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Microbiology Test II


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Name the 5 diseases that N. Gonerrhea will cause?
Cervicitis (leads to PID)
N. Meningitis (NM)what is the age distrubution?
Infants (1-5)
-5%-10% fatality
Young Aduls (12-29)
-Up to 25% Fatality
How do you spread Menigitis
Repiratory Route
Must be in close contact
What makes a person more susceptible to NM
Crowed Places
Age (immunity doesnt start developing until after 5)
Complement Defiency
How does NG Enter the system, replicate and spread
1-Recognizes a receptor (ligand)
2-Attatches to Non cilliated epithelium via Microvilli
3-Adjacent Ciliate cells sloughed off
4- Replication (up into urethra/ cervix)
5-Internalized (vaculoe)
6- Vacuole fuses w/ BM
7-Leaves and goes into Subepithelial C
8-Host has an Immune Response
What are some of the disseminated disease of NG
-gets there via the blood stream (Strains are serum resistant)
Skin and Joints
What are some of the disseminated diseases of NM
What are the Virulence Factors of NG and NM
-Pili (scavenger for Fe, antiphagocytic, attach to CD46 receptor)
-Capsule (in NM// 13 variable serotype capsules)
-Endotoxin (NM)
-Proteins from Outer Membrane
(Porin B-stops the maturing of phagosomes, Opacity Proteins- bind to CD66, invade cells, IgA1 Protease-Invade hos mucusal immunity, cleave lysosome associated proteins and promote intracelluar survival)
-Genetic Adapatibility
can change surface proteins during infection, pili and capsule have lots of antignenic characteristics (results from slipped strand mispairing, rep. sequences, and ability to transform)
How does one diagonose NG or NM
Gram Stain
Immunologic not useful
Molecular-Amplified probes
What Antibiotics can I use
Usually Chlamydia is a co-infecion so one can use Azithromycin and Doxycycline

Penincillin for NM (can inculed Ceftriaxone)
Name the 3 Aniboitic prophalaxis given to people in close contact w/ people that have NM
Rifampin, Ciprofloxacin, Ceftriaxone
Are polysaccharid vaccines effective for infants
no long lasting immunity either
Conjugate vaccines are under development for serotypes
A,C,Y, and W135
What is Group B Capsule
Polysialic Acid, Polysacch, that occurs in Human Tissue
-Non Immunogenic
-30 yrs of failure
What does Influenza look like
Gram Negative Coccobacilli
Pleiomorphic in Tissues
Complicated Growth Requirements
-Heme Factor 10
-NAD Factor 5
-Factors that are given by RBC
-CO2 enhaces growth
-Have Encapsulated (sero) and Non-Encapsulated (non-sero)types// Can invade non immune hosts
6 serotypes
Hib is the most Invasive Serotype
How does Influenza interact w/ the Host
Normal Flora
Usually in Nasopharynx
What 8 Diseases does Influenza Cause?
Bacteremia- bacteria in blood
Meningitis- infection of CNS
Cellulitis-infection of soft tissues (facial/periorbital)
Conjuctivitis-infection of conjuctiva (associated w/ Brazilian Purpuric Fever)
Septic Arthritis-infection in joint (esp. weight bearing joints)
Epiglottis-cellutitis of supraglottic tissues (can be fatal due to Acute Rspiratory Obstruction, Med. ER)
Ottis Media- infection of the Middle Ear
Sinusitius- infection of the sinus cavities
How does Influenza cause the Diseases(how is it spread)?
It is is from Aerosol droplets or Direct contact, it will then colonize in the Nasopharynx
What is the Incidence of Influenza
Pre Vaccine
-1 out of 200 (Hib infections)
-20,000 cases reported to CDC of which 95% are under 5 yrs
-Mortality was 3-10%
-Morbitity was 15-30%

Post Vaccine (drop by 99%)
-2001 about 1600 cases
-325 less than 5 yrs old
-2003 there were less than 2,000 cases
Non encapsulated incidence has remained unchanged
What is the Epidemiology of Influenza
Its in the Normal Flora of Humans
Located in the Nasopharynx
Most are Nonencapsulated// less than 5% are encapsulated
Seasonal (Sep-Dec and March-May)
What are the Symptoms of Influenza
Depends on the Disease that results from the Hib
How does one diagnose Influenza
Gram Stain
Direct Detection
How does Influenza relate to dentistry
Since Hib colonizes in the nasopharynx then it is transmissible via repiratory secretion
List the Mechanisms that Influenza uses to cause disease
1) Attaches to the Mucous, Non ciliated epithelial cells
2)Cilia slouhed off of adjacent cells
3)Tight Junctions Break and Bacteria infiltrate between cells
4)Multiply and Asend into Repiratory Structures// Disseminate through the blood stream
What increases someones risk for influenza (5 things)?
Immune Status
-Babies w/ no more maternal AB (will continue until age 3 or 4)
-People w/ the following conditions (Asplenia, Immunodefiencies- No gamma globulin, low gamma globulin, lymphoma, Multiple myeloma)
-Genetic (AA,NA, HA and Eurpoean lineages are at increased risk due to blood group phenotypes, HLA antigens)
-Underlying Pulmonary Disease
-Pre Respiratory VIRAL Infection
-Day Care// Exposure to Smoking
What are its Virulent Factors
(What make it a Bad Mama Jamma)?
-Antiphagocytic,Type B capsule is polyribitol phosphate and the AB dont appear until 3 or 4 years after birth
IgA1 Protease
How do you treat Influenza?
Invasive Diseases: 3rd Generation Cephalosporins

Non Invasive: Doxycyclin or Quinolones

Resistant to Ampicillin (40%)
Upper repiratory illness
-cause of the flu
Haemophilis means?
means blood loving (requires blood containing medium for growth
-Hematin-needed for cytochrom system
-NAD-needed for metabolic activity
Influenza means?
Attacks the lungs
There are 6 capsule types (A-f) which one is bad
Capsule b= BAD
The nonencapsulated HI can only cause the local infections of
Otis Media
When the Hib bacteria die they release an ENDOtoxin? what is it
LPS lipid A leading to a violent immune response
Giving steroids 15-20 before antiboitic can help
What are the 3rd Generation Cephalosporin Antibiotics uses to trea Hib
Cefotaxime and Cefriaxone
How is TB Spread in the US
-What allows it to continually be spread globally?
US- Inhaling Aerosols from a person coughing, sneezing, talking
Globally- contaiminated milk
(underdeveloped contries lacking programs to control TB in cows)
-It will continually spread b/c Crowded living condiions, Population w/ little resitance, and People w/ Pulmonary TB and Suptum + smears are VERY contagious
What is the difference between primary, latent and reactivated TB?
Primary TB is the initial infection it is when TB first infiltrates your body and is taken up by macrophages who cant digest it
Latent TB- is when it has been closed off in a Caseous Necrosis, the immune system was effective at getting the bacteria under control
Reactivated TB is when the host immune response is compromised and the TB w/ in the caseous necrosis begin to grow and start another infection
Why are HIV patients at higher risk for contracting TB? (170X greater risk)
Who else is at risk
B/c there immune systems are compromised your CD4 and CD8 and Macrophages have to be in tip top shape or they will not be able to secrete lymphokines (attract macrophages) and phagocytose the TB
Others at risk:
Lymphoma patient and those recieving corticosteriods
What are the symptoms of someone w/ ACTIVE TB?
-Assoc. w/ Systems and Not Assoc. w/ Systems
Can be absent or mild
-Night Sweats
-Anorexia (loss of apeptite)
Associated w/ Organ Systems
-Pulmonary TB pt have cough
-Vertenral TB pt have back pain
How is PPD testing done and how are the results interperted?
-When do u see false positives
-What are the 3 categories for peolple that the CDC requires the TB test
Person is given 5 units of Purified Protein derivative (PPD) intradermally
-false positive are from non TB mycobacterium (seen in immune supressed, malnourshied and elderly pt)
-1 (Healthcare worker)increased risk of exposure (e.g., close contacts of TB cases, health care workers).
2 (Immigrant)increased risk of TB infection (e.g., foreign born from area of high TB prevalence, homeless).
3 (Prior Exposure)increased risk of developing active tuberculosis if latent infection is present (e.g., HIV, receiving immunosuppressive drugs such as corticosteroids, lymphoma).

Results are interperted dependeing of the group
What is the treatment for TB
Why do so many antibiotics need to be used?
4 drugs
For the 4 monthes
-P: Pyrazinamide

For the next 4 months
Isoniazmide and Rifampin
-extended the amount of months for pts w/high risk of relapse (HIV pt)

There are drug resistant TB and MDR (multi drug resistant) TB
What are the side effects of antituberculosis treatment that need to be considered for chemoprophalysis
-this risk increases w/ __?
Chemoprohalyxis treatment is the antibiotic Isoniazid (INH)
-to people that are PPD + w/ high risk of REACTIVATION of TB
-Risk of Hepatitis increase w/ Age, if the pt has risk factors for TB, and if the pt is from a group that has high incidence of TB
TB is apart of what Genus
What does the Tubercle Bacilli look like
Thin Rods
Lipid Laden Cell wall that make them Acid Fast on Stain
Grows slowly dividing every 12-24 hours
How does TB relate to Dentistry?
High speed instruments create aerosols
-Use Eye Wear and Suction
What is the Incidence of TB
-19th century
-Early 20th century
-Minority Population
-2002 CDC Analysis
-19th century: it was 30% of all adult deaths
-Early 20th century: decline b/c of improved sanitation and living conditions
-1950's: More decline due to chemotherapy
-1990's:Increase(2ndary) due increased # of immigrants, homeless, incarcirated, AIDS
-Minorities have been hit the hardest
-5.2% per 100,000
Globally what is going on w/ TB?
Every 10 sec someone dies of TB
Number 2 Infectious cause of Death (AIDs is #1)
1 billion people worldwide have latent TB (50 million w/ drug resistant strains)
What is going on in Zambia in regards to TB?
Developing countries with limited health care resources tend to be the hardest hit. For example, in Zambia, over 70% of the country's population is latently infected with tuberculosis. In addition, an estimated 20% of the Zambian population is infected with HIV. A recent study found that 98% of tuberculosis patients in Zambia who are between the ages of 20 and 40 are also infected with HIV.
Explain the Mechanism that allow TB is able to Infect.
-Inhale Aerosol
-Goes to Middle or Lower part of lungs (Initiates Primary Infection)
-Alveolar Macrophages Attack TB BUT they are not destroyed , they will multiply and survive in macrophages
-Spread via the lymphatics or blood stream to distant foci
-Immune response occurs in 3 to 6 weeks (macrophages are now able to phagocyosis and there is destrucion of lung tissue (necrosis-caseous)
-This caseous tissue is then surrounded by macrophages, giant cells(langhan cells), fibroblast, and collagen deposits that will calcify
-W/in the granuloma the bacteria are kept in control but remain viable (Latent Stage)
-If host immune defense goes down the bacteria can GROW again
How could one identify a latent TB?
What needs to be in its best shape to fight off TB
Via chest x-ray (Ghon Complexes-fibrotic calcified lesions)
CD4 and CD8 Lymphocytes and Macrophages
What is Pulmonary TB
TB that develops soon after exposure
-More common in children
-Affect mid and lower lung
-Reactivation occurs in the apical or subapical part of the lung
-Chest x-ray you will see Ghon Complexes consitant w/ Caseous Necrosis and AFB
What is Extrapulmonary TB
-Organ Systems
-Multiple Organ Systems
-Oral Cavity TB (where)
Almost any organ system can be involved
If multiple organ systems are involve it is called Milary TB
TB in oral cavity is Rare
-Tongue and Hard Palate
-most pateints had ulcers
-bone or salivary involvement
-Biopsy is required for diagnosis
What are the structural features of Mycobacteria
-Which prevents gram staining of these bacteria
-Slightly curved or Straight Bacilli
- 0.2-0.6
-High Lipid Content (Waxes w/ Mycolic Acid)
-Gram-Positive (but stain poorly
The high lipid content is the reason for the poor gram stain
What are the steps in Acid Fast Staining
- What is the color of the bacteria after the staining
1-Carbol Fuchsin (red stain) + Phenol (stains cell wall)
2- Acid Alcohol (ethanol and HCL) added to discolorize
3-Other bacteria will decolorize
4-Methylene Blue is added
5-Mycobacteria keeps its RED stain while other bacteria are blue
What does it mean when a smear is positive?
-What do you do?
-How do you treat your pt?
-Why is a + smear so important?
+ Test means Mycobac.
-For Respiratory Specimens: A Nucleic Acid Amplification Test (PCR or Transcription Mediated Amplification); This will determine if it is TB
-If pt tested postive you could treat them w/ Antibiotics "PIER"
-Importance of + Smears: Take 6-8 weeks to culture, Estimates how infected and individual is (semi-quanitative, and can be used to see how effective the therapy is going for a pt you are treating
What are the factors that have to be taken into consideration when cultivating mycobacteria from clinical specimens?
- Treatment of Containated vs. Noncontaimated
-Growth Conditions
-Time for Growth
If a specimen is contaminated (has other bacteria such as normal flora)you must first isolate the bacteria w/ N-Acetyl L-Cysteine and then use 1% NOH then centrifuge to concentrate b/c Mycobacterium cells walls are pretty resistant
If not contaminated then process directly or centrifuge to concentrate
-Growth Conditions (Cultivating):Either by a Solid Media(slow;8 weeks;Enhanced by CO2), Broth (more rapid), or Lysis by Centrifugation (best for MAC from blood)
-Time for Growth
TB complex and Avium Complex are slow growers it takes up to 12 weeks for it to grow
Most Mycobacterium like 35 degrees celcius
-Look on slide 15 for more specifics
What are the two main species in the M. Tuberculosis complex
-What diseases do they cause
-How are they transmitted
M. Tuberculosis and M. Bovis(cattle)
-5 species in the complex and they all cause TB
-Transmitted via Aerosols
-Treat w/ PER(note there is no "I") and Streptomycin for 6-24 months or and take tablets (NH+RMP or INH + RMP and PZA)
What are the mechanisms for aqurired drug resistance of these organisms
Primary:prior to therapy
Secondary:emerges during therapy
-Become Resitant to these drugs easily (Streptomycin>Ethambutal>Rifampin>INH>RMP+INH)
This is why many drugs have to be used when treating a pt w/ TB
ONLY Associated w/ Mutation encoded on Chromosomal Genes (not plasmid, conjugation etc)
What is M. Leprae?
-Where is it located
-What will a person look like if they have it
-How does it spread
-Incubation Period
-Who are natural carriers of it?
M. Leprae is the cause of Leprosy:chronic granulomatous disease (the nose is where it colonizes and how it is transmitted)
-Skin Lesions
-Peripheral Neuropathy
-Perpherial Skin thickening
-Incubation Period:2 to 40 years
Prevent Transmission:
Must have Prolonged contact to get it (Jesus didnt catch it from the woman who touched his garment)
Human and the 9 Banded Armadillo are Natural Host
-Paubacillary: 100mg dapsone daily// RPM monthly for 6 monts
-Multibacillary: 100 mg of dapsone daily//clofazamine 50mg daily and RMP once a month for 2 years or more
-Gram stainin characteristics?
-Types of Infections?
-At Risk Populaions?
Doesnt gram stain well b/c of its mycolic acid in the cell wall
Infections Chronic Suppurative Granulomatious Infecttions- swelling, abscess formation, draining sinuses//
Most infections are in immunocompromised hosts
Treatment: SXT, Minocycline and Surgical Drainage)
Where is Actinomyces found in the body?
-What infections does it cause?
Normal Flora
-Mouth, Colon and Vagina
Causes Tissue and Abscess Infections assoc. w/ formation of Sulfur Granules
-Polymicrobial (often found w/ Aerobic and Anerobic bacteria)
A. israelii, naeslundii, odontolyticus, viscosus and meyeri
Thoracic and disseminated disease
Abdominal and pelvic (PID)
chronic (your teeth are ok but your gums have to come out)
Treatment w/ Penicillin 10-20 million units a day and then 0.5 Amoxicillin for 6 months
Surgery or Remove IUD or Prosthetic Devices
Which 2 bacteria are the only bacteria that are ACID FAST
Mycobacteria and Nocardia
-Need suffient amount for acid fast staining
(Mycobacteria 10E3-10E4 per ml of sputum)
What is the other method of staining Mycobacterium besides the Acid fast way?
-How do you do it? (6 steps)
1-Heat Fix Specimen (must do b/c high lipid content will make the bacteria not adhere well)
2-Flood w/ Red Carbol Fuchsion for 3 minutes them rinse w/ tap water
3-Flood w/ Acid Alcohol for 3 minutes and rinse w/ water
4-Counterstain w/ Methylene Blue for 1 minute
6- Heat on warmer
With a Florescent Stain on Mycobacteria what color do they change into?
-What is the advantage of this test?
Bright Orange// Orange Yellow
(w/ a blue light source)
-Can screen many samples in a short time
(Can also use a fluorochrome stain with phenolic auramine-rhodamine, a modified acid-alcohol decolorizer and potassium permanganate counterstain)
The Mycobacterium's High Lipid content is responsible for these characteristics
slow growth
resistance to detergents resistance to common antibacterial antibiotics antigenicity
What is postexposure therapy of TB based on?
Age (less than 35)and induration at 8 weeks is greater than 15mm
INH chemical Hepatitis increases at age 35
What are the clincal features of the major diseases caused by the major chlamydiaceae?
Sm. Obligate Intracelluar Parasistes
Cant be gram stained

Chlamydia Trachomatis:
-Eye(Inclusive Conjuctivitis
// Trachoma)
-Sex (Non-gonococcal Urethriis//Lymphogranuloma Venerum)
Chlamydophila Psitaci (BIRDS)
Chylamydophila Pneumoniae
-Coronary Arthritis Disease?

Chlamydophila Pneumoniae
Name the 2 Syndromes caused by Legionella Pneumophila
-mortality rates
Legionella Pneumophilia is a fastidious GRAM NEGATIVE BACILLUS
-Legionnaries Disease: Multisystem disease, pneumonia, high fatality
(Headach,Cough, Fever, Pneumonia, Liver Degeneration, Cardiac Arrest
-Pontiac Fever:Non Pneumonia, Self limited, Acute Febrile, illness w/ NO MORTALITY (Flu-like symptoms, resembled an allergic disease, headache, dizzness, muscle pain, resolved in 2-5 days)
What is the basic structure of Legionella?
-How is it transmitted
Aerobic, Gram Negative Bacillus
Affect Unicellular Organisms in the groud or water
-Invade phagocytotic cells by using the complement receptor
-MOD is unclear (Proposed that it is spread via Aerosols as in defective ari conditioning, aneshesia equipment, pulmonary assistance equipment>> inhaled>>deposited on air spaces in lungs>> Severe Pneumonia is produced
What are the structural characteristics of Mycoplamataceae?
-what is there normal reservior?
No Peptidylglycan in cell wall
(like Chlyamydia)
-Have plastic membrane, contains sterol
-The SMALLEST BACTERIA (pass through membrane filters)
-Colonies look like fried egg w/ central growth zone
-Need cholesterol and FA for growth
-Antibiotics target Glycolipids and Glycoproteins (membrane proteins-Tetracycline
-Found in Repiratory Tract// Genitourinary Tract
What is the MOT, Symptoms, Mechanisms for Pathogenesis, and targeted population caused by Mycoplasm Pneumoniae?
(1) Fusion w/ Host cells
(2) Superantigen Formed
(3)Release of Cytokines, TNFa, IL1, IL2, IL6
(4)Exchange Antigens w/ the host
(5)Autoimmune RXN (IgM directed against RBC)
(6)Cold Aggultination
2nd Mechanism:
Host Response to Infection
(1)Lymphocytes and Phagocytes Infiltrate
(2)Surgically excise the thymus befor infection prevents development of lung infiltrate

Targeted Population:
MP>>Children and Young Adults
UU,MH>> Sexually Transmitted in Adults, Pulmonary Infect in Newborns (contracted in Utero, increased risk for low birth babies)
3 Species of Mycoplasma
M. Pneumoniae
M. Hominis
Ureaplasma Urelyticum
UU metabolizes this for growth
Urea (produces urease)
-ATP is generated by an electrochemical gradient prod by ammonia derived from the break down of UREA
Antibiotic means
Against Life
-substance or semisynthetic derivative that is from one microbe that can kill another microbe
-Chemotheraputic Agent
Targets of Antibiotics
Bacteria, Fungi, Parasites(uni/multi) and Viruses
-Bacteria//Fungi are focuses for TEST
Besides Antibiotics what are some other chemotheraputic agents
Plant Alkaloids
Analogues of endogenous molecules that aid in replication or viability of cell
What are the 3 types of treatment?
(1)Treat Infection from supported material from cultured microbes and there susceptibility to drug

(2)Treat Infection Empiracally, based on most likely microbes and there probable susceptability

(3)Prophalytically to prevent infection
When do DENTIST use Antibiotics?
Acute Dental Infections
Endocarditis pt
Immunocompromised Pt
What should you consider when giving a drug (5 things)?
Drug to drug/ food interactions


Side Effects//Toxicities

Microbe Susceptible?

Access of Drug and how long it will act on the infected area
Inhibition of growth of bacteria
Kill bacteria
Broad Spectrum Antibiotic vs Narrow Spectrum Antibiotic
B= Kills a wide variety of bacteri
N=Kills specific types of bacteria
Describe the 2 ways you can test to see if a bacteria is sensitive to the Antibiotic
Disk Diffusion Assay: Measure diameter of growth inhibited
on a paper disk w/ antibiotic and bacteria (agar plate)

Microdilution Broth Test:Measures lowest concentration at which the antibiotic inhibits growth in broth inoculated w/ bacteria
The lower the MIC Value the ___ the drug
What are the 4 Target sites for Bacteria
Folate Synthesis
Cell Wall Synthesis
Protein Synthesis
Nucleic Acid Synthesis
Folate Synthesis inhibitors are ___. They act by depleting the cell of folate that is needed for ___.

This is a DIhydrofolate Syntheisis Inhibitor

This is a DIhydrofolate Reductase Inhibitor
Bacteriostatic; Thymadine Synthesis


Do humans have Sulfonamides or Dihydrofolate
The dihydrofolate drugs act by depleting what?
How do cell wall inhibitor work?

Name 2 drugs that do this?
Bacteriocidial b/c the inhibit cell wall synthesis

Beta Lactam: Binds to transpeptidase and inhibits cross linking of peptidylglycan layer

Vacomycin: binds to D-alanine terminus thus blocking polyer elongation
Bacteria can synthesize this E and make penicillin inactive
Beta Lactamase
-MIC goes up if there is alot of this in a culture
Protein Synthesis inhibitors act by binding to the __ or __ ribosomal subunit
30 or 50s
-this blocks formation of the initiation complex
-translocates mRNA
-Blocks Elongation
-Causes Miscoding
Name 4 Protein Synthesis Inhibitors
Macrolides (Erythromycin)
Aminoglycosides (Gentamicin)
Name the 2 Nucleic acid inhibitors and what there action is?
Quinolones: blocks DNA gyrase (allows DNA to uncoil for replication)
Rifampin:inhibits DNA-dependent RNA polymerase
Component of Fungi cell walls that is the target of antibiotics (not is mammals)
Antibiotics will bind to it and mess up membrane permeabiltity

-Fluconazoles// other azoles: inhibits Erg. Synthesis

-Nystatin and Amphotericin B: Will bind Erg creating holes in the membrane
Antibiotics used in Combos
-Why is it important
-Give 2 EX
Emphirical Therapy>> Prevents emergence of Resistance

-Pen + Beta Lact. Inhibitors

-Pen + Aminoglycoside (Gentamicin)
How do bacteria aquire there resitance?
Decrease Intracellular levels of the drug
-decreasing uptake
-increasing efflux

Increase Inactivation of drug
-Alter the target of the drug
-Increase Amount
-Decrease Affinity

Increase Repair of Drug Effect
What made bacteris resisant to penn
Beta Lactamase increase expression

Alter affinity for Penn binding proteins

Increased Activity for efflux transporters of inner and outer membrances of Gram - bacteria
What are the mechanisms of aquired resistance
Gene amplification
Gene mutation
Gene transfer
What are the ways for gene transfer?
Conjugation: transfer of R plasmids between bacterial cells
Transposons: transfer of resistance genes between plasmids and plasmids and chromosomes
Transduction: transfer of resistance genes from bacteriophage and bacteria
What is Pharmokinetics
Drug Access and Duration

Drug formulation, route of administration, and absorption
Drug distribution from vasculature into infected tissue
Drug elimination from body by excretion or enzymatically catalyzed biotransformation
What are the problems associated w/ clinical use of antibiotics
Side Effects (organs, or fetal risk-tetragenocity)
Drug to drug interaction
Name the complication associated w/ these organs and the drug that corresponds

Gastrointestinal Tract
Many orallly administered: nausea
Aminoglycosides: proximal tubular necrosis
Macrolides: cholestatic hepatitis
Penicillins: seizures
Which drugs have effect on fetus
Discoloration of teeth and altered bone growth
Altered bone growth
8th cranial nerve damage
Antibiotics As Allergens
Generally, incomplete antigens
Reactive metabolite (hapten) binds covalently to protein or DNA to form immunogen
Initial exposure elicits synthesis of immunoglobulin
Reexposure elicits symptoms of antigen-antibody interactions
Name 1-4 Hypersensitivity rxn and the associated mediators and response
Type Mediators Syndrome
I (immediate) IgE, mast cell activation Anaphylaxis,
complement Cytolysis of cell bound to hapten
complement Inflammation due to antigen-antibody deposits
IV (delayed) cytotoxic
T cells Rashes
2 Examples of Cross Reactivity
Drugs with similar chemical component may elicit allergic response in sensitized patient
Sulfonamide antibiotics and sulfonamide diuretics
Beta lactam penicillins and cephalosporins
KNOW-Drug to Drug Interactions
Altered cytochome P450 enzymes of drug biotransformation
Inhibited by macrolides and -azoles
Increased by rifampin
Altered drug effect due to suppression of gastrointestinal flora
Oral contraceptives
Oral anticoagulants
Know-Super Antigens
Appearance of bacteriological and clinical evidence of new infection during Rx of primary one
Overgrowth of normal flora difficult to treat
Clostridium, Pseudomonas, Staphylococci, Candida
Risk higher with broad spectrum drugs
Pen G<tetracycline<3rd generation cephalosporins
What is Psudomembraneous Colitis
Effects of toxin from overgrowth of anaerobe Clostridium difficile
Diarrhea, fever, blood and mucus in stool, mucosal lesions of large intestine
Potentially fatal
Caused by clindamycins, penicillins⬦.
Rx: oral vancomycin, metronidazole
Antibiotics of Orodental Infections
Penicillin V p.o.
Amoxicilliin, cephalosporins
Macrolide, clindamycin if penicillin allergy
Oral candidiasis (thrush)
Topical nystatin, an -azole p.o.
Prophylaxis for Bacteria Endocarditis
Oral dose 1 hour prior to procedure
Normalize dose for body weight in children
Standard drug choice
Drug choice in patient with penicillin allergy
Cephalosporin (if penicillin allergy manifests only as rash)
What is the basic structure and gram stain for Bordetella Perfussis and Corynebacterium?
-Small Coccobaccilli
-Gram Negative Bacilli (Rods)
-Filamentous Agglutanin (adheres to RBC)

-Gram Positive Bacilli
-Non motile
What is the epidemiology of BP and CB Infecions?
-Target Population
-Geographic Distribution
BP Infections
-Whooping Cough and Respiratory Syndromes (Repiratory Tract Infection)
-Humans (Children)
-Geographically ?

What will I see clinically in BP and CB?
BP Clinically: (0ccurs during early phase, spread by respiratory droplets, vaccination decresed this microbe)
-Acute Encephalopathy
-Convalesent Phases

-Pharyngeal Infections:
Pharyngitis// Tonsilitis,Hypoxia due to airway obstructions, Fever, Lymphadentitis

-Cutaneous Infections:Psudomembrane
-Systemic Complications, Perpheral Neuropathy, Myocarditis and Congestive Heart Failure

Complications are life threatening>> Loss of Motor Function and Congestive Heart Failure
What are the mechanisms for Pathogenesis, Virulence Factors, and Host Response?
-Colonize on Ciliated Cells in Repiratory Mucosa
-Undergo Phase Variation of Toxic Expression

-Colonizes in the host nasopharyngeal cavity//skin
-Produces DPT
-Immunity is from AB response to toxin
How is BP and CB treated?
-Gram Stain/Culture

-DPT// LPS-free
-Erythromycin and Tetracycline in early phases
-Pt Isolation

-Vaccinated w/ DPT
-Pennicillin and Erytrmycin
-Adult Titer are low
-Passive Immunzation via Anti toxin Sera
3 species of Bordetella
B. Perfussis
B. Paraperfussis
B. Bronchoseptica (Animals)
What are the toxins in BP?
PT:ADP Ribosylating>> Hypoglycemia, Leukocyte Infiltration, Lymphocytosis
HLT: Dermonecrotic, Vasoconstrictive
AC:Interferes w/ cAMP regulation// PMN inhibitor
TC: Destroy ciliated cells
How do the Enterics Infect?
S. Typhi- GI Mucosa, LP, Peyer's Patches and Blood= Typhoid Fever, Septicemias, and Acute Gastroentericitis

Deck Info