Biology 105 Final 2025

Question 1

To recover from tetanus or botulism

A. Antibiotics are necessary along with washing of the intestines or wound to remove the bacteria
B. Supporting therapy is used until the person
recovers
C. The person has to actually grow new nerve endings since the toxins bind irreversibly
D. All of the above are
correct

Answer 1

All of the above are
correct

Question 2

Botulinum toxin causes muscle paralysis by

A. Binding to the stimulatory nerves at the synapse and blocking releases of signaling molecules that tell the muscle to contract
B. Actively growing and reproducing in the nerve cells and causing nerve cell death
C. Triggering the immune system to attack and damage the nerves
D. The mechanism of botulinum toxin is unknown

Answer 2

A. Binding to the stimulatory nerves at the synapse and blocking releases of signaling molecules that tell the muscle to contract

Question 3

The bacteria that cause tuberculosis and leprosy are able to remain viable outside of the body for many months. How is this possible?

A.
These bacteria produce a very thick capsule that keeps them from drying out
B.
These bacteria have a waxy substance in their cell wall that keeps them from drying out
C.
These bacteria have flagella that allow them to swim or move to an appropriate location in the environment where conditions for survival are the greatest
D.
These bacteria have an uncanny ability to seek out their host so that they won’t dry up

Answer 3

These bacteria have a waxy substance in their cell wall that keeps them from drying out

Question 4

In today’s time, it is deemed unnecessary to quarantine people infected with leprosy. This is because

A. Leprosy is not very contagious and, in fact, takes ears of intimate contact with an infected person before it is transmitted
B. Leprosy is fully treatable
C. Leprosy takes years to manifest signs and symptoms and people rarelv die from Leprosv
D. All of the above are
correct

Answer 4

All of the above are
correct

Question 5

A person is brought to the ER with high fever, stiff neck, dizziness, confusion, and headache. Which of the following may the person be suffering from?

A. Pneumonia
B. Meningitis or encephalitis
C. Infectious mononucleosis
D. Rabies

Answer 5

Meningitis or encephalitis

Question 6

Listeria is more problematic for pregnant women and their fetus, the immunocompromised, and older people. It is primarily associated with which of the following foods?

A. Ground beef
B. Deli meats, dairy, and other undercooked meats
C. Pasteurized cheese and milk
D. Eggs

Answer 6

Deli meats, dairy, and other undercooked meats

Question 7

Listeria bacteria have an interesting way of spreading from one host cell to another without ever really leaving the original host cell. Listeria bacteria achieve this means of spread by

A. Causing the host cells to fuse with nearby cells
B. Circulating in the lymphatic system within macrophages
C.
Causing the host cell to form a pedestal/pseudopod structure that pushes the bacteria from the infected cell into nearby cells
D. Destroying the molecules that hold tissue cells together thereby allowing deeper penetration into tissues

Answer 7

Causing the host cell to form a pedestal/pseudopod structure that pushes the bacteria from the infected cell into nearby cells

Question 8

Neisseria meningitidis is a gram - cocci that causes meningitis outbreaks among college students. This organism is particularly virulent and leads to septic shock because of a process called blebbing. Blebbing is when

A. The organism sheds part of it’s outermembrane
B. The organisms resist phagocytosis
C. The organism changes it’s membrane proteins to hide from or avoid the immune system
D. The organism grows and reproduces at very high speeds when the host is immunocompromised

Answer 8

The organism sheds part of it’s outermembrane

Question 9

A new and promising treatment for C. difficile and pseudomembranous colitis is

A. Antibiotics to kill the infecting organisms
B. Change in the patient’s diet
C. Using leaches to suck the toxins out of the patient’s blood
D. Fecal transplant
where feces from a healthy donor is given to the patient

Answer 9

Fecal transplant
where feces from a healthy donor is given to the patient

Question 10

A young man is being treated with several antibiotics simultaneously for Leprosy. After several weeks of treatment, he develops watery, foul-smelling, blood stools. A colonoscopy reveals patches of yellowish lesions in the large intestine. The probable cause is

A. Giardia intestinalis
B. Vibrio cholerae
C. Clostridium difficile
D. Salmonella enterica

Answer 10

Clostridium difficile

Question 11

Shiga-like toxin is an enterotoxin that inhibits protein synthesis, kills cells, and can result in death of the infected individual. Shiga-like toxin is produced by

A. Virulent E. coli and Salmonella species
B. Vibrio cholera
C. Type Ill pathogens
D. All intestinal pathogens that cause diarrhea

Answer 11

Virulent E. coli and Salmonella species

Question 12

Type Ill secretion systems

A. Inject toxins directly into host cells
B. Increase intimacy of the attachment of bacterial cells to the host by injecting a receptor into the host cell
C. Cause cytoskeletal rearrangements and pedestal formation to occUr
D. All of the above

Answer 12

All of the above

Question 13

Vibrio cholerae is transmitted by

A. Miasmas or bad air
B. Fecal-oral route
C. Contact transmission from person to person
D. Contaminated water

Answer 13

Fecal-oral route and Contaminated water

Question 14

Cholera toxin
A. Is an AB toxin where B is a receptor and A is the toxin that enters the cells
B. Is classified as an exotoxin because it is secreted
C. Is an enterotoxin that causes diarrhea
D. All of the above

Answer 14

All of the above

Question 15

RSV (respiratory syncytial virus) causes mild, cold-like symptoms in adults but causes a very serious respiratory infection in young children and infants. RSV can spread quickly within a host and therefore lead to very severe symptoms rather quickly. This is because RSV spreads within a host when

A. Virus particles spread via blood and lymph causing viremia
B. Infected cells fuse with neighboring uninfected cells to form a large syncytium
C.
Virus particles cross the blood:brain barrier and lead to simultaneous meningitis and encephalitis
D. Virus particles are absorbed into the bloodstream from fecal-contaminated food or drink

Answer 15

Infected cells fuse with neighboring uninfected cells to form a large syncytium

Question 16

Legionaire’s disease is unique in that

A.
The organism that causes it lives as an internal parasite of amoebas that commonly inhabit water cooling systems and humidifiers
B. It is generally asymptomatic or very mild in healthy individuals
C.
Inside the human host, the bacteria lives as an internal parasite of macrophages where it escapes detection from the immune system
D. All of the above

Answer 16

All of the above

Question 17

Cigarette smoke is known to inhibit the cilia that line the respiratory tract and effectively prevent movement of the ciliary escalator. How might this lead to an increased risk of pneumonia?

A. Exposure to cigarettes increases one’s risk of exposure to microbes since bacteria can collect on cigarette filters
В.
The ciliary escalator is responsible for trapping dust and microbes in mucous and moving the mucous up and out of the respiratory tract
C.
The ciliary escalator moves mucous downward to the lower respiratory tract to deliver infection-fighting mucous and antibodies
D. All of the above are correct

Answer 17

The ciliary escalator is responsible for trapping dust and microbes in mucous and moving the mucous up and out of the respiratory tract

Question 18

CASE STUDY
A man in his mid-40’s visited a physician complaining of shortness of breath and a persistent cough for over three weeks. Upon examination, the doctor noted that the client had a history of asthma and intravenous drug use.
Believing the patient to have an upper respiratory disturbance, the physician ordered a steroid to reduce inflammation and swelling of airways. Two weeks later, the man’s signs and symptoms were worse. He began to experience periods of dizziness and extreme fatigue. Worried that something was terribly wrong, he sought help at an emergency room. When he arrived, his blood pressure was low and he appeared dehydrated. The ER staff administered a rapid IV infusion of fluids, took blood for analysis, and x-rayed his chest. The x-ray film revealed an inflamed (abnormally enlarged) heart and fluid (pneumonia) throughout the lungs. The blood culture grew Streptococcus pneumoniae, a bacterium commonly found as part of the normal flora of healthy individuals.
*1.How could the man have developed bacteremia?
2.What factors in the medical treatment may have exacerbated the infection?
3. What factors in the man’s history may have led to his infection?

Answer 18

1. From a dirty needle, From his lung infection that grew more severe, From taking the steroids prescribed by the doctor
2. The steroid ordered by the doctor to reduce inflammation could have compromised the man’s immune response
3. He had a persistent cough and shortness of breath, so he clearly came in with
   respiratory issues, The man had a history of IV drug use

Question 19

Which of the following are minute, hemorrhagic skin lesions?
A. Petechiae
B. Interferons
C. Interleukins
D. Lymphangitis

Answer 19

Petechiae

Question 20

Viremia refers to
A. Viruses in the blood that cause illness
B. Blood poisoning due to toxins
C. The presence of bacteria in the blood
D. Inflammation of the lymphatic vessels due to pathogens in the blood

Answer 20

Viruses in the blood that cause illness

Question 21

A friend of yours shares their perspective on HIV with you. They reason that since HIV is an emerging disease, it hasn’t undergone coevolution with humans for a very long time. Further, your friend predicts that HIV will remain virulent for hundreds or even thousands of years. How do you respond to their prediction?
A. I disagree. I tell my friend that coevolution should lead to decreased virulence in HIV virus.
B. I disagree. I tell my friend that HIV should remain virulent because it requires host to host contact (STD) and so should evolve milder over time.
C. I agree. I tell my friend that despite host-to-host
transmission, HIV should remain virulent because of its dormancy period. Transmission has already occurred before the host is sick enough to be immobilized.

Answer 21

I agree. I tell my friend that despite host-to-host
transmission, HIV should remain virulent because of its dormancy period. Transmission has already occurred before the host is sick enough to be immobilized.

Question 22

Why does Malaria remain highly virulent after many many years of coevolution with human and other hosts?

A.
Because malaria requires host to host contact for transmission and high virulence aids that mode of transmission
B.
Because malaria is waterborne
C. Because malaria is transmitted by a vector, which does not require host mobilization
D. Because an immobilized host (very sick) has an increased risk of mosquito bite so virulence aids transmission

Answer 22

Because malaria is transmitted by a vector, which does not require host mobilization AND Because an immobilized host (very sick) has an increased risk of mosquito bite so virulence aids transmission

Question 23

What types of pathogens are able to maintain high virulence with no fitness cost?
A. Those transmitted by direct contact
B. Those transmitted by vector
C. Those transmitted by droplet transmission
D. Those transmitted by water

Answer 23

Those transmitted by vector

Question 24

Evolutionary fitness can be roughly defined as an organism’s contribution to future generations. Those that are more fit have more offspring and those that are less fit have less offspring. For a pathogen/parasite, evolutionary fitness is not that simple and relates to reproduction AND…

A. How effectively it overwhelms the host
B. How virulent it is
C. How long it can remain viable
outside of the host
D. Rate of transmission to new hosts

Answer 24

Rate of transmission to new hosts

Question 25

When looking at a graph of host resistance and pathogen virulence, we see an oscillating pattern often coined as "The Red Queen Hypothesis". Why do we see an oscillating pattern? A. Because both virulence in a pathogen and resistance in a host continue to increase over time indefinitely B. Because as host resistance decreases, pathogen virulence must increase C. Because both virulence in a pathogen and resistance in a host continue to decrease over time indefinitely D. Because both the pathogen and the host use all their resources to gain an advantage over the other but really neither one ever gets ahead of the other

Answer 25

Because both the pathogen and the host use all their resources to gain an advantage over the other but really neither one ever gets ahead of the other

Question 26

In reciprocal coevolution, the host will evolve greater and greater resistance and in turn, the pathogen will evolve greater and greater virulence. A. True B. False

Answer 26

FALSE

Question 27

Which of the following is NOT true regarding reciprocal evolution? A. Coevolution stimulates mutual evolutionary response in the traits of interacting populations В. Coevolution requires that organisms live in very close association with each other C. Coevolution always results in pathogens becoming more virulent over time D. The host will continue to evolve greater and greater resistance overtime until it is completely resistant and unaffected by the pathogen

Answer 27

Coevolution always results in pathogens becoming more virulent over time

Question 28

The necessary conditions for host-pathogen coevolution includes A. Genetic variation for resistance in the host population B. Genetic variation for virulence in the pathogen population C. A close association of the host and pathogen (the pathogen spends part or all of its life cycle on or in the host) D. All of the above

Answer 28

All of the above

Question 29

Pathogens spread by host-host contact should cause mild disease to be successful

Answer 29

-if a host is too sick, it will not be moving about, spreading the pathogen

Question 30

Pathogens spread via vector or non-living reservoir should be able to cause serious disease and still be successful

Answer 30

-the sicker the host is, the more likely it is to get bitten by vector

Question 31

Describe briefly the central nervous system (CNS) and peripheral nervous system (PNS).

Answer 31

The CNS includes the brain and spinal cord, responsible for processing and sending out information. The PNS includes all the nerves outside the CNS, transmitting signals between the CNS and the rest of the body.

Question 32

How do organisms gain access to the CNS?

Answer 32

Organisms may enter the CNS through: Bloodstream (hematogenous spread) Nerve pathways (e.g., rabies virus via peripheral nerves) Direct invasion (e.g., skull fractures, surgery) Infection from nearby areas (e.g., sinuses, middle ear)

Question 33

What is meningitis and what is encephalitis?

Answer 33

Meningitis: Inflammation of the protective membranes (meninges) surrounding the brain and spinal cord. Encephalitis: Inflammation of the brain itself.

Question 34

Signs and symptoms of bacterial meningitis and encephalitis, and why immediate treatment is crucial:

Answer 34

Bacterial meningitis: Fever, headache, stiff neck, nausea, photophobia, altered mental status. Encephalitis: Fever, confusion, seizures, personality changes, coma. Immediate treatment is necessary because both conditions can progress rapidly, causing permanent brain damage or death.

Question 35

Bacteria causing 90% of bacterial meningitis and related facts:

Answer 35

Major species: Neisseria meningitidis (vaccine available; causes college outbreaks) Streptococcus pneumoniae (vaccine available) Haemophilus influenzae type b (Hib) (vaccine available) Others: Listeria monocytogenes (found in undercooked meats, deli meats, cheeses) Group B Streptococcus (normal vaginal flora; neonatal meningitis)

Question 36

Listeria’s method to spread and evade immune system:

Answer 36

Listeria uses actin rockets to propel itself through host cells. This intracellular movement allows it to avoid extracellular immune detection (like antibodies or complement).

Question 37

What is Hansen’s Disease (Leprosy)?

Answer 37

Caused by Mycobacterium leprae Features: acid-fast, slow-growing, prefers cooler body regions (like extremities) Signs/symptoms: Tuberculoid leprosy: Mild, localized skin lesions, loss of sensation. Lepromatous leprosy: Severe, disfiguring lesions, widespread nerve damage. Difference: Tuberculoid involves strong immune response; lepromatous involves poor immune response.

Question 38

CNS or PNS? Contagious? Quarantine?

Answer 38

Leprosy affects the PNS. It is not highly contagious and requires prolonged, close contact. Quarantine is not necessary.

Question 39

What is Botulism? Why is it an intoxication?

Answer 39

Botulism is caused by the botulinum toxin from Clostridium botulinum. It’s an intoxication because the toxin, not the bacteria, causes symptoms. Three forms: Foodborne (ingestion of toxin-contaminated food) Infant (ingestion of spores, often in honey) Wound (spores enter an open wound) Symptoms: Weakness, blurred vision, dry mouth, descending paralysis.

Question 40

How does botulinum toxin cause paralysis?

Answer 40

It blocks acetylcholine release at neuromuscular junctions. This prevents muscle contraction, leading to flaccid paralysis.

Question 41

How is botulism prevented?

Answer 41

Properly canning food, avoiding bulging cans, no honey for infants <1 year, wound care.

Question 42

What is tetanus and how is it acquired?

Answer 42

Caused by Clostridium tetani. Acquired through wound contamination with spores (e.g., from soil). Symptoms: Lockjaw, muscle spasms, difficulty swallowing.

Question 43

How does tetanospasmin cause symptoms?

Answer 43

Toxin blocks inhibitory neurotransmitter release, leading to continuous muscle contraction.

Question 44

Is there a vaccine for tetanus?

Answer 44

Yes, the DTaP and Tdap vaccines protect against tetanus, diphtheria, and pertussis.

Question 45

What is viral meningitis and why are many of its viruses called enteroviruses?

Answer 45

Viral meningitis is a less severe form of meningitis caused by viruses. Enteroviruses (like coxsackievirus) are called so because they infect the GI tract. Transmission: Fecal-oral route, respiratory secretions.

Question 46

What is poliomyelitis? What causes it?

Answer 46

Caused by the poliovirus. Signs/symptoms: Fever, fatigue, headache, stiffness, paralysis. Four forms: Asymptomatic (90% of cases) Abortive polio (mild illness) Non-paralytic polio (meningitis-like) Paralytic polio (flaccid paralysis) Transmission: Fecal-oral route, contaminated water.

Question 47

What is an iron lung and why were they used?

Answer 47

A negative pressure ventilator used to help polio patients with respiratory muscle paralysis. Hospitals were filled with them during polio epidemics in the 20th century.

Question 48

Is there a vaccine for polio and how is it being used globally?

Answer 48

Yes: IPV (inactivated polio vaccine) and OPV (oral polio vaccine) The WHO uses mass vaccination campaigns to eradicate polio globally, targeting children in endemic regions.

Question 49

Structure and function of the gastrointestinal (GI) tract:

Answer 49

The GI tract includes the mouth, esophagus, stomach, small and large intestines, rectum, and anus. Lined with a mucous membrane that: Protects against digestive enzymes and pathogens Absorbs nutrients Secretes mucus and enzymes

Question 50

Normal microbiota in the mouth and intestines:

Answer 50

Mouth: Streptococcus spp., Lactobacillus, Actinomyces Intestines: Small intestine: fewer microbes due to bile and digestive enzymes Large intestine: rich microbiota, including E. coli, Bacteroides, and Clostridium

Question 51

Process of dental caries to periodontal disease:

Answer 51

Dental caries (cavities): Bacteria (e.g., Streptococcus mutans) metabolize sugars, producing acids that demineralize enamel. Gingivitis: Inflammation of gums from plaque accumulation. Periodontitis: Advanced gum disease with destruction of bone and soft tissue.

Question 52

Effect of Helicobacter pylori on the stomach lining:

Answer 52

H. pylori damages stomach lining by: Penetrating mucus Producing urease (neutralizes stomach acid) Causing inflammation and ulcers

Question 53

Virulence factors of H. pylori:

Answer 53

Urease: neutralizes gastric acid Flagella: helps movement through mucus Adhesins: help attachment to epithelial cells Toxins: damage epithelial cells and promote inflammation Evades phagocytosis by surviving inside cells

Question 54

Ulcers: symptoms, treatment, prevention:

Answer 54

Symptoms: Burning stomach pain, nausea, bloating Treatment: Antibiotics (e.g., clarithromycin) + acid reducers (e.g., proton pump inhibitors) Prevention: Avoid NSAIDs overuse, reduce stress, good hygiene

Question 55

Bacterial gastroenteritis & prevention:

Answer 55

Inflammation of stomach/intestines caused by bacteria (e.g., E. coli, Salmonella, Shigella) Symptoms: Diarrhea, cramps, vomiting, fever Prevention: Handwashing, proper food handling, safe water, vaccines (e.g., for cholera or typhoid)

Question 56

Cholera and its mechanism:

Answer 56

Caused by Vibrio cholerae Cholera toxin: Part B: binds to intestinal cells Part A: activates adenylate cyclase → increases cAMP → massive water/electrolyte efflux Leads to severe watery diarrhea

Question 57

Rice-water stool & cholera treatment/prevention:

Answer 57

Rice-water stool: Watery diarrhea with mucus and flecks, resembles water after rinsing rice Treatment: Oral rehydration therapy (ORT), IV fluids, antibiotics Prevention: Clean water, sanitation, oral cholera vaccine

Question 58

Antimicrobial-associated diarrhea & fecal transplants:

Answer 58

Caused by C. difficile overgrowth after antibiotic use Symptoms: severe diarrhea, colitis Fecal transplants restore healthy gut microbiota by introducing stool from a healthy donor

Question 59

Salmonellosis – uniqueness & recurrence:

Answer 59

Salmonella can invade intestinal cells, survive in phagosomes, and spread via bloodstream to liver, spleen, or gallbladder (can cause chronic carrier state) Recurrent infections possible from gallbladder reservoirs

Question 60

Type III secretion system (E. coli & Salmonella):

Answer 60

Molecular syringe-like structure Injects toxins and receptors into host cells Promotes pedestal formation, cytoskeletal changes, host manipulation for invasion

Question 61

Viral gastroenteritis – causes, diagnosis, treatment, prevention:

Answer 61

Caused by Norovirus, Rotavirus, Adenovirus Symptoms: Vomiting, diarrhea, fever Diagnosis: Clinical signs or PCR Treatment: Supportive (fluids) Prevention: Hand hygiene, Rotavirus vaccine, disinfect surfaces

Question 62

Cholera and The Big Stink:

Answer 62

Cholera: Reinforces Vibrio cholerae transmission via water, historical outbreaks, public health measures. The Big Stink: London’s 1858 sewage crisis → sparked modern sanitation systems and understanding of fecal-oral disease transmission.

Question 63

Tuberculosis (TB):

Answer 63

Cause: Mycobacterium tuberculosis (acid-fast bacillus with waxy mycolic acid cell wall). Transmission: Airborne droplets from coughing, sneezing, talking. Primary TB: Initial infection; often asymptomatic or with mild flu-like symptoms. Secondary TB: Reactivation of latent TB when immune system weakens; causes cough, night sweats, weight loss, blood-tinged sputum. Disseminated TB: Bacteria spread via blood to other organs (bone, liver, kidneys, brain); also called miliary TB.

Question 64

Respiratory system structure and microbiota:

Answer 64

Upper respiratory system: Nose, nasal cavity, pharynx, larynx. Contains normal microbiota (e.g., Streptococcus, Staphylococcus). Lower respiratory system: Trachea, bronchi, bronchioles, alveoli. Normally axenic (free of microbes) due to: Ciliary mucous escalator: Cilia move mucus and trapped particles up and out of the lungs. Alveolar macrophages: Engulf and destroy pathogens in the alveoli.

Question 65

Streptococcal pharyngitis (strep throat):

Answer 65

Cause: Streptococcus pyogenes (Group A strep). Virulence factors: M protein: Prevents phagocytosis. Streptolysins: Lyse red and white blood cells. Hyaluronidase: Helps invasion into tissues. C5a peptidase: Inhibits immune cell recruitment. Scarlet fever toxin: Requires a lysogenized strain producing pyrogenic toxin (superantigen). Causes rash, strawberry tongue, fever.

Question 66

Sinusitis and otitis media:

Answer 66

Causes: Often Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis. Sinusitis: Facial pain, pressure, nasal congestion. Otitis media (middle ear infection): Ear pain, fever, hearing loss (common in children). Treatment: Antibiotics, decongestants. Prevention: Vaccines (e.g., Hib, pneumococcal), avoiding upper respiratory infections.

Question 67

Common colds:

Answer 67

Causes: Mainly rhinoviruses, but also coronaviruses, adenoviruses. Symptoms: Sneezing, runny nose, sore throat, mild cough. No vaccine: Over 200 viral strains, high mutation rate, and short immunity.

Question 68

Corynebacterium diphtheriae and diphtheria toxin:

Answer 68

Transmission: Respiratory droplets or skin contact. Diphtheria toxin: An A-B exotoxin that halts protein synthesis in host cells. Pseudomembrane: Grayish film in throat composed of dead cells, fibrin, and bacteria—can block airway.

Question 69

Lower respiratory infections—rarity and danger:

Answer 69

Rare due to defense mechanisms (cilia, macrophages). Dangerous because infections can impair gas exchange and cause systemic illness.

Question 70

Pneumonia:

Answer 70

Definition: Inflammation and fluid in alveoli. Pneumococcal pneumonia: Cause: Streptococcus pneumoniae. Symptoms: High fever, productive cough, chest pain, difficulty breathing. Diagnosis: Chest X-ray, sputum culture. Treatment: Antibiotics (penicillin), vaccine available (PCV13, PPSV23). Klebsiella pneumoniae: Often nosocomial (hospital-acquired). Produces thick, bloody sputum due to tissue necrosis. More resistant to antibiotics.

Question 71

Viral respiratory diseases – SARS & RSV:

Answer 71

Severe Acute Respiratory Syndrome (SARS): Cause: SARS-CoV (a coronavirus). Transmission: Droplets, close contact. Symptoms: Fever, dry cough, difficulty breathing. Prevention: Isolation, hygiene, travel restrictions. Respiratory Syncytial Virus (RSV): Cause: RSV, a paramyxovirus. Transmission: Respiratory droplets. Symptoms in children: Bronchiolitis, wheezing, respiratory distress. Symptoms in adults: Cold-like or mild respiratory symptoms. Syncytium: Infected cells fuse to form multinucleated cells → cell damage, virus spread.

Question 72

Other causes of pneumonia:

Answer 72

Pneumonic plague: Cause: Yersinia pestis. Transmitted via respiratory droplets; highly fatal without treatment. Inhalational anthrax: Cause: Bacillus anthracis spores. Spores inhaled → severe respiratory distress and toxemia.

Question 73

Septicemia vs. Bacteremia vs. Toxemia:

Answer 73

Bacteremia: Bacteria in blood. Septicemia: Infection in blood → inflammation, shock. Toxemia: Microbial toxins in blood.

Question 74

Lymphangitis & Petechiae

Answer 74

Lymphangitis: Red streaks from infected lymph vessels. Petechiae: Tiny skin hemorrhages. Both = signs of systemic infection.

Question 75

Septicemia Organisms & Source

Answer 75

Common: E. coli, Staph, Strep, Pseudomonas. Often from normal flora, especially in immunocompromised.

Question 76

Plague

Answer 76

Cause: Yersinia pestis via flea bites (rats are reservoir). Bubonic: Lymph node swelling (buboes). Pneumonic: Lung infection, airborne spread.

Question 77

Lyme Disease

Answer 77

Cause: Borrelia burgdorferi, spread by ticks. 3 phases: rash → neuro/joint issues → arthritis. Rising cases: Climate & habitat changes.

Question 78

Malaria

Answer 78

Cause: Plasmodium via mosquito. Cycle: Liver → RBCs → fever/chills. Prevention: Nets, antimalarials.

Question 79

Toxoplasmosis

Answer 79

Cause: Toxoplasma gondii, from cat feces/raw meat. Dangerous in pregnancy or immunocompromised.

Question 80

Viremia

Answer 80

Viruses in the bloodstream.

Question 81

Infectious Mononucleosis (Mono)

Answer 81

Cause: EBV. Spread: Saliva. Teens: Fatigue, sore throat, swollen nodes. Risks: Chronic fatigue, lymphoma in some.

Question 82

Ebola & Marburg

Answer 82

Cause: Filoviruses. Spread: Body fluids. Symptoms: Fever, bleeding, organ failure. Reservoir: Fruit bats. Ebola vaccine available.

Question 83

Key Evolutionary Terms:

Answer 83

Mutation: Random genetic change. Variation: Genetic differences in a population. Fitness: Ability to survive and reproduce. Populations evolve as favorable traits increase over generations.

Question 84

Pathogen Fitness Factors:

Answer 84

Fitness ≠ just multiplication. Transmission is key—a pathogen must spread to new hosts. High virulence can reduce fitness if it hinders transmission.

Question 85

Symptoms & Transmission:

Answer 85

Symptoms often aid transmission (e.g., coughing). Direct contact disease: Too severe = host is immobilized → reduced spread. Vector/waterborne disease: Can still transmit even if host is immobile → transmission persists.

Question 86

Coevolution vs. Environmental Evolution:

Answer 86

Coevolution: Two species evolve in response to each other. Arms race: Each evolves defenses/offenses over time (e.g., host immunity vs. pathogen virulence).

Question 87

Heliconius & Passiflora Example:

Answer 87

Butterflies lay eggs on Passiflora leaves. Plant evolves egg mimics, toxins to deter laying. Butterfly evolves to resist toxins and detect mimics.

Question 88

Coevolution Limits:

Answer 88

Evolution can’t go on forever. Too much virulence → kills host too fast. Too much resistance → costly to host’s energy/resources.

Question 89

Red Queen Hypothesis:

Answer 89

Hosts and pathogens must keep evolving just to keep up. “Run to stay in place” – constant evolutionary battle.

Question 90

Myxoma Virus & Australian Rabbits:

Answer 90

Virus released to reduce invasive rabbit population. Initially highly deadly, but over time: Virus became less virulent (killed too fast → fewer transmissions). Rabbits evolved resistance. Outcome: High virulence → killed too fast → poor spread. Intermediate → best balance for transmission. Low virulence → not competitive enough.

Question 91

Trade-offs in Virulence:

Answer 91

If host resists, pathogen may lose virulence. If pathogen is weak, host may lose resistance. Trade-off: Maximize spread without killing host too fast.

Question 92

Malaria = No Trade-off:

Answer 92

Transmitted by mosquito vector, even from very sick hosts. No pressure to reduce virulence.

Question 93

Malaria Host Resistance Examples:

Answer 93

Sickle-cell trait: Alters hemoglobin → resists Plasmodium. G6PD deficiency: Damages infected RBCs. Duffy-negative blood group: Resists P. vivax entry.

Question 94

HIV = No Trade-off:

Answer 94

Spread occurs before severe symptoms, via bodily fluids. Human resistance: CCR5-Δ32 mutation: Prevents virus entry into cells.

Question 95

Hypotheses on Virulence Evolution:

Answer 95

If virulence lowers transmission, it will evolve to decrease. If transmission unaffected, high virulence may persist.