• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/174

Click to flip

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;

174 Cards in this Set

  • Front
  • Back
What is epidemiology?
The study of patterns and distribution of disease
What is the attack rate?
The number of cases developing in a group of people who were exposed to the infectious agent
How is infectious disease spread?
From RESERVOIR THEN TRANSMITTED TO PERSON
List and explain the terminology used to describe the rates of disease in a population:
-endemic = disease constantly present in a particular geographical area
-epidemic = disease with an unusually high occurrence
-pandemic = a worldwide severe epidemic
-morbidity = illness (morbidity rate)
-mortality = death
-incidence= the number of new cases of a disease in a population
-prevalence = the total number of cases of a disease in a population at risk at a point in time
endemic
disease constantly present in a particular geographical area
epidemic
disease with an unusually high occurrence
pandemic
-pandemic = a worldwide severe epidemic
morbidity
illness (morbidity rate)
incidence
the number of new cases of a disease in a population
prevalence
the total number of cases of a disease in a population at risk at a point in time
What are the roles for the Centers for Disease Control and Prevention?
Compile the MMWR – morbidity and mortality report. And write news stories on the issue
What are the roles for the WHO?
Compile weekly epidemiological records and stories
Name the types of infections that human carriers can have and give examples of each.
-symptomatic infection = cold virus
-asymptomatic infection = neisseria gonnorhea
-carriers
When are infections easiest to control?
When humans are the only carriers
Give some examples of non-human animal reservoirs, and what infectious agents they may carry
-poultry – salmonella, campylobacter = diarrheal diseases
-rodents = Yersinia Pestis = causes plague
-bats and raccons – rabies virus
-zoonoses
What are zoonoses?
Diseases of animals transmitted to humans, but primarily exist in other animals
Name an environmental reservoir and a bacterium that resides in it.
Soil – clostridium
What is horizontal transmission?
The transmission of a pathogen from one person to another through the air, by physical contact, by ingestion of food or water, or via a living agent such as an insect
What is vertical transmission
The transmission of a pathogen from a pregnant woman to her fetus, or from a mother to her infant during childbirth or breast feeding.
What is direct contact?
When one person physically touches another
What is indirect contact?
Transfer of pathodgens via inanimate objects (FOMITES) such as clothing, table tops, doorknobs, and drinking glasses.
What is a fomite?
An inanimate object
What is droplet transmission?
Coughing or sneezing droplets that come out of the mouth which others nearby can inhale
Food and water can harvest pathogens.
Thus acting as a reservoir
What reservoir is the hardest to control?
Air
What does the term vector mean?
Any organism that can carry a disease. Usually these are arthropods such as mosquitoes, fleas, lice, and ticks.
Fleas, acting as vectors, carry what pathogen?
Yersinia Pestis =plague causing
Mosquitoes, acting as vectors, carry what pathogen?
Plasmodium species = malaria
Explain the transmission of the bubonic plague:
-a flea transmits > Y. pestis to a human
-bacterium is carried to a lymph node
-Bubo (dramatic swelling of lymph nodes) develops within days
-Y. Pestis begins nterfering wth the immune response (inflammatory)
-multiplying bacteria spill into the bloodstream
-50-75% mortality of untreated
-there is no person to person transmission of this
How is the bubonic plage able to become Pneumonic Plage and thus be transferable from person to person?
Bubonic plague can colonize the lungs, at which point this is now called pneumonic plague. Then, it can transfer from person to person
What are the characteristics of Pneumonic Plague?
The transmitted Y. pestis is fully armed because it is in its fully virulent form thanks to being in the previous host.
-100% mortality rate if untreated within 2-3 days
Mycobacterium Tuberculosis is what kind of disease and has what symptoms?
Chronic and symptoms are cough, fever, weight loss, night sweats, “consumption” (white death)
How is Tuberculosis transmitted?
-Droplets of infected person are inhaled
-in the lungs, M. TB is ingested by a macrophage; multiplies slowly (GT>12 hr)
-Organism can be carried to other body sites
-unable to destroy intracellular M. tb, t cells and activated macrophages wall off the infected site by forming a granuloma.
-infection may be contained, patient converts to PPD+ (purified Protein derivative)
Distinuguish between the latent and active form of M. tb:
-latent infection – TB is held in check by the immune system; no disease and non-transmissible
-active infection – TB actively multiplies, symptoms are present and transmissible
What is the consequence of infection by mycobacterium tuberculosis?
More than 90 percent never have symptoms
-1 percent have immediate illness
-5 to 10 percent have a latent infection which reactivates later as immune system wanes
---- 5 to 10 percent number goes up A LOT if patient has AIDS
Approximately how much of the global population is infected with M. tb?
1/3
How can we control M. tb?
-treat people who have active M. tb with a combo of two or more antimicrobial meds for MONTHS
-Prevent development of active M. tb via a vaccine which is used in many countries but isn’t effective, and recipient converts to PPD+ anyways. But in America, we monitor exposure and treat latent infections with Isoniazid or Rifampin, for MONTHs
What are some targets of antibacterial drugs
-Cell wall synthesis
-nucleic acid synthesis
-cell membrane integrity
-metabolic pathways
-protein synthesis
What is the therapeutic index tell us about dosage?
Compares lowest dose toxic to the patient / dose used therapeutically

Higher therapeutic index = safer drug
What are the characteristics of Pneumonic Plague?
The transmitted Y. pestis is fully armed because it is in its fully virulent form thanks to being in the previous host.
-100% mortality rate if untreated within 2-3 days
What does bacteriostatic imply about drugs?
Drugs that inhibit growth of bacteria
Mycobacterium Tuberculosis is what kind of disease and has what symptoms?
Chronic and symptoms are cough, fever, weight loss, night sweats, “consumption” (white death)
How is Tuberculosis transmitted?
-Droplets of infected person are inhaled
-in the lungs, M. TB is ingested by a macrophage; multiplies slowly (GT>12 hr)
-Organism can be carried to other body sites
-unable to destroy intracellular M. tb, t cells and activated macrophages wall off the infected site by forming a granuloma.
-infection may be contained, patient converts to PPD+ (purified Protein derivative)
Distinuguish between the latent and active form of M. tb:
-latent infection – TB is held in check by the immune system; no disease and non-transmissible
-active infection – TB actively multiplies, symptoms are present and transmissible
What is the consequence of infection by mycobacterium tuberculosis?
More than 90 percent never have symptoms
-1 percent have immediate illness
-5 to 10 percent have a latent infection which reactivates later as immune system wanes
---- 5 to 10 percent number goes up A LOT if patient has AIDS
Approximately how much of the global population is infected with M. tb?
1/3
How can we control M. tb?
-treat people who have active M. tb with a combo of two or more antimicrobial meds for MONTHS
-Prevent development of active M. tb via a vaccine which is used in many countries but isn’t effective, and recipient converts to PPD+ anyways. But in America, we monitor exposure and treat latent infections with Isoniazid or Rifampin, for MONTHs
What are some targets of antibacterial drugs
-Cell wall synthesis
-nucleic acid synthesis
-cell membrane integrity
-metabolic pathways
-protein synthesis
What is the therapeutic index tell us about dosage?
Compares lowest dose toxic to the patient / dose used therapeutically

Higher therapeutic index = safer drug
What does bacteriostatic imply about drugs?
Drugs that inhibit growth of bacteria
What does bactericidal imply about drugs that effect bacteria?
These drugs kill bacteria
What does broad spectrum imply about the spectrum of activity of an antimicrobial drug?
Antimicrobials that affect a wide range of bacteria
What does narrow-spectrum imply about the spectrum of activity of an antimicrobial drug?
Antimicrobials that affect a limited range of bacteria
What is half-life?
Time when half the drug is left in the blood
What are some adverse of antibiotics?
-allergic reation
-toxic effects at high concentrations etc.
-suppresion of the normal microbiota
-antibiotic associated colitis due to growth of clostridium difficile after competing microbes are destroyed
Explain intrinsic/innate resistance
Like mycoplasma is resistant to penicillin because it has no cell wall. Bacteria that are just innately resistant to an antibiotic
Explain acquired resistance
Resistant to antimicrobials via mutation
What are the stages of syphilis?
-primary – 3 weeks after infection, chancres, highly infection
-secondary – rash develops/exists for 2 to 10 weeks to years
-tertiary – neurosyphillis, cardiovascular syphilis, gumma formation, years later (1/3 of time); not infectious
-congenital – damage to the fetus
What drug was developed that as a chemotherapeutic agent to kill syphilis
Salvarsan – is an arsenic
Give an example of beta-lactam drugs
Penicillin G as an example
List some characteristics about B-lactam drugs
-therapeutic index
-not effective against…
-acid-______
-destroyed by __________
-high
-most gram negatives
-sensitive
-penicilliinase AKA B-lactamases
Explain the development of folliculitis, caused by Staph aureus
Folliculitis = hair follicle localized staph growth
-furuncle growth spreads to subcutaneous tissue
-carbuncle – usually back of neck = multiple furuncles
Carbuncles are more serious than furuncles. What can they lead to ?
Bacteremia = bacteria in the blood. This can develop into
-septicemia = blood stream infections which can spread to bones and organs
What is the target of beta – lactam drugs?
Peptidoglycan synthesizing transpeptidases (NAM bridges) AKA penicillin binding proteins
Which bacteria are antibiotics derived from?
Penicillium, streptomyces, bacillus
List some characteristics about B-lactam drugs
-therapeutic index
-not effective against…
-acid-______
-destroyed by __________
-high
-most gram negatives
-sensitive
-penicilliinase AKA B-lactamases
What are some families of penicillins?
-natural
-penicillinase-resistant
-broad spectrum penicillins
-penicillins + beta lactamase inhibitor
Give an example of a beta lactamase inhibitor
Augmentin
What are two ways the susceptibility of a strain to an antimicrobial drug can be assessed?
MIC – minimum inhibitory concentration
Kirby-bauer test – disk – must use a chart that correlates zone size to susceptibility
How can resistance to antimicrobial drugs be established. Name two methods
1 – spontaneous mutation
2 – gene transfer
Explain how spontaneous mutation that yields antimicrobial resistance via a single step, is countered.
Using combination therapy – multiple drugs lower the chance that a spontaneous mutation can survive the drug.
Explain how spontaneous mutations that yield antimicrobial resistance via multi-step mechanisms are countered.
Multi-step S – s – even smaller s – R.

This is countered by making sure patient empties the bottle of antibiotics prescribed.
Explain how gene transfer can cause antimicrobial resistance
Resistance plasmids (R plasmids) can be transferred. These can even encode resistance to multiple antimicrobial medications.
What is the solution to preventing antimicrobial resistance via gene transfer?
Stop letting microbes see what we have in store to kill them. STOP USING ANTIBACTERIAL SHIT WHEN YOU DON’T NEED IT.
List some examples of emerging antimicrobial resistance
-neisseria gonorrhea
-vancomycin resistant enterococci
-methicillin resistant staphylococcus aureus
-vancomycin intermediate staph aur.
-vacomycin resistant staph aur.
-streptococcus pneumonia
-mycobacterium tuberculosis
Wound infections can be nosocomial or healthcare associated. Explain the difference
Nosocomial is hospital acquired infection whereas healthcare associated includes infections you can get from locations in the medical arena (dr’s office, nursing homes, etc.
What is the difference between the microscopic morphology of staphylococcus and streptococcus?
Staph is grape-like clusters

Strep is chains
Both staph and strep are anaerobes, which one is what type of anaerobe?
Staph – falcultative anaerobe – can switch between fermenting and o2.

Strep – aerotolerant – can live in 02 rich environments but still does fermentation
Of Staph and Strep, one of these needs coagulase. Which one is it?
Staph – because it does something that needs to convert fibrinogen to fibrin to make clots…
Food-borne intoxication by a toxigenic strain of staph aureus leads to ….
Enterotoxin (entero means intenstinal tract)

Bacterium grows in the food and produces toxin which is consumed and causes vomiting and nausea
Scalded skin syndrome affects primarily ____ and ___ separates layers of the epidermis
Under 5; exfoliatin; bacterium grows in lesion, synthesizes toxin and the toxin spreads systematically causing skin to peel off.
Staphylococcal toxic shock causes _______ primarily in _______ resulting in _________
Toxic shock syndrome toxin (TSST); women; high fever, rash, low bp, organ failure and death.
Explain the epidemiology of staphylococcal toxic shock.
Women menstruating used superabsorbent tampons which contained polyacrylate which bound Mg++, causing toxin production to increase because all the mg++ was leaving the body to the tampon.
How do you prevent staph infections?
Wash your hands nigga
What do the following virulence factors of staph aureus do?
1 – capsule
2 – coagulase
3 – exfoliatin
4 – hyaluronase
5 – leukocidin
6 – lipase
7 – proteases
8 – protein A
9 – Toxic Shock Syndrome Toxin
1 – inhibits phagocytosis
2 – may impede progress of leukocytes into infected area by producing clots in surrounding capillaries
3 – separates layers of the epidermis, causing scalded skin syndrome
4 – breaks down hyaluronic acid component of tissue thereby promoting infection
5 - kills white blood cells by producing holes in their cytoplasmic membrane
6 – breaks down fats by hydrolyizing the bond between glycerol and the fatty acids
7 – degrade collagen and other tissue proteins
8 – binds to Fc portion of antibody inhibiting phagocytosis (by blocking attachment to Fc receptors on white blood cells)
9 – causes rash, diarrhea, and shock
Name three streptococcus species?
Viridians strep; streptococcus pyogenes (Group A strep); streptococcus pneumonia
Explain viridians strep?
Part of the normal microbiota; occasional oppurtunists; alpha – hemolytic – greenish hemolysis
Explain streptococcus pyogenes (Group A strep)
Pathogen; causes “strep throat”; beta – hemolytic (clear hemolysis
Explain streptococcus pneumonia
Oppurtunists (old people, sick people, get pneumonia quicker than healthier people); alpha hemolytic
Strep throat is a disease caused by group A strep. Explain the symptoms
Streptococcal pharyngitis
Sore, red throat, whitish pus; fever enlarged lymph nodes
How is strep throat spread? And what age range is most susceptible?
Spread via droplet transmission

Mainly 5 – 15 yr olds.
Strep throat itself is not a serious disease. However, if not treated, the aftermath can be pretty bad. What is the aftermath?
Sequelae – which has two symptoms – rheumatic fever and glomerulonephritis
Rheumatic fever results in damage to tissues. Particularly which one?

It also makes the patient susceptible to infections by _____ flora and antibiotics must be taken for _____.
Heart tissue

normal

years
Rheumatic fever makes one more susceptible to infections by normal flora. How long must you take antibiotics for if you get rheumatic fever?
For years. To avoid reinfection and heart valve infection
What does glomerulonephritis do to the kidneys?
Damages them, because antigen-antibody complexes get packed in there disrupting normal flow of blood.
Some toxigenic strains of Streptococcus pyogenes (group A strep) cause scarlet fever, what is this caused by?
Caused by erythrogenic toxin which is an SPE released by certain strains of S. pyogenes at the site of infection.
Some toxigenic strains of Streptococcus pyogenes (group A strep) result in what diseases?
-scarlet fever
-streptococcal toxic shock (more severe than staph. Toxic shock because toxin is more concentrated damage locations
-necrotizing fasciitis “flesh eating disease”
What is the mechanism of attack by toxins called superantigens?
They bind to outside of MHC class II molecules AND T cell receptors, circumventing specificity. Since about 5 to 20% T cells respond, there is an overwhelming release of cytokines that can actually be fatal.
What are two examples of Superantigens
Staph enterotoxin and TSST.
Streptococcus Pneumoniae causes Pneumonia. What are some predisposing factors and what are the symptoms?
Respiratory infections, elderly age, alcohol/drug abuse are all predisposing factors. The symptoms are inflammation of the lungs causing an interference with O2 exchange.
How fatal is Pneumonia without treatment with antibiotics?
30%
Explain the pathogenesis of Pneumonia
It’s a capsule and interfers with C3b deposition.
What is the stomach’s role in regards to intestinal pathogens?
Since its acidic, most bacteria cannot survive such an environment loaded with pepsin (protein cutting enzyme)
Explain the anatomy of the small intestine
-Giant surface area
-Villi which have microvilli on them
-digestive fluids and enzymes are secreted, nutrients are absorbed (about 9 liters of electrolytes and fluids a day)
-little or no normal flora
Explain the anatomy of the large intestine
-Fluid absorption, not nutrient
-storage
-lots of normal flora
Explain the general process by which bacteria diseases of the lower digestive tract occur
Bacteria are ingested which colonize the intestine and thus cause disease whose symptom is usually diarrhea.
Explain the concept of infection dose
Can be low (around 10) or high (thousands?)
How are bacterial diseases of the lower digestive tract transmitted?
Fecal orally, direct contact, or via food and water
What is the generic pathogenic mechanism followed by bacterial diseases of the lower digestive tract?
-attachment
-toxin production; this results in increased electrolytes and thus water being secreted leaving watery diarrhea and in the case of shiga toxin and cholera: cell death by inhibiting protein synthesis resulting in bloody diarrhea
-cell invasion; thus the bacterium induces its own uptake instead of nutrient uptake and the invasion leads to an inflammatory response resulting in blood, pus, mucus.
-loss of microvilli due to substances delivered by bacterium into the cell which rearrange the actin
Areas where diarrhea is a problem are areas that lack adequate care in what arenas?
-sewage treatment, water treatment, medical care, nutrition
Explain the epidemiology of Vibrio Cholerae.

Infection Dose, reservoir, etc.
It has a high infectious dose because it is killed by acid and thus a high dose is needed so that some survive the stomach ; and exists in contaminated water, food
Explain the symptoms and pathogenesis of Cholera
It colonizes the small intestine. Adheres to the small intestine via adhesion and releases enterotoxin.

This causes increase of Cl- secretion which causes water to follow via osmosis and Na+ to follow via the electrochemical gradient. Up to 20 L a day of fluids can be lost. Rapid dehydration leads to death.
Explain treatment options for Cholera
Rehydration is the solution. Can be accomplished in two ways:
-IV
-oral rehydration solution (contains water, glucose, electrolytes). Newer starch based solutions are even more effective
Explain how acquisition of cholera can be prevented
Through water and sewage treatment
Explain the epidemiology of Shigella
Low infectious dose
Explain the symptoms and pathogenesis of shigella
It is invasive and moves from cell to cell directly by attaching to M cells(which normally take in microbes and transfer them to macrophages in Peyer’s patches) and being transported across the epithelium

Symptoms are inflammation, dysentery (small volume of feces, usually blood and pus), and fever
How can shigella be prevented?
By washing hands and sewage treatment
Explain which one of the species of shigella produces shiga toxin and what effect does shiga toxin have.
Shigella dysenteriae produces shiga toxin which disables the ribosomes of cells thus inhibiting protein synthesis and killing cells.
How is shigella treated?
Antibiotics and fluids
What is ETEC?
Enterogenic E. Coli, makes cholera-like toxin
ETEC makes what kind of toxin?
A cholera like toxic
What is EHEC AKA STEC?
Enterohemorragic E. Coli aka Shiga Toxin Producing E. coli
Explain the symptoms and pathogenesis of Enterohemmoragic E. coli AKA shigatoxin producing e. coli
Symptoms are bloody diarrhea, and in 10% of cases Hemolytic uremic Syndrome (HUS) which lyses red blood cells and is life threatening since kidney failure results.

The shiga toxin is phage encoded and damages endothelial cells
Explain the epidemiology of EHEC aka STEC
-75% of cases in summer months
-reservoir is cattle and thus meat and manure leading to contaminated food and water
-low infectious dose
Explain how EHEC can be prevented
Washing hands and cooking food thoroughly
What is the treatment of EHEC?
No antibiotics, just supportive shit.
List some other intestinal pathogens
Norovirus, Salmonella, Campylobacter, Yersinia Enterocolitica, Vibrio Parahaemolyticus
Giaradia is a parasitic disease. Explain some general info/epidemiology
-Low infectious dose
-intestinal pathogen
-survives in the environment
-animal reservoirs
There are two forms of Giardia Lambila, name them
Trophozoite and Cyst
Explain the Trophozoite form of Giardia Lambila
-growing form (actively feeding)
-non-infectious
-in the small intestine
-does not survive in the environment
Explain the Cyst form of Giardia Lambila
-infectious (ID: 10 to 100 cysts)
-dormant, survival form
-formed as parasite SLOWLY passes out of GI tract
Explain the pathogenesis of Giardia Lambila
-Adheres to small intestine
-coats and damages epithelial tissue interfering with absorption.
-fats are not absorbed and thus you get a fatty stool. This stool will float.
-lactase is inhibited and thus lactose will not be broken down. Lactose is a source of energy that bacteria love, and now they are going to get it.
How is giardia lambila diagnosed?
There are three things you can do. First is a fecal exam. Second, you can test for antigen in the feces. Finally, you can do a string test which involves swallowing a capsule with a string on it that will be taped to your cheeks, only to use it to pull the capsule back up with a sample of your intestines a couple hours later.
How can you prevent getting infected with Giardia Lambila
The usual tactics… wash your fucking hands and get the water treated
Explain some general information about Malaria
Its transferred via mosquitoes being the vectors. The mosquito then, is obviously a very important part of the life cycle. Once you’ve been infected, your RBCs are targeted and cyclical symptoms begin. This means that every 2 to 3 days the same round of symptoms repeat themselves: chills, fevers, sweats (Paroxysm). About 1 million deaths per year because of this
Explain the life cycle of Malaria
Once the mosquito injects the virus into your body, the spores head for the liver. There they grow, and certain species make hypnozoites which can hide in the liver for long periods of time and cause relapse. These spores develop into merozoites which infect Red blood cells and are now in their active feeding form, the Trophozoite. These trophozoites become merozoites and burst out and infect more RBCs. In the RBCs gametocytes also form which are sucked up by mosquitos and thus transferred to other hosts.
What is the damage caused by all malaria?
Inflammatory response leads to paroxysm

And

Anemia – unhealthy RBCs
What is the damage caused by malaria of plasmodium falciparum?
Cerebral malaria – capillaries in brain are clogged.
Bilharzia refers to …
Schistosomiasis
What is some general info about schistosomiasis?
It’s a worm in the blood – blood fluke
-requires 2 hosts: a human for the sexual stage where these fuckers live in “copulatory embrace” and a snail for the asexual stage
Explain the life cycle of schistosomaiasis
EGG is excreted from human and hatches upon contact with water. MIRACIDIUM swims and enters snail. CERCARIA is released from the snail and burrows into human skin. ADULTs live in copulatory embrace in blood vessels. EGGs are deposited in capillaries near bladder and not all eggs can be expelled….
Explain the pathogenesis of schistosomaiasis
Adults can mask themselves with blood proteins, and
the eggs are highly antigenic, granulomas are formed around them are not expelled.
Explain the epidemiology of schistosomaiasis
Poor sanitation and snail hosts are reservoirs
How can schistosomaiasis be controlled
By treating infected humans and eliminating snail hosts
Which type of HIV is the major source of HIV in the world?
HIV 1
Which HIV is less common and exists mostly in Africa and causes a slower disease course
HIV 2
In adults, which rank the following in terms of contribution of HIV infection prevalence:
Heterosexual, injection drug use, homosexual (male to male)
1 – heterosexual
2 – injection drug use
3 – homosexual
What kinds of barriers reduce exposure to HIV
Condoms, male circumcision
How does transmission of HIV occur?
Through blood and genital secretions
What is the effect of STDs on risk of exposure to HIV?
Increased risk if STDs are present
What proportion of infants born to HIV-1 mothers become infected? And how does transmission occur here.
1/3 – vertical transmission – blood, genital secretions, and breast milk
How is HIV diagnosed?
Detection of HIV specific antibodies, ELISA followed by western blot to confirm
What is seroconversion in regards to HIV
Presence of HIV antibodies
Upon primary infection to HIV, what symptoms are observed?
Flu-like symptoms, fever
With HIV, what is the virus doing during the asymptomatic phase (after primary infection)?
For about 10 years, virus replication continues but no disease is observed
The first two phases of HIV infection are called primary and asymptomatic. What is the third stage called?
AIDS – this is the disease. T helper cells (CD4) deciline to less than 200 cells per microliter. This suppression of the immune system lets opportunistic infections flourish.
What is the typical set point in HIV disease progression?
Low set point – AIDS hits around 10 years after primary infection.
What is the rapid set point in HIV disease progression?
High viral set point – meaning AIDS hits between 1 and 5 years after primary infection
In HIV replication, how does HIV enter a CD4 cell?
It binds the CD4 receptor and then finds whats called a coreceptor. Most of the time it is CCR5. Both CCR5 and CD4 receptor are required for HIV to enter the cell.
How does HIV replicate once inside CD4 cell?
It begins reverse transcription. A viral polymerase that takes RNA genome and makes a DNA copy of it. Reverse transcriptase is very error prone… no proofreading mechanism. This means mutations are carried into the next virus particle. Integrase takes viral genome (now DNA) and integrates into host cell genome. The genome is transcribed and assembly occurs and virues lyses the T host cell and infects other T cells.
What are some possible antiretroviral therapy mechanisms?
-RT inhibitors, block reverse transcriptase nucleoside analogs, AZT (
-protease inhibitors – viral protease is needed to cleave gag into functional units (assembly stage)
-fusion inhibitor – blocks entry to CD4 by blocking late stages of receptor binding/entry.
What is HAART?
Highly active antiretroviral therapy.
Explain the benefits of monotherapy and the eventual result
One antiviral is used. The viral levels go down for a long time, but eventually, the virus will mutate and circumvents one retrovirus
Explain the benefits of HAART?
Put three drugs together and virus has a hell of time coming up with a mutation that can evade ALL THREE antivirals simulataneously
How is short-course monotherapy used to reduce mother to child transmission of HIV.
One drug used during pregnancy or even during labor can reduce transmission by about 10%.

Combining drugs reduce it even further to about 5%
Vaccines for HIV have progressed a little bit. Where are attenuated virus/antigen in a vector/protein analogs viruses first tested?
In animal models – rodents and monkeys to see if an immune response occurs.

First test in small animals and see if immune response occurs.

Then test in non-human primates and if it slows disease a little or protection is observed, humans are tested.
There are three phases in testing HIV vaccines in humans. Explain the phases
First phase involves safety testing using about 100 people

Second phase is the same but with a larger group

Phase 3 is on even larger scale (N= 1000s) and observe if protection is provided?
How long does it take to get vaccine to human testing stage 3 from the first test in animals?
About 10 years
What were the results of the STEP/MERCK trail which used an adenovirus vector?
Vaccinated group was MORE infected than the controls….
The Thai/RV144 trail results are valuable because… why?
Since they used a second booster to rev the immune system, 26 percent fewer infections occurred in the vaccinated group, however the p value was quite small (.18) whereas a value of .5 is needed to be declared statistically relevant.
Bacillus anthracis –
- Is it transmissible person to person?
- Can antibiotics help?
- How hardy is the agent?
- Vaccine available?
-No.
-Antibiotics are available
-Very hardy
-Vaccine is available for highly susceptible people – military or researchers
Botulinum Toxin
- Is it transmissible person to person?
- Can antibiotics help?
- How hardy is the agent?
- Vaccine available?
-No
-No, there is an anti-toxin tho.
-very hardy
-vaccine is available in limited supply
Yersinia Pestis
- Is it transmissible person to person?
- Can antibiotics help?
- How hardy is the agent?
- Vaccine available?
-Only in pneumonic plague
-Yes. But they may not be approved for wide-scale use
-no
-no vaccine
Smallpox Virus
- Is it transmissible person to person?
- Can antibiotics help?
- How hardy is the agent?
- Vaccine available?
-Yes
-No
-Not very
-YES