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How does humoral immunity work?

Uses antibodies (produced by B cells) to help kill invading microbes

What two things must happen in order to activate B cells?

-B cell must bind free antigen
-APC (macrophage) activates helper T cell

Where do B cells get antigens?

-Free antigens circulate in the blood
-When B cells finds matching antigen, it will bind and ingest (endocytosis) antibody-antigen, complex antigen is saved and presented in MHCll
-B cell becomes anigen-presenting cell

What are antigens?

-Generally large molecules found on the surface of cells
-Trigger an immune response in our bodies
-Include LPS and viral capsid proteins
-Are bound to by antibodies

How does humoral immunity help to eliminate pathogens from our bodies?

-By producing antibodies

How do antigen-presenting macrophages activate B cells?

Indirectly through helper T cells which recognize antigens bound to MHC

What do T cells have to perform the same functions of antibodies?

Antigen receptors

How can T cells identify antigens?

-T cell receptors bind to antigens presented in the MHC l or MHC ll

What happens when a T cell binds to an antigen presenting cell?

It releases cytokines

What do cytokines do?

-Increase leukocyte activity
-Activate B cells with bound antigen
-Stimulate T cell division

What is produced by clonal selection?

Effector cells and memory cells

Why is humoral immunity not an effective way to combat viral infections?

-Extracellular pathogens or toxins can be coated with antibodies, making them easier to destroy
-Viruses are intracellular parasites, and spend the majority of their time inside a cell
-Viral antigens are not seen by immune system because they are hidden within the cell

What are the two branches of acquired immune response?

-Humoral (antibody mediated) immuntiy
-Cell mediated immunity

Key players in Humoral Immunity

-B cells
-Helper T cells
-APC macrophage

Key players in Cell mediated immunity

-APC macrophage
-Helper T cells
-Cytotoxic T cells

How are viral infections detected by the immune system?

-Cells infected with a virus will present the viral antigen in a MHC-l complex
-Like a secret flag to the immune system

Which cell recognize the MHC-1 complex on viral cells?

Cytotoxic T cells (kill human cells infected by virus or with cancer)

What happens when cytotoxic T cellsare activated?

They secrete a protein called perforin

What does perforin do?

creates holes in cell membrane, killing the cell

What happens when a viral cell is lysed after cytotoxic T cells kill it

-Its viral particles are released into the blood where they are detected by the Humoral immunity, wider immune response

What is required to kill a virus?

Both Humoral and cell mediated immunity

Which branch of the acquired immune system acts against cancer cells?

Cell mediated immunity

How does our immune system recognize cancer cells?

-Cancer cells display unusual proteins that are displayed in MHC 1 complex
-Cancer cells can over-express various cell-surface molecules
-Cancer cells can also cause a down-regulation in MHC 1 so it is no longer present, missing display case all together

How are cancer cells destroyed?

-"Unusual" proteins recognized as antigens and destroyed by Cytotoxic T cells
-Natural Killer Cells

What is a natural Killer cell and what does it do?

-Cells that recognize abnormal cells
-Works independently, doesn't need antigen presentation or cytokine activation to function
-Destroys cells in the same way as Cytotoxic T cells

HIV infects helper T cells, why do people with HIV have weaker immune systems?

-Their B cells and cytotoxic T cells are not activated and can not destroy invading pathogens

What would cancer rates in people with HIV look like compared to healthy people?

They would be higher

Cell Mediated Immunty...
(A) Is responsible for destroying extracellular pathogens
(B) Is responsible for destroying cancerous cells
(C) Includes the inflammatory response
(D) Involves B and T cells
(E) Is triggered by antigens presented in MHC-ll

(B) Is responsible for destroying cancerous cells

When are memory cells created?

During primary immune response

What are vaccines?

A mixture of dead or much less virulent (pathogenic) bacteria or viruses

How do vaccines work?

-They mimic primary immune response to generate memory cells that will be quickly activated in a real encounter with a pathogen

What were the characteristics of early vaccines?

-they were inactivated whole agent vaccines (dead bacteria and viruses)
-Contained surface antigens but were non viable and non infectious
-Not effective against some types of pathogens

What type of pathogen are inactivated (killed) vaccines NOT effective against?
(A) Gram neg bacteria
(B) Gram pos bacteria
(C) Intracellular pathogens (viruses)
(D) Eukaryotic Worms
(E) None of the above

(C) intracellular pathogens (viruses)
- intracelluar pathogens go inside your cells, but if we try to use a dead pathogen as a vaccine it cant make its way into the cell to mimic viral infection

Problems with inactivated (killed) whole agent vaccines

1. only activates humoral immune response (pathogens dont enter cells so not effective against intracellular pathogens)
2. Pathogen does not replicate so fixed amount of antigen (more antigen=more memory cells= longer immunity)
3. Not effective against exotoxins
4. Surface mollecules are only weakly antigenic

Whay are whole agent vaccines not effective against exotoxins?

because when dead pathogens are injected into your body, they cant create exotoxins, so your body would still be unfamiliar with them.

What are the types of vaccines?

-Inactivated (killed) whole-agent vaccines
-Attenuated (weakened) whole agent vaccines
-Subunit vaccines

What are inactivated whole-agent vaccines and what are some examples?

-Killed completely
-Used for pathogens where live vaccine is too hazardous
-Rabies, Influenza

What is a toxoid vaccine?

-Inactivated toxins
-Tetanus and diptheria

What are attenuated whole agent vaccines?

-weakened but not killed
-Closer mimic to actual infection, confers lifelong immunity

What are subunit vaccines?

-use antigens that elicit the strongest immune response
-Hepatitis B (viral protein coat)

Boosters are additional doses of vaccines given after the original dose to help increase immunity against that antigen. What type of vaccines are boosters most commonly required for?
(A) inactivated (killed) whole agent vaccines
(B) Toxoids
(C) Attenuated (weakened) whole agent
(D) Subunit vaccines
(E) All of the above

(A) Inactivated (Killed) whole agent vaccines
-because inactivated or killed vaccines only have a certain number of antigens, you need another dose so that your body can maintain its immunity

What are the types of acquired immunity?

Active imunity and Passive immunity

What is Active Immunity?

-develops when a person is exposed to antigens, becomes ill, and then recovers
-Duration of immunity varies-lifelong for measles, years for intestinal illnesses
-Can be natural (you get sick) or artificial (vaccine)

What is Passive immunity?

-The transfer of antibodies gives temporary immunity (weeks or months)
-Can be natural (mother to infant) or artificial (anti-venom)

What causes the flu?

-The influenza virus (enveloped RNA virus)
-Influenza virus has HA and NA proteins on its viral cell wall

What are the antigens for the influenza virus?
(A) Nucleic acids (RNA)
(B) Capsid proteins
(C) Envelope proteins (NA and HA)
(D) All of the above

(C) Envelope proteins (NA and HA)

How does the influenza virus avoid the effects of vaccines?

-Errors are mad in the replication of influenza RNA (common in RNA viruses because they lack proofreading enzyme)
-The resulting mutations lead to the formation of different surface proteins, which our immune system will not recognize (antigenetic drift)

How are the influenza vaccines different every year?

-each flu vaccine contains 3 different strains of the influenza virus
-chosen based on the strains of influenza that are predicted to be most common in the coming year

What are the types of flu vaccines?

-Flu shot (killed virus)
-Nasal spray such as FluMist (live attenuated virus)

Side effects of the inactivated (killed) influenza vaccine include soreness, redness, or swelling where the shot was given. What branch of our immune system is primarily responsible for these side effects?
(A) innate immune response
(B) Humoral (antibody-mediated) immune response
(C) Cell-mediated immune response
(D) A, B, and C
(E) Impossible to say

(A) Innate immune response
-inflammatory response is part of innate immunity

Why does it take up to to weeks for protection to develop after receiving an inactivated (killed) flu vaccine?
(A) The virus must multiply to high enough levels to trigger an immune response
(B) It takes time for naiive B cells to become activated and produce antibodies
(C) T cells must migrate to the site of infection
(D) Cytokine levels must reach a minimum concentration to activate B cells
(E) It takes time for memory B cells to be formed

(B) It takes time for naiive B cells to become activated and produce antibodies

-Morphological arrangement
-Gram Stain
-Diagnostic Test

-Coccus, non motile
-Gram Positive +
-Capsule In some species
- Catalase -

-Morphological arrangement
-Gram Stain
-Diagnostic test

-Coccus, non motile
-Irregular clusters
-Gram positive+
-In some species
-Catalase + (growth on MSA)
-Tolerate high salt, resistant to drying and many chemical agents

Why is Mannitol Salt Agar (MSA) a selective growth media only allowing Staphylococcus (but not streptococcus) to grow?
(A) Streptococcus can not use mannitol(sugar)
(B) Streptococcus can not tolerate the high salt
(C) Only bacteria that make hemolysins can grow on MSA
(D) Catalase is required to grow on MSA
(E) All of the above

(B) Streptococcus can not tolerate the high salt

What causes hemolysis of red blood cells?

exotoxins called hemolysins

How do hemolysins work?

-They wedge into membranes to make large holes (pores), causing cell lysis
-Complete hemolysin has 7 subunits


Alpha=Partial hemolysis
Beta= Complete hemolysis
Gama= no hemolysis

What does it mean when we say RBC hemolysis is an in vitro effect

Happens in the lab

What do the hemolysins target in vivo (in the body)?

Many cells, heart, skeletal muscle fibers, leukocytes, and RBC
-RBC produce the most obvious results

Why is Staphylococcus aureus the most medically important Stapphylococcus?

-They are common in nosocomial infections
-They have extreme drug resistance (MRSA & VRSA)
-Ability to colonize or invade wide number of sites
-Have the ability to survive outside the host

What are some Staphylococcus aureus diagnostic tests?

-Coagulase (enzyme that causes blood to coagulate and form clots) produced by S. aureus
-Mannitol Salt Agar

How is staph differentiated in an MSA experiment?

-both Staphylococcus species will grow, but only S. aureus will ferment mannitol and turn media yellow

What makes S. aureus so prevalent in nosocomal infections?

- It is readily transmitted by inanimate objects
-ex: bed dressings, tools, catheters, contaminated needles
-S. aureus is part of our transient microflora, 20-50% of people

How is coagulase beneficial to S. aureus being an effective pathogen?

-Causes blood clots to form around S. aureus effectively helping it hide from the immune system

How does Staphylokinase contribute to the virulence factor of S. aureus?

-Dissolves clot so that S. aureus can sneak away

How do digestive enzymes contribute to the virulence factor of S. aureus?

-Dissolve connective tissue t promote spread of infection

How do hemolysins contribute to the virulence factorof S. aureus?

lyse a variety of cells, including RBC, WBC, heart, and muscle cells

Why is coagulase considered a virulence factor?
(A) It lyses blood cells providing food for S. aureus
(B) It forms blood clots making it harder for immune cells to phagocytize S. aureus
(C) It forms blood clots which hides S. aureus antigens from the immune system
(D) B and C
(E)All of the Above

(D) B and C
-Coagulase forms blood clots making it harder for immune cells to phagocytize S. aureus
-Coagulase forms blood clots which hides S. aureus antigens from the immune system

Why are S. aureus nosocomal infections so much worse than most infections?

-Hospital strains of S. aureus are generally antibiotic-resistant
-cause staph infections after surgery

What are cutaneous infections?

-Localized infections
-infection of hair follicles leads to skin abscesses. Usually resolved without any further problems

Systemic infections have variety

-often result from cutaneous infection with access to bloodstream
-Can infect most organs (aided by virulence factors allowing passage through bloodstream)

What are the sites of infection for systemic infections?

-Heart Lining
-Lower respiratory tract

What is scalded skin syndrome?

-Systemic S. aureus infection; symptoms caused by toxin that reaches the skin
-Causes skin to peel
-Common in newborns (contracted through umbilical stump)

What is Toxic shock syndrome?

-Vaginal S. aureus that can proliferate in tampons and produce pyrogenic toxin

What are pyrogenic toxins?

-Bind directly to T cell antigen receptors and MHC-ll, leading to overstimulation of acquired of immune system
-Leads to non-specific activation of T cells, releasing large amounts of cytokines

How is streptococcus differentiated?

-By patterns in blood hemolysis

You are trying to identify a bacterial sample isolated from the respiratory tract of a patient. The bacteria is a gram + cocci, and does not produce catalase. What two additional diagnostic tests do you need to run to determine whether the bacteria is S. pneumonia or S. pyogenes?
(A) Coagulas and hemolysis
(B) Coagulase and antibiotic sensitivity
(C) Hemolysis and antibiotic sensitivity
(D) MSA and hemolysis
(E)MSA and antibiotic sensitivity

(C) Hemolysis and antibiotic sensitivity

What is the main reservoir for S. pyogenes?

-10% of the human population are transient carriers of virulent strains of S. pyogenes in their nasopharynx

What is S. pyogenes sensitive to?


What 3 major diseases are caused by S. pyogenes?

-Streptococcal pharyngitis (strep throat)
-Scarlet fever

What helps Streptococcus pyogenes attach to cells?

-Its M protein (part of the fimbria)

What helps S. pyogenes resist phagocytosis?

-Its capsule made of hyaluronic acid
-M protein coats the bacteria with self proteins which resists phagocytosis, doesn't allow MAC to enter membrane

What does the Protein G of S. pyogenes do?

-binds to antibodies and confuses immune system

What are the secreted virulence factors of S. pyogenes?

-Hemolysins (streptolysins) lyse WBC, muscle, heart fibers
-Toxins (toxic shock syndrome)
-Enzymes (ex. streptokinase) that degrade tissues or promote invasion

Which of the following statements about the M protein is false?
(A) It is part of hemolysin, and lyses various cells in the body
(B) It is part of fimbriae, allowing attachment to cells in the body
(C) It coats the bacteria with "self" proteins, preventing phagocytosis
(D) It prevents MAC from getting into the cell membrane
(E)All of the above statements are true about the M protein

(A) Is not part of hemolysin and does not lyse various cells in the body
-also is the only antigen on S. pyogenes that elicits and acquired immune response

What does S. pyogenes rely on to infect?

-sufficient number of bacteria
-an opportune portal of entry

Where are S. pyogenes infections most common?

-in adolescents (direct contact, poor hygiene)
-Immunocompromised individuals

How to reduce infection of S. pyogenes?

-activities that reduce the the microbial load (hand washing) will reduce incidence and transmission

Why are there no vaccinations for S. pyogenes?

-Because antibodies to some variants of the M protein bind to our heart valves (results in autoimmunity: Rheumatic fever)
-Antibodies produced to attack the M protein react (bind) to heart, joints, skin and brain cells

S. pyogenes localized diseases: Cutaneous- what is IMPETIGO?

- Yellow, itchy crusts that are puss filled, highly transmittable
-Portal of entry is broken skin (abrasion)

S. pyogenes localized diseases: Pharynx- What is Strep Throat?

-Infections in mucous membranes of tonsils or pharynx
-Causes redness, edema, difficulty swallowing.
-Often accompanied by fever
-Pus-filled tonsils

S. pyogenes: Systemic Diseases

-Causes most invasive or virulent strains
-Can be fatal (septicemia)

What is Septicemia?

pathogens proliferating in the blood (blood infection); usually accompanied by a fever

What is Scarlet Fever

-Systemic infection
-10% of strep throat cases result in scarlet fever
-Caused by strains of S. pyogenes infected by a dormant (lysogenic) virus
-Viral genes cause secretion of super antigen into blood stream
-Symptoms include spotty inflammation (strawberry tongue), and persistent fever
-Historically fatal in 10-20% of cases, but now successfully treated with antibiotics

What is childbirth fever?

-Mothers die shortly after child birth due to systemic infection w/ S. pyogenes
-Transferred by unwashed hands of doctors and midwives
-Easy access to uterus and blood
-Handwashing and sanitization technique reduced mortality dramatically

S. pneumoniae

-Responsible for majority of bacterial pneumonia cases
-Carried by 33% of people in the nasopharynx
-can not live outside of the host for a long time

What is the morphology of S. pneumoniae


Who gets infected by S. pneumoniae?

-Weakened immune
-Those constantly exposed to high doses

What is the main virulence factor for S. pneumoniae?

-capsule that evades phagocytosis

Why can 30% of the population carry S. pneumoniae in their nasopharynx but not have pneumonia?
(A) They carry less pathogenic strains of S. pneumoniae
(B) Their immune system is functioning normally and keeps S. pneumonaie from invading the body
(C) They carry low abundances of S. pneumonaie
(D) They carry strains of S. pneumoniae that lack a capsule
(E) All of the above

(B) Their immune system is functioning normally and keeps S. pneumoniae from invading the body

S. pneumoniae lower respiratory tract infections

-Immune system prevent our own microflora from entering the lower respiratory tract
-Immunocompromised could contract large amounts of S. pneumonaie and develop pneumonia

What is lobular pneumoniae?

-S. pneumoniae that colonizes and infects the alveoli

What is bronchial pneumoniae?

-S. pneumoniae that colonizes in the bronchioles

S. pneumoniae Upper respiratory tract infections

-Middle ear infections (esp in children) and other upper respiratory tract infections

S. pneumoniae Secondary infections

-Migrates from site of primary infection to the blood or meninges
-Most common cause of bacterial meningitis in adults (can be fatal)

Why do mothers in third trimester undergo group B strep testing?

-If it is positive, the mother is given antibiotics to prevent transmission during delivery

Group B Streptococcus

-Newborns (vaginal birth) at risk of infectionby group B streptococcus, which resides in vaginal tract
-Causes fatal pneumonia, septicemia, and meningitis
-Leads to 5000 deaths a year

What us the upper respiratoy system?

-Bronchii up

What is the lower respiratory system?

-Bronchioles and alveoli

How is our respiratory system defended against invaiders?

-Air eddies in nasal cavity slow movement of particles into respiratory tract
-Competitive inhibition from resident microflora
-Cilia in nasal cavity, pharynx, larynx, trachea, bronchi (mucociliary escalator)
-Microbes in alveoli are engulfed by resident (alveolar macrophages)

What is the result of our bodys protection against invaders in the respiratory tract?

-Oral cavity and nasopharynx are colonized by harmless microflora (aid in preventing pathogen colonization)
-Lower respiratory system is generally sterile (no resident microflora)

What are the sites of infectionin the upper respiratory system?

-Sinus infections
-Ear infections

Infection of the pharynx (pharyngitis)

-Sore throat that may be accompanied by a fever

infection of the larynx (laryngitis)

-Sore throat and often loss of voice

Sinus infections

-usually bacterial infection in the hollow sinuses of the skull
-blocks drainage and causes mucous accumulation
-swelling results in pressure induced pain

Ear infections

-Caused by Streptococcus, S. aureus, and P. aeruginosa
-Usually middle ear infections caused by migrating microbes from the pharynx up the Eustachian tube
-More common in young children because eustachian tubes are short and more horizontal
-Inflammation and pus development behind tympanic membrane
-Deafening, painful to swallow


-infected and inflamed bronchi

Which statement(s) about the microbes that cause sinus infections are true?
(A) The pain associated with sinus infections results from inflammation
(B) Some bacteria that cause sinus infections can have antibiotic resistance, making treatment challenging
(C) Sinus infections are caused by opportunistic pathogens such as S. pneumoniae or S. aureus
(D) Most bacteria that cause sinus infections are part of our transient microflora
(E) All of the above

(E) All of the above

Studies have shown that babies who are breastfed have fewer ear infections. Why does this occur?
(A) Breastfed babies are not exposed to as many bacteria
(B) Breastfed babies have been exposed to more bacteria, and therefore have more immunity
(C) Breastfed babies get antibodies from the breast milk
(D) Breastfed babies get leukocytes from the breast milk
(E) Breastfed babies have longer Eustachian tubes

(C) Breastfed babies get antibodies from the breast milk

Lower respiratory tract infections

-Less common but more serious
-pathogen must overcome host defenses (mucociliary escalator, alveolar macrophages)
-Infections are more common in immunocompromised and chronic smokers (smoke paralyzes ciliary escalator)

Which of the following statements is FALSE?
(A) Lower respiratory tract infections are more common than upper respiratory tract infections because once bacteria reach the alveoli there are few defenses
(B) Lower respiratory tract infections are more severe than upper respiratory tract infections because the lower respiratory tract is generally sterile
(C) Lower respiratory tract infections are more common in chronic smokers

(A) Lower respiratory tract infections are more common than upper respiratory tract infections because once bacteria reach the alveoli there are few defenses
-Lower respiratory tract infections are not more common


-Leading cause from infectious disease in the US (common in AIDS patients and elderly)
-Mortality ranges from 30% (no treatment) to 5% (prompt treatment)
-Produces bloody sputum
-Can migrate from site of infection to blood or meninges

What are the types of pneumonia viruses?

-Klebsiella pneumonia
-Pseudomonas aeruginosa
-Mycoplasma pneumoniae

Klebsiella pneumonia

-More destructive form of pneumonia, higher mortality rate
-Causes extensive destruction of lung tissue

Pseudomonas aeruginosa

-opportunistic pathogen that causes pneumonia in immunocompromised patients
-Produces attachment pili, commonly found on non-living surfaces

Mycoplasma Pneumonia

-Milder form of pneumonia
-Mycoplasma has no cell walls and lacks much cellular macinery
-relies on host, cannot live outside humans

Legionnaire's Disease
-Bacterial cause
-where it replicates
-how its transmitted

-Discovered in 1976 after an Americans Legion convention resulted in several deaths
-Caused by Legionella pneumophila
-Replicate inside alveolar macrophages and eventually rupture cell
-Symptoms: Impaired respiration, fevers, diarrhea, vomiting, and pain in abdomen and chest
-death results from systemic shock and kidney failure (5-30%)
-Transmitted by water (can withstand chlorine)

What branch of the immune system will be activated if you are infected with Legionella pneumophila?
(A) Passive immunity
(B) Humoral immunity
(C) Cell-mediated immune system
(D) all of the above

(C) cell mediated immunity

What bacteria causes Tuberculosis (TB)?

-Caused by Mycobacterium tuberculosis

What is the course of infection for a primary infection of TB?

-10-100 cells for a minimum dose
-Bacteria are inhaled and phagocytized by alveolar macrophages
-Bacteria reproduce inside the macrophages (slowly) until they eventually lyse the cell
-3 to 4 weeks after infection, tubercules form (accumulation of infected macrophages and other immune cells)
-In 95% of the cases the immune system surpresses bacteria at the primary infection stage

What are the two things that can happen after the primary infection of TB?

-Become nonsymptomatic latent TB (not infectious)
-Progress to secondary infection (active TB infection)

What happens during the secondary infection of TB?

1) Bacteria escape tubercles and infect new areas
2) Growth of tubercles leads to necrosis and rupture of lung tissue (allows M. tuberculosis to spread to other parts of the lung)
-Symptoms: violent cough, malaise, extreme fatigue, blood in sputum, wasting away (in advanced state)
3)Disease waxes and wanes in severity (bouts of illness followed by bouts of recovery)
-fatality rate 60% within 5-10 years if left untreted

How is TB transmitted?

Transmitted by respiratory droplets from infected individuals (which are resistant to drying)
-transmission is high in crowded, poortly ventalated households

What is the generation time like for Myobacterium (TB)

-Very long, 15-20 hours, grows very slowly
-has long incubation time, 6-8 weeks
-Hard to culture and identify pathogen via diagnostic tests

What makes Myobacterium (TB) so resistant to drying?

-Cell wall contains large amounts of lipids, creating a waxy coat
-Viable in dried sputum for up to 6 months

Why was TB originally called the white plague?

-Name created by Robert Koch
- When TB first came about it affected the poor in europe in the 1800's and had a mortality rate of almost 25% before antibiotics

What did Koch do after he found that TB was transmitted in droplets from the mouth?

-He led efforts to improve sanitation and encourage people to cover their cough

What was the first cure for TB?

Streptomyocin (1946)

Why did TB make a resurgence in the 1980's?

-Latent TB more likely to become active TB in immunocompromised
-The emergence of drug resistant strains of TB
-Increasing world population and travel

What is the current treatment for TB?

-6 months of an antibiotic drug cocktail

What are the current effects of TB?

Causes 3 million deaths a year (mostly in Asia and Africa)
-incidence is on the rise, especially in AIDS patients with antibiotic resistant strains

How much of the worlds population is infected with TB?

-1/3 of the worlds population
(lowest rates are in the US)

What percent of TB cases will progress to active TB?
What percent of active TB infections are fatal without treatment?

- 10% progress to active TB
- 50% are fatal without treatment

Where are infection rates of TB the highest in the US? Why?

-Highest TB rates are in the US
-Because of large immigrant population and rigorous testing program

What is a Manoux test?

-Test to diagnose TB
-Purified TB protein injected just under the skin
-Measures resp. from cell-mediated immune system
-Memory cells will react to proteins and produce hardening around the injection site in 48 hrs

How does someone confirm TB after a positive Manoux test?

-Chest X-ray
-DNA testing

Why has the prevalence of Tuberculosis been on the rise since the 1980s?
(A) Increase in immunocompromised individuals.
(B) The development of antibiotic resistant strains
(C) Increasing world population and travel
(D) AIDS pandemic
(E) all of the above

(E) all of the bove

How is infection prevented in the urogenital tract?

- regular flushing w/acidic urine, valves in kidney prevent backflow

What role does lactobacilli play in the vagina?

-It creates a low pH, which inhibits most other microbes

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