the tube (c)Also linked to a computer for analysis |
|
|
Chlamydiae Facts
|
- Obligate intracellular parasites
- Cannot grow on agar - Need a living cell in which to grow - They are unable to synthesize their own pools of ATP, or regenerate NAD+ oxidation; they depend on the host for this. - Cell wall resembles that of a Gram-negative organism - Possess ribosomes and synthesize their own proteins - Sensitive to antibiotics - Life cycle: a) Elementary bodies-enters host and initiates infection b) Then changes into the reticulate/initial body-larger, noninfectious (within 8 hours) C) Forms an inclusion body in the host cell, which become new elementary bodies, which then get released and can infect new host cells. (glycogen inclusions) After 35 hours or so, cell bursts and releases these bodies. |
|
|
Eye Infections from Chlamydia trachomatis
|
Trachoma-a chronic follicular conjunctivitis- chronic inflammation of eyelids
a) One of the leading causes of preventable blindness in the world. Vision loss due to scarring - Inclusion Conjunctivitis a) Acute infection in infants-“ophthalmia neonatorum” --> Gonorrhea also causes this!! Lab test: Can be grown in the yolk sac of chick embyos - can be grown in tissue culture; McCoy cell line (mouse cell line) |
|
|
The Rickettsiae
|
- Does not cause eye disease!
Obligate intracellular parasites just like Chlamydia - Small - Infections transmitted by infected arthropods; lice, ticks, fleas, and/or mites - Diseases 1. Typhus-from lice (during WWI) 2. Spotted fevers (ex. Rocky Mountain Spotted Fever) 3. Q fever-the only one not transmitted by transmitted by an arthropod. It is a pneumonia transmitted by respiration. 4. Generalized infections, sometimes with a rash |
|
|
Fungi facts
|
Eukaryotic – true nucleus
2. May cause subacute to chronic diseases 3. Aerobic 4. Reproduction a. Asexual spores – conidia b. Sexual spores – ascospores, basidospores, etc c. Buds or blastoconidia in yeasts Laboratory Identification 1. Growth on Sabouraud’s agar -->pH of 5.0 – fungi likes an acid pH 2.Microscopic observation 3.Spore morphology 4.Serologic tests 5.Immunofluorescent techniques |
|
|
Fungal diseases of the eye
|
1. Conjunctivitis
2. Keratitis 3. Keratoconjunctivitis – mainly caused by species of fusarium (common air contaminant) 4. Endophthalmitis – caused by Candida species; very serious disease caused by normal human flora 5. Chorioretinitis – Histoplasma capsulatum, Coccidioides immitis, & Candida species 6. These are mainly in the immunocompromised |
|
|
Molds form filaments called
|
hyphae
|
|
|
Many hyphae form a mat called
|
Many hyphae form a mat called a mycelium. This is what you see on spoiled food.
|
|
|
Types of Fungi
1. Yeasts 2. Molds |
1.usually what it looks like at body temperature
2. usually what it looks like at room temperature. |
|
|
yeast facts
|
A. Unicellular
B. Spherical or ellipsoidal in shape C. 3-15 um in diameter D. Most reproduce by budding (blastospores) E. Few yeasts reproduce by binary fission |
|
|
Molds
-Two types of Hyphae |
1. Vegetative – penetrate the supporting medium to absorb nutrients, like the roots of trees
2. Aerial – bear the reproductive structures --> contain the spores and are identified by their arrangement. |
|
|
Candida albicans eye diseases
|
A.Endophthalmitis
B.Keratitis |
|
|
Candida albicans facts
|
- a fungus
1.Normal flora of the skin, GI tract, and genital tract 2.Regarded as yeasts – under special conditions they form pseudohyphae -->never gets extremely long. Can have different morphological appearances. If you grow on specialized media (Cornmeal agar/ Rice extract agar --> forms chlamydospores) 3.They form germ tubes when incubated in serum of any kind |
|
|
systemic Candida Infections
|
- Thrush -->highly inflamed mouth area (tongue/cheek). Normally seen in children. When children are given antibiotics, it wipes out the normal flora in the mouth, so that this fungi no longer has other competition, and grows.
- Vaginal - Diaper rash - Chronic mucocutaneous candidiasis - Esophagitis - Intestinal - Urinary tract - Disseminate infections – in the immunocompromised – kidneys, brain, heart, and eye |
|
|
Aspergillus facts
|
- a fungus
1. Grow rapidly 2. Have septate hyphae 3. Widely distributed in nature (hospital air and nosocomial infections) 4. Common air organism 5. Appears as black and fuzzy colonies when grown on media |
|
|
Aspergillis opportunists
|
1.A. fumigatus
2.A. flavus 3.A. niger --> found in spoiled food |
|
|
Aspergillosis
|
a. Lung or allergies Type 1 Hypersensitivity response
b. Farmer’s lung 1) Can get from pitching hay c. Invasive – pre-existing disease (ex. TB); fungus grows in tissue producing a “fungus ball”, which has to be surgically removed (cut it out of lung) d. Acute pneumonia in the immunocompromised |
|
|
Fusarium Keratitis
|
- Became a problem in 2007 when a contact lens solutions manufacture was infected.
- Fungal keratitis is a serious and painful corneal disease caused by a fungal organism. Until now, fungal keratitis has rarely been reported in the healthy contact lens wearing population |
|
|
Cryptococcus neoformans
|
Fungal pathogen
lung, meninges – spread by pigeon’s fecal matter 1. This is a true yeast 2. Has a large capsule 3. yeast-like mold (di-morphic) |
|
|
Histoplasma capsulatum
|
Fungal pathogen
– soils containing bird, chicken, or bat droppings 1. dimorphic 2.Pneumonia that resembles TB |
|
|
Blastomyces dermatitidis
|
Fungal Pathogen
- soil 1.Di-morphic 2.Lesions on the skin |
|
|
Acanthamoeba
|
A protozoa
single celled organism that is free living in fresh water, soil, sewage, and sea water. Get infected in swimming pools. |
|
|
Acanthamoeba infections
|
1. Keratitis – minor trauma to eye precedes infection – hay, dust, sawdust, water, contact lenses (soaking solutions)
2. Granulomatous amebic encephalitis – opportunist – immunocompromised, diabetic, alcoholic 3. Ear infections 4. Respiratory tract infections |
|
|
Toxoplasma gondii facts
|
A. Protozoan causing Toxoplasmosis (banana shaped)
B.Tropozoids live in the cysts and when the cyst bursts, infection occurs - Particularly threatening to AIDS patients and to the developing fetus 1. Can have serious brain damage if fetus is not aborted |
|
|
Toxoplasma gondii Syndromes
|
1.Mononucleosis
2.Congenital infection – severe consequences if acquired during 1st trimester 3.Infections of immunocompromised involves the brain and heart 4.Chorioretinitis – lesions on retina and choroid caused by cyst form of parasite a.Can go blind due to this organism (rare) |
|
|
Toxoplasma gondii transmission via
|
1. Eating undercooked meat
2. Breathing in oocysts from kitty litter |
|
|
Toxacara canis
|
A hemolith
-– from dogs, especially puppies 1.A larval nematode (roundworm) a.Recognizes it is no longer in the dog and does not complete it’s life cycle Life Cycle 1.Dogs and cats transmit eggs 2.Children playing in the soil ingest the eggs and become infected a.Commonly found in a sandbox 3.Mature in small intestine 4.Penetrate intestinal mucosa and are carried by the blood to the liver, lungs, and other sites 5.Lesions occur in the liver, brain, eye, spinal cord, lungs, hearts muscles, kidney, and lymph nodes 6.Occurs mainly in children 1-4 years old 7.Contaminated soil or sand boxes |
|
|
Toxacara canis Eye infections
|
a. Choroiditis
b. Iritis c. Chorioretinitis |
|
|
Demodex folliculorum
|
Arthropod
follicle mite 1. It invades the hair follicles and sebaceous glands of humans and domestic animals 2. It has been found in the skin of every part of the human body 3. Eyelashes – chronic erythema, acne, keratitis |
|
|
Virus Structure
-Capsid |
is made up of capsomeres – a protein coat with nucleic acid inside.
2. Envelope virus: contains a membrane on the outside of the capsid. Can be ctyoplasmic, lipid or nuclear membrane. Example: Influenza has an envelope. |
|
|
Viral Replication
|
– several steps must occur before the virus can grow
1.Adsorption or attachment to receptors of susceptible cells 2.Penetration – endocytosis or fusion of viral envelope with the cell membrane 3.Uncoating of capsid – leading to the release of nucleic acid 4.Replication of viral genome: occurs either in the cytoplasm or nucleus. a.DNA viruses multiply in the nucleus b.RNA viruses multiply in the cytoplasm 5.Maturation – assembly of virus particles. 6.Release of virions from cells – budding, cell lysis, or exocytosis, depending on the virus |
|
|
Identification of Virus in body: Titer method
|
a 4-fold rise in the titer
1) Stage 1: Acute Stage 2) Stage 2: Convelescent stage --> 3 weeks later. It is difficult to take blood from this stage because patients do not usually go back to doctor when they are feeling better. 3) Years later: you will still see rise in titer but it will be much lower to Convalescent stage. It (a) Take blood from both stages and see a 4-fold rise in antibody - Thus we know the person was infected with a certain virus at some point in life |
|
|
Lytic infections –
|
virus replicates and kills cells
|
|
|
Latent Viral Infections
|
a.Primary acute infection
b. At resolution of disease you start to feel better c.Virus persists, in a cryptic form until it is reactivated (“hides” in nerve tissue until reactivated) d.Symptoms recur as well as virus production e.Ex. Varicella-zoster (chicken pox/shingles), herpes simplex, CMV, and Epstein-Barr |
|
|
Stages in Viral Pathogenesis
|
a.Entry and primary replication
b.Spread to target tissues c.Incubation period – days, weeks, months, years d.Cellular damage and clinical illness which may cause: 1) Cell death 2)Immune-mediated pathogenesis (chronic hepatitis) 3)No apparent effect |
|
|
Host cell defense factors against viruses
|
a)Antibody response
b)Complement c)Cell-mediated immunity (T cells) – important with viral infections. d)Interferons (produced by virally infected cells). Cells pick up interferons and it helps to protect them. e)Phagocytosis f)Fever – a good thing, as long as it is not too high, because viruses won’t grow if they don’t “like” the temperature |
|
|
Treatment for viruses
|
1.Antibiotics do not work against viruses!!!!
2.Antiviral chemotherapy 3.Stages of growth are targeted: mainly the replication of viral nucleic acid a.Immunoglobulins – passive immunization 1)Ex. Rabies virus, hepatitis A virus, hepatitis B virus, measles virus f.Viral Vaccines – active immunization |
|
|
Types of Viral Vaccines
|
Live attenuated virus vaccines (ex. polio) Your body responds by producing antibodies
b)Killed virus vaccines – response not as good as with live attenuated virus vaccines, but don’t have to worry about mutations (influenza virus vaccine) c)Purified protein vaccine – recombinant DNA technology (ex. hepatitis B virus) d)Subunit vaccine (ex. influenza virus) – take portions of viral particle and use in vaccine |
|
|
Adenoviruses facts
|
- discovered during screenings of throat washings and cultures of adenoids and tonsils (lymphoid tissue in the throat – around area of tonsil). This is how it got its name.
-Linear, double stranded DNA (infectious portion of virus) -Non-enveloped (no lipid envelope – naked virus, icosahedral symmetry (20 sided figure) - Several capsid proteins – hexon (6-sided), penton base, fiber (contains the viral attachment protein) Replication: Virus attachment – via penton fiber structure (“knobs” on the tips of viral fibers) to membrane of host cell 2. Assembly of the virus occurs in the nucleus of the cell. |
|
|
Illnesses associated with adenoviruses
1. Ocular infections: |
Transmitted by direct inoculation of the eye by virus-contaminated hands, ophthalmologic instruments, or bodies of water in which groups of children swim together
a. Epidemic keratoconjunctivitis (EKC) – AKA “shipyard eye” because of an epidemic among dockworkers; serogroups 8, 19, & 37 --> most common b. Pharyngoconjunctival fever (PCF) – serogroups 3, 7, & 14 c. Acute nonspecific follicular conjunctivitis-serogroups 1 -11, & 19 *KNOW the serogroup numbers for ocular infections* |
|
|
Epidemic keratoconjunctivitis serogroups
|
8, 19, 37
|
|
|
Pharyngoconjunctival fever (PCF) – sero group
|
serogroups 3, 7, & 14
|
|
|
c. Acute nonspecific follicular conjunctivitis-serogroups
|
1, 11, & 19
|
|
|
Adenovirus systemic diseases
|
Other diseases:
a. Respiratory diseases: i. Acute febrile pharyngitis (sore throat, fever) ii. Acute respiratory disease (ARD) in military recruits: due to crowded conditions and fatigue (which decreases resistance). iii. Pneumonia can result b. Gastrointestinal disease (diarrhea, upset stomach) c. Acute hemorrhagic cystitis d. Systemic adenoviral infections (in immunocompromised hosts) |
|
|
Adenovirus Lab teting
|
Virus isolation: take material from where patient is experiencing symptoms (ex. stool, urine, throat and conjunctiva) and culture in primary human embryonic kidney tissue
2. Serology – look for (antibodies): a. Complement-fixing antibodies (IgG and IgM) b. Neutralization (patient’s serum plus virus, if neutralized, can’t infect cells) c. Hemagglutination-inhibition (the Ab prevents clumping of RBC’s) |
|
|
Adenovrius prevention
|
Formalin (solution of formaldehyde) inactivated vaccine: serogroups 3, 4 and 7.
- Live attenuated vaccine: serogroups 4 and 7, enteric-coated capsule (given to military recruits, not to general public). It is enteric coated so that it can get through stomach into intestines. - Wash hands frequently, be aware of fomites – inanimate objects that can harbor infectious agents |
|
|
Herpes simplex virus type 1
|
above the waist – 90% is in the oropharyngeal area):
a. Oropharynx is predominantly infected i. Kissing, exchange of saliva, ii. Primary infection occurs early in life b. Direct contact: oral-genital c. Respiratory secretions d. Then usually goes to trigeminal ganglia (latent until resistance is low) ocular/oral symptoms. It can hide in the nervous system in the trigeminal, superior cervical or ciliary ganglion) |
|
|
Herpes simplex virus type 2
|
(can affect same tissues as HSV Type I but mostly below the waist):
a. Sexually transmitted (usually); oral-genital contact, oral-oral contact b. Perinatal infection (an infected mother passes herpes to newborn baby through birth canal if genital herpes) c. Antibodies seldom found before adolescence d. 40 - 60 million infected individuals in US (500,000 new cases/year) e. Can go to lumbar and sacral root ganglia (latency) genital region REMEMBER #2 is BELOW the waist. #1 is ABOVE the waist. |
|
|
Ocular Herpes
|
Ocular herpes: keratoconjunctivitis
a. Primary infection b. Recurrent infection: i. Formation of dendritic ulcers ii. They can progress to deep stromal keratitis iii. Leading to scarring and loss of vision |
|
|
Herpes Immunity
|
1. Incomplete, reinfection, reactivation
2. Antibodies develop too late to be helpful: therefore they play no role in recurrence 3. Cellular immune mechanisms control both primary and recurrent infection 4. Suppression results in spread and severe disease. |
|
|
Viral cures??
|
these drugs inhibit the synthesis of DNA, however there are no known drugs that cure a viral infection. KNOW this fact.
|
|
|
Varicella-Zoster Virus (VZV)
|
Zoster = “Shingles” = reactivation of latent virus
Anyone who has ever had chicken pox or has had a live vaccine has these viruses hiding in them – this may or may not reappear as shingles 1. Respiratory tract 2. Spread to skin epithelial cells – chickenpox 3. Appear 14 - 21 days after exposure |
|
|
Varicella-Zoster Virus (VZV) Clinical Significance
|
Clinical Significance
i. Primary and recurrent diseases are quite distinct ii. Not life-threatening in normal, healthy individual; but there are severe complications in immunocompromised |
|
|
Varicella-Zoster Virus (VZV) Vaccines
|
Vaccine – live, attenuated virus was developed in 1995
2. Given to children 1 year or older 3. Now one of the routine childhood vaccines 4. Also recommended for non-immune adults who are at risk of being exposed to contagious individuals 5. Varicella-zoster immune globulin is given to susceptible individuals who have been exposed to chickenpox or zoster lesion fluid (which contains the virus) 5. Has no effect on the occurrence of zoster 6. Live attenuated vaccine vaccine against zoster now exists. |
|
|
Retrovirus
|
Contain an enzyme called reverse transcriptase virus contains single strained RNA that is copied into DNA, which is then converted back to RNA to form viral proteins.
C. Converts a single-stranded RNA viral genome into a double-stranded viral DNA D. RNA serves as a template for DNA synthesis. |
|
|
AIDS (Acquired Immune Deficiency Syndrome) Symptoms:
First reported in the USA in 1981 |
1. Severe pneumonia – from Pneumocystis carinii (an opportunistic parasite, once thought to be protozoan, but now thought to be associated closely with yeast, treated with antibiotics but later comes back – can cause death. Usually this yeast poses no threat unless you are severely immunocompromised)
2. Kaposi’s sarcoma – a skin cancer. 3. Sudden weight loss 4. Swollen lymph nodes 5. General suppression of immune function |
|
|
HIV Replication First Phase
|
First phase = virus attaches to cell and enters; reverse transcription, & integration of virus into host genome
a. Attachment occurs by SU fragment on surface of HIV (1) binds to CD4 molecule; affects helper T cells, lymphocytes, monocytes, and dendritic cells (2) all are cells that function in the immune system b. Viral entry occurs by means of TM (fusion) glycoprotein which triggers fusion between viral envelope and cell membrane c. Reverse transcription of viral RNA by an RNA-directed DNA polymerase (1) Process takes place in the cytoplasm d. Integration of the provirus into host cell DNA e. Transported to the nucleus with the aid of MA (matrix protein) f. Viral integrase cleaves the chromosomal DNA and inserts the provirus. 2. |
|
|
HIV Replication Second Phase
|
Second phase = synthesis and processing of genomes, mRNAs, structural proteins; uses the host cell machinery
a. Transcription and translation b. Assembly and maturation of infectious progeny c. Virus buds out of cell 3. End result = cell death |
|
|
HIV transmission
|
I. Transmission – four routes:
1. Sexual contact – virus is present in both semen & vaginal secretions 2. Transfusions – whole blood, plasma, clotting factors, or cellular fractions of blood a. We now have tests to detect virus or its components (to screen blood) 3. Contaminated needles – either accidentally or through shared needles or syringes by drug users 4. Perinatal – there is a 15% to 40% chance of transmitting infection to newborn a. transplacentally or breast feeding (virus is in breast milk) |
|
|
AIDS Pathogenysis
|
1. Pathology results from either tissue destruction by the virus itself or the host’s response to the virus-infected cells (ex. CD8 cells)
2. Also, the immunodeficient state that leads to opportunistic diseases – patient cannot fight off infections *important* most die from complications of the virus, but not the virus itself. |
|
|
Development of HIV to AIDS usually takes:
|
Development from HIV infection to AIDS takes an average of 10 years, and if untreated, is itself uniformly fatal within 2 years
|
|
|
Initial Phase of HIV
|
(1) Macrophages within the genital tract
(2) Blood carries them to dendritic cells throughout the lymphoid tissue (3) Then to CD4+ lymphocytes (Helper T cells are necessary in signaling for immunity) (4) Get an Acute Phase viremia (a) Several weeks after initial infection (b) Virus multiplies rapidly (c) 1/3 to 2/3 experience an acute disease syndrome (similar to infectious mononucleosis) (5) During this period there is a very high level of virus replication occurring in CD4+ cells (helper T cells) (6) Seroconversion (convert to having antibodies in blood): 1 to 10 weeks after initial infection (7) Lymph nodes become infected and later serve as sites of virus persistence during the asymptomatic period |
|
|
Latent Phase of HIV
|
b. Latent period
(1) Acute phase viremia is eventually reduced with the appearance of an HIV-specific cytotoxic T lymphocyte response, followed by humoral antibody response [both cellular and circulating antibody response] (2) Latent period lasts from months to many years following acute infection |
|
|
Clinical Complications of AIDS during latency period
|
(3) Clinical Complications during latent period
(a) Latent period lasts on the average of 10 years (b) Persistent, generalized lymphadenopathy (swollen lymph nodes) (c) Diarrhea – from Cryptosporidium parvo (parasite in water) (d) Chronic fevers (e) Night sweats (f) Weight loss (g) Common opportunistic infections (i) Herpes-zoster (ii) Candidiasis (a yeast that is part of normal flora) (iii) Occur repeatedly (h) CD4+ count remains normal or gradually declines [it is greater than 200cells/ul] |
|
|
Progression of HIV to AIDS based on
|
(7) When below CD4 helper cells are 200 cells/ul = frequent and serious diseases and opportunistic infections (person has AIDS) --> the critical time.
|
|
|
End stages of AIDS
|
(4) All of the following cells/tissues are affected:
(a) Langerhans cells in the skin (b) Dendritic cells in lymph nodes (c) Monocytes in bone marrow (d) Eye – ischemia (deficiency in blood) in the retina (i) Can lead to retinitis (ii) Can see the damage in the retina (e) Anemia |
|
|
Opportunistic Infections in AIDS – be aware of these infections!!!
|
a. Toxoplasma – protozoan parasite from raw meat or cat feces, same grouping as malaria parasite – can lie dormant, get brain cysts which later open and can cause blindness
b. Cryptococcus – in pigeon feces; organisms are breathed in and can cause meningitis --> yeast that has a capsule that is a virulence factor. *Know* c. Mycobacteria Lung diseasesL a. Pneumocystis carinii pneumonia b. Mycobacterial infections common (1) 30% of AIDS patients die from tuberculosis Gastrointestinal tract a. CMV colitis b. Protozoal parasitic diseases – Cryptosporidium (opportunistic) c. Gram-negative enteric organisms 5. Latent herpes virus 6. Mucocutaneous candidiasis (oral, esophageal, or vaginal) Kaposi’s sarcoma (KS) – involves the skin, mucous membranes, and deep viscera b. Various lymphomas – including those of the CNS |
|
|
AIDS/HIV treatment
|
1. Every step in the HIV replication cycle is a potential target for an antiviral drug
2. Those directed against reverse transcriptase (enzyme) and viral protease have thus far been successful 3. Combinations of three different drugs used, which works and also limits mutations a. It is rare that the virus will be resistant to a mixture of drugs (cocktail) c. Nucleoside Reverse Transcriptase Inhibitors (1) Target the reverse transcriptase itself (2) Advantage = have no effect on host blood-forming elements & lack cross-resistance with nucleoside analog reverse transcriptase inhibitors d. Protease Inhibitors (more recent drugs) |
|
|
AIDS and HAART
|
1. HAART = Highly Active Anti-Retroviral Treatment
2. Increased the life expectancy of patients 3. Reduced opportunistic infections 4. CMV is the second-most opportunistic infection (20-40% of AIDS patients) 5. After HAART, 7.5% of patients AZT therapy of pregnant women has reduced perinatal transmission by 70% followed by several weeks of AZT to the newborn |
|
|
CMV (Cytomegalovirus)Facts
|
1. It is a member of the Betaherpesvirinae (a member of the Herpes family)
2. Differs from HSV and VZV, but within the family 3. Infected cells are typically greatly enlarged and multinucleated 4. An opportunistic invader 5. In symptomatic cases, the kidney, liver, and CNS are commonly affected 6. Primary infection as an adult may result in a mononucleosis syndrome. 7. Most common intrauterine viral infection |
|
|
Ocular effects of CMV
|
8. f. Ocular effects include:
(1) Chorioretinitis |
|
|
Eye infections from Adenovirus
|
– “naked virus”
A. Acute viral infection of the ocular adnexa and cornea, most common cause of red eye. B. Infections are usually acute, self-limiting forms of follicular keratoconjunctivitis, so patient may not complain of symptoms and not seek care. |
|
|
Adenoviral Eye Syndrome
|
1. Epidemic Keratoconjuntivitis (EKC) – “Hot red eye”
a. Most commonly Adenovirus Type 8 and 19, also 2-4, 7-11, 14, 16, 39, 37 reported b. Epidemiology: Iatrogenic outbreaks |
|
|
Adenovirus Pathogenesis
|
a. Virus prefers intact epithelium of conjunctiva, cornea and upper respiratory tract – likes the conjunctiva the most. Many patients have a cold prior to having an eye infection.
b. Incubation of 2-14 days during which the virus is contagious |
|
|
Acute Stage of Adenovirus
|
- begins with viral replication in epithelium, which leads to the clinical presentation. If virus is actively replicating on the conjunciva you get “a hot red eye”
d. Sx: sudden watery discharge, punctate kerititis, tenderness, swelling, follicular and papillary conjunctival responses, psuedomembrane formation and variable conjunctival hemorrhage. Follicles look like clear elevations, with blood vessels running around the sides. KNOW THIS FOR THE TEST!! Definitely will be asked about the clinical presentation of this virus! |
|
|
When are we most worried about the effects of adenovirus?
|
f. We are more worried when patient begins to feel better delayed hypersensitivity reaction leads to corneal infiltrates which can block vision (normally seen 10-12 days after infection). Because patient feels better, they might ignore the infiltrates and will not return to office. Schedule a Follow-Up, especially if infiltrates are seen on the visual axis. We can help prevent corneal scarring via the infiltrates if treated with a steroid.
|
|
|
Herpes Simplex Facts
|
1. Most common infectious cause of corneal blindness in developed countries
c. Has flu like symptoms occasionally with vesicles on the eye lid and possible conjunctivitis d. May be associated with preauricular adenopathy or folliculosis e. May be taken for a cold-like virus f. Unilateral orbital, or bilateral (but not in recurrent infections) g. Virus is self limiting |
|
|
Herpes Simplex 1 occurs
|
above the waist
|
|
|
Herpes Simplex 2 occurs
|
below the waist
|
|
|
Latency period of Herpes Simplex
|
Latent period where the virus lies dormant in the trigeminal ganglion. Reactivating during times or emotional or physical stress, trauma (including surgery), UV exposure, menstruation, concurrent infectious disease
ii. Most clinical ocular infections are due to reactivation. Virus travels along the trigeminal nerve to the terminal end resulting in “fever blisters”, “cold sores”, and ulcers on ocular surfaces. |
|
|
H. Simplex Blepharitis
|
i. Vesicles on the eye lid become ulcerated and crusty (Vesicular blepharitis) after a week and heal without scarring. H. Simplex Blepharitis: Generally heals on its own, without scarring.
|
|
|
Herpes and the Cornea
|
k. Cornea involvement – may produce epithelial, stromal, or endothelial disease either alone or in combination. Likes the epithelium the most!
1. Classic appearance is of a dendrite: linear or serpentine branching ulcer. It follows the branching of the trigeminal nerve. It stains with Rose Bengal, and Lisamine Green. i. The cornea is the most common location of recurrent HSV disease ii. Recurrent HSV infection is unilateral in 90% of cases iii. May initially present as punctate keratitis that coalesces into a dendritic pattern Very early stages of HSV epithelial infection may or may not stain, but it will soon coalesce into the dendrites. Some forms of HSV may form large ameboid, map-like geogprahic ulcers. - Corneal hypoesthesia (reduced sensation) ii. Neurotrophic Ulcers: Sterile, non-healing ulcers (keratopathy) |
|
|
Dendritic ulcers
|
– contain live Herpes virus. Break out follows pattern of corneal nerves.
Terminal endbulbs - end of each dendrite is swollen and enlarged. Dendrites are swollen and can be stained with Rose Bengal |
|
|
Herpes and the Stroma
|
Stromal reaction typically absent or subclinical – occasionally a moderate inflammatory reaction may occur under the dendrite, causing “Ghost dendrites”. Clinically appears as a white haze surrounding the dendrite. Stromal haze or scaring may occur. Want to treat will a topical antiviral, but can’t add steroid until epithelium is intact.
|
|
|
Differentiating between Herpes Simplex and Herpes Zoster!!!!
|
lDifferential signs: the depressed and ulcerated HSV lesions with terminal end- bulbs are different from the elevated, plaque-like “pseudo-dendrites” of Herpes Zoster.
|
|
|
What should you never use to treat SV Epithelial Keratitis?
|
c. Never use topical steroids initially with infections HSV Epithelial Keratitis. Worsens the viral effects on the epithelium. Can use under special circumstances for stromal disease only when the epithelium has healed over.
|
|
|
General Herpes Simplex Treatment guidelines
|
- Infectious forms of Simplex are treated with antivirals
- Immune or inflammatory causes required steroids, but with antiviral cover. - If in doubt, avoid steroids. |
|
|
Herpes Zoster
2 Types |
1. Varicella (chicken pox) – Primary Herpes Zoster infection (children)
2. Zoster (shingles) – Secondary Herpes Zoster infection (adults). Infection of the eye is known as Herpes Zoster Opthalmicus |
|
|
3. Ocular Herpes Zoster
|
a. Prodromal Flu-like illness
b. Pain over distribution of ophthalmic nerve c. Rash with even distribution (elevated unlike HSV) d. Lasts 7 days e. Respects the midline f. Nasociliary nerve involvement tends to lead to ophthalmic nerve involvement i. “Hutchinson’s sign” |
|
|
HIV Retinopathy Microvascular disease
|
1. Cotton wool spots 30-70% HIV px, 100% AIDS, usually resolves in 6-8 weeks. As you become more immunosupressed you develop more spots.
2. Hemorrhages 8-40% 3. Microanuerisms B. AIDS Retinopathy Ultrastructural Changes 1. Loss and degeneration of pericytes 2. Swollen endothelial cells 3. Thickened basal lamina 4. Narrowed capillary lumen |
|
|
HIV and cotton wool spots
|
4. Risk for opportunistic retinal infection --> loss of blood retinal barrier
D. Cotton Wool Spots- can come and go throughout the infection. Patients with cotton wool spots also tend to have lower CD4 counts. 1. Pathogenesis a. Microvascular changes b. HIV infection of vascular endothelial cells c. Deposition of circulating immune complexes d. Alteration of blood flow |
|
|
HIV Conjunctival Microvascular Changes
|
1. 75% of patients
2. Alterations in blood flow 3. Comma shaped dilations of blood vesicles – very subtle 4. Sludging of blood flow 5. Perilimbal bulbar conjunctiva 6. Not clinically significant |
|
|
Retinal HIV Infection
|
1. Found in all retinal layers – especially like glia
2. Reduced VA – even if retina looks clear 3. Reduced color vision 4. Reduced contrast sensitivity 5. Reduced ERG 6. Visual field loss |
|
|
Dry Eye Syndrome in HIV Infected Patients
|
1. Sicca complex similar to Sjogren’s
2. Immune system attacks lacrimal gland 3. HIV alters immune environment of lacrimal gland 4. Lymphadenopathy 5. Keratoconjunctivitis sicca |
|
|
Keratoconjunctivitis sicca and HIV
|
a. Tested HIV infected men
b. 21% had signs and symptoms of dry eye c. Positive Schirmer d. Sjogren’s like syndrome in 7% of HIV infected men e. One study showed absence of Sjogren’s like symptoms in patients on HAART |
|
|
Two forms of CMV
|
a. Fulminant: - Progresses more quickly. Confluent areas of retinal whitening. Venous sheathing. Hemorrhaging “cottage cheese” fundus.
b. Indolent: - Progresses more slowly. Granular patches adjacent to retinal vessels with occasional hemorrhages. Virus can lead to an absolute field loss, “brush fire” appearance. |
|
|
Clinical appearance of Fulminant Retinopathy
|
a. Pizza Fundus
b. Cottage cheese and Catsup fundus c. Necrosis d. Hemorrhage e. Exudates f. Vascular sheathing g. Uveitis and Vitritis 9. Symptoms of CMV a. Asymptomatic b. Blurry or cloudy vision c. Floaters (because of vitritis) d. Flashes of light e. Loss of central or peripheral vision |
|
|
CMV Clinical Course
|
a. Absolute field loss
b. Loss of VA with ONH or Macula involvement c. (+) RAPD with ONH involvement d. Uveitis and Vitritis e. Without treatment invades the entire retina in 3-6 months f. Retinal detachment g. Blindness |
|
|
Molluscum Contagiosum facts
|
1. Benign epidermal tumor
2. Keratotic “wart-like” growth 3. Spread by direct and indirect contact |
|
|
Toxoplasmosis
|
1. Ocular Toxoplasmosis (10-20% of AIDs patients)
2. Discrete lesions 3. Full thickness necrosis 4. Minimal hemorrhage 5. Minimal vascular sheathing 6. Marked vitritis 7. See a lot of vitreal inflammation, makes it hard to get in with a lenses. |
|
|
Microsporidial Keratitis
|
1. Obligate, intracellular protozoal parasite
2. Painful, bilateral, chronic corneal epithelialopathy 3. Coarse, diffuse punctate corneal infiltrates 4. Severely immunocompromised 5. Usually only reported in AIDS patients. |
|
|
Microsporidial Keratoconjunctivitis Diagnosis
|
1. Clinical appearance
2. Conjunctival (not corneal) scrapping 3. Advise laboratory of possible microsporidial etiology |
|
|
Fungal Chorioretinitis endophthalmitis
|
1. Cryptococcus neoformans, Candida albicans, Sporothrix schenckii
2. CD4 count less than 50 cells/mm3 3. All cause chorioretinitis with risk to endopthalmitis 4. Small white retinal infiltrates 5. Spread to overlying vitreous – fluffy lesions 6. Vitreal abscess |
|
|
Ocular Kaposi Sarcoma
|
1. Vascular malignancy
2. Skin of eyelids 3. Mucous membranes of conjunctiva 4. 20% of AIDs patient not on HAART 5. Rate has decreased by 2/3 after introduction of HAART 6. Cofactor of Human Herpes Virus Type 8 and immune dysfunction 7. Spread through deep kissing and sexual contact 8. Sexual transmission particularly among men 9. Lesions around the eye occur on the lid and conjunctiva 10. Systemic Tx: a. HAART is the most common and successful treatment b. Anti cancer drugs are another treatment option |
|
|
Tetracyclines and clortetracyclines are
|
BACTERIOSTATIC antibiotics isolated from streptomyces.
Can be short, intermediate, or long acting. Broad spectrum against both + and -, aerobic and anaerobic bacteria, spirochetes, mycoplasma, richettisa and chlamydia and protoza |
|
|
What is Tetracycline available in
|
1% suspension and ointment for topical use.
Oral administration is available but it should not be taken with meals and dairy products |
|
|
Tretracyclines inhbits the
|
bacteria's protein synthesis by bindings to the 30s but ACTING on 50s by preventing tRNA from binding.
|
|
|
Tetracycline is recommended for
|
prophylaxis of gonococcal opthalmia neomatum.
Chylamidial can also be treated topically with tetracyclien but is not fulyl effective because it also needs to be treated systemically. |
|
|
In adults ora tretracycline is the DRUG OF CHOICE FOR TREATING
|
CHLAMYDIAL DISEASES INCLUDING CONJUNCTIVITS AND TRACHOMA.
|
|
|
oral tetracyclines can be effective for
|
notuberculous phlyctenular keratoconjunctivitis, non infected corneal ulcers, lepharitis, keratitis, meiobmianitis and chalazia
|
|
|
Tetracyclines should not be given to women in the last half of pregnancy, lactating women and children under 8 years old BECAUSE
|
it causes negative nigtrogen balance and increase blood urea nitrogen --> INHBITIS BONE growth and discolor teeth.
Psudotumor cerebri can occur |
|
|
Drug of choice for treating chlamydial diseases including inclusion conj and trachoma
|
ORAL TETRACYCLINE
|
|
|
Doxycycline/Vaibramycin is diffrent from tetracycline because it can be taken
|
orally without regard to meals and diary products
Note: can also be used to treat Chlamydial inclusion conj |
|
|
Tetracycline analogs include
|
Doxycycline/Vibramycin
Minocycline |
|
|
Macrolide Antibiotics include and work by
|
Erythromycin, Azithromycin, Clarithromycin
|
|
|
Erthyromycin is this type of antibiotic and works via
|
its a macrolide and works by inhibiting protein sythensis by binding to 50s subunit.
It is BACTERIOSTATIC and works against Gram + only available in 5 mg ointment for topical use. |
|
|
Drug of choice for legionnaire's disease and mycoplasma pneumoniae
|
Erythromycin, a macrolide
it is also good against gonococcal neonatorum and neonatal conj. due to chlyamidia trachomatis. |
|
|
Which macrolide is the drug of choice for Chlamydial inclusion Con?
|
Azithromycin, administered orally
|
|
|
Chloramphenicol works by
|
binding to the P site on the 50S subunit
It is BACTERIOSTATIC active against Gram +,-, rickettsia, chlamydia, sprochetes and mycoplasm |
|
|
The use of chloramphenicol is limited due to _______- and is only given whne
|
its ability to cause fatal aplastic anemia, even when used topically on the eye!!
it is limited to treatment of endopthalmitis following trauma or surgery, as it can easily penetrate the blood aqueoues barrier |
|
|
side effects of Chloramphenicol include
|
reversible bone marrow depression, reticulocytopenia, anemia, aplastic anemia.
These commmonly occur weeks to months AFTER therapy. Toxic reaction is known as "gray syndrome". Can also lead to OPTIC ATROPHY |
|
|
Which drug can lead to optic atrophy?
|
Chloramphenicol
|
|
|
Clindamycin works by
|
binding to the 50s subunit.
It is BACTERIOSTATIC, and can be used alone or in combo with sulfadizzine to treat ocular toxoplasmosis. Can lead to C. difficle |
|
|
Sodium sulfacetamide and sulfisoxazole work by
|
inhiiting folic acid synthesis. They are BACTERIOSTATIC against +,-, actinomyces, chlamydia, plasmodia, and toxoplasma.
Are only used topically! |
|
|
T/F A number of staph are completely resistant to sulfa drugs
|
T
|
|
|
What % of Sodium sulfacetamide soln is most common for treating routine bac. conj?
|
10%
|
|
|
Side effects to Sodium sulfacetamide include
|
photosensitization, hypersensitivity reactions, topical 30% is reported to produce a decrease in corneal sensitivity.
|
|
|
Oral short acting sulfa drugs are used to treat
|
trachoma, and ocular toxoplasmosis
|
|
|
Pyrmethamine and Trimethprin work by
|
inhibiting folic acid synthesis, not allowing the reduction step to occur.
These drugs are bacterioSTATIC Are powerful synergists with sulfa drugs |
|
|
Pyrmethamine and Trimethprin side effectins include
|
white blood cell and plately depression, or megaloblastic anemia, may also cause stinging, itching, and hyperemia
|
|
|
Nalidix acid is a
|
1st generation quinolone, against Gram +, no ocular applications
|
|
|
2nd generation quinolones include
|
ciprofloxacin, norfloxacin, and ofloxacin. Good gainst + and some -
|
|
|
Third generation quinolone includes
|
levofloxacin, very effective against gram + and atypical pathogens
|
|
|
4th generation quinolones include
|
Moxifloxacin and gatifloxacin, vast increase against gram + and against anaerobic organisms and atypical pathogens
|
|
|
Ciprofloxacin is a 2nd gen quinolone that is avaiable
|
sstemically and topically .3%
it inhibits supercoling 2 drops q 2 hours for 2 days and then 2 drops q 4 hours for next 5 days |
|
|
Ciropoflaxin is used in the treatment of
|
bacterial ulcerse and conjunctivitis
|
|
|
Norfloxacin is a 2nd gen quinolone that is available as a topical opthalmic sol called
|
Chibroxin, used for surface ocular infections
|
|
|
Ofoxacin is a 2nd gen quinolone that is topically available and is called
|
ocuflox, indicated for surface ocular infections
|
|
|
Levofloxacin is a 3rd gen quinolon called
|
Quizin
|
|
|
Moxifloxacine and gatifloxacin are 4th gen quinolones avaible in _______% solutiosn
|
Mox is .5%
Gat is .3% these block DNA gyrase AND topisomerase 4 --> works well against gram - Also has a large bicylclic amino side change at psotion C-7, making it a large ize and thus blocking the bacterias ability to pump out the drug. |
|
|
T/F research hasd determiend that 4th gen quinolones are more efficacious against gram + then second and third drugs and equally efficacious from gram -
|
true
|
