1
Q
What is septicemia?
A
Pathogen in blood.
2
Q
What proportion of septicemia cases are hospital-acquired?
A
1/3 of all cases.
3
Q
What hospital source commonly leads to septicemia?
A
Catheters.
4
Q
How do catheters contribute to septicemia?
A
That’s how it enters the blood.
5
Q
What are early symptoms of septicemia?
A
Fever, chills, breathing difficulty.
6
Q
What does SIRS stand for?
A
Systematic inflammatory response syndrome.
7
Q
What does “S” stand for in SIRS?
A
Systematic.
8
Q
What does “R” stand for in SIRS?
A
Response.
9
Q
What is the final stage of sepsis?
A
Shock.
10
Q
What is puerperal sepsis?
A
Infection after childbirth.
11
Q
What organism causes puerperal sepsis?
A
GAS (Streptococcus pyogenes).
12
Q
What is the treatment for puerperal sepsis?
A
Penicillin.
13
Q
When was measles declared eliminated in Canada?
A
1998.
14
Q
Why are more people getting sick with measles now?
A
It is so contagious and more people are susceptible due to not being immunized or under-immunized.
15
Q
How is measles described in terms of transmissibility?
A
Textbook worst in terms of transmissibility to others.
16
Q
How does measles spread?
A
Through the air.
17
Q
What are early symptoms of measles?
A
Fever, cough, red eyes, runny nose.
18
Q
What oral sign can appear in measles?
A
White spots in the mouth.
19
Q
What happens later in measles infection?
A
A distinctive red rash develops.
20
Q
What were most measles cases in Canada linked to?
A
International travelers.
21
Q
What global trend is happening with measles outbreaks?
A
Outbreaks around the world are rising.
22
Q
Why is the pool of susceptible people increasing?
A
Not being immunized or under-immunized.
23
Q
Why have immunization rates declined since the pandemic?
A
Pandemic took resources away and increased anti-vaccine sentiment.
24
Q
What percentage of people need to be vaccinated to stop measles spread?
A
95%.
25
What vaccine prevents measles?
MMR vaccine.
26
How many doses does the MMR vaccine have?
Two doses.
27
When is the first MMR dose given?
Around 12 months of age.
28
When is the second MMR dose given?
Between 4–6 years old.
29
What issue exists with some millennials and Gen Xers?
May have only received one dose.
30
How many measles cases have been reported in Canada so far this year?
More than 500 cases.
31
Where were the majority of cases in Canada?
Ontario.
32
How many cases were reported in all of last year?
147 cases.
33
Can measles still spike even after being declared eliminated?
Yes, occasional spikes occur.
34
Do all measles patients recover at home?
No, some need hospital admission.
35
What serious complications can measles cause?
Pneumonia, brain swelling, death.
36
How long can it take for measles symptoms to appear?
About 10 days.
37
Why is measles exposure hard to trace?
Exposure can happen anywhere (doctor’s offices, restaurants, airports).
38
Why was a 7-month-old child especially at risk in the example?
Had not yet received first dose of MMR vaccine.
39
What condition made the child more vulnerable to measles?
Cystic fibrosis and immunocompromised.
40
What risk threatens Canada’s measles elimination status?
Local transmission for a year.
41
Why is there concern about measles returning?
Due to decreased vaccination and increased spread.
42
What are the five main causative agents of meningitis?
Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae, Listeria monocytogenes, E. coli.
43
What is the focus of meningitis diagnosis?
CSF (cerebrospinal fluid).
44
Why is CSF important in meningitis diagnosis?
It bathes the entire nervous tissue.
45
Where is CSF collected from?
Lumbar region (tail region of the spinal cord).
46
What is the first procedure performed on CSF?
Gram stain.
47
What is the best first diagnostic step for meningitis?
Gram stain.
48
If asked “Which meningitis is spread by food?” what is the answer?
Listeria monocytogenes.
49
What types of details are commonly tested in meningitis questions?
Demographic, transmission, treatment.
50
Why is chloramphenicol not used for all meningitis patients?
Because of adverse effects.
51
What is the best treatment for meningitis?
Third-generation cephalosporins.
52
What is a key prevention strategy for meningitis?
Avoid sharing items.
53
Where are meningitis organisms commonly carried?
Nasopharyngeal region.
54
How does sharing contribute to meningitis spread?
Sharing means saliva can spread organisms.
55
What is the mechanism of tetanus?
Blocks the release of the inhibitory neurotransmitter GABA.
56
What is the role of GABA in normal muscle function?
Helps muscles relax.
57
What is the normal cycle of muscle activity?
Contraction and relaxation.
58
What happens to muscle activity in tetanus?
Relaxation does not happen.
59
What is the result of blocked GABA in tetanus?
Muscles go into spasm.
60
What are early symptoms of tetanus?
Restlessness, grouchiness, drooling, lockjaw, stiff neck.
61
How is stiff neck in tetanus different from meningitis?
Do not use Kernig’s sign.
62
What are advanced symptoms of tetanus?
Back spasms and opisthotonos.
63
What is opisthotonos?
Severe spasm with body arching backward.
64
What serious complication can result from severe spasms?
Spinal fracture.
65
Is death in tetanus caused by spinal fracture?
No.
66
What causes death in tetanus?
Respiratory failure and cardiovascular failure.
67
What causes tetanus?
Powerful exotoxin.
68
How is tetanus prevented?
DTaP vaccine.
69
How often should adults receive a tetanus booster?
Every 10 years.
70
What organism causes botulism?
Clostridium botulinum.
71
How is botulism described in terms of severity?
Lethal form of food poisoning.
72
What type of foods are botulism most associated with?
Low-acid canned foods.
73
What processed food example was mentioned for botulism?
Sausages.
74
What canned food examples were listed for botulism risk?
Corn, beans, low-acid fruits, mushrooms.
75
Why are tomatoes usually not a main concern in botulism?
They are highly acidic.
76
What toxin types affect humans in botulism?
A, B, E, F.
77
Which botulinum toxin type is most lethal?
Type A.
78
What is the fatality rate of toxin B and E?
About 25%.
79
Which toxin types affect animals and not humans?
C, D, and G.
80
How does botulism compare to tetanus?
Opposite.
81
What are early symptoms of botulism?
Dizziness, abdominal cramps, nausea.
82
What GI symptom occurs in infants with botulism?
Constipation (“floppy baby syndrome”).
83
What GI symptom occurs in adults with botulism?
Diarrhea.
84
What neurological symptoms are seen in botulism?
Dilated pupils, blurred vision, double vision.
85
Why are neurological symptoms important in botulism?
Important warning signs.
86
Where does botulism act in the body?
Neuromuscular junction.
87
What neurotransmitter is blocked in botulism?
Acetylcholine.
88
What is the result of blocking acetylcholine?
Flaccid paralysis.
89
What systems, if affected, can lead to death in botulism?
Cardiovascular and respiratory systems.
90
Which toxin is especially associated with fatal outcomes?
Toxin A.
91
Can contaminated food look normal in botulism?
Yes.
92
Can contaminated food smell normal in botulism?
Yes.
93
What is the danger despite normal appearance and smell?
It may still contain powerful exotoxin.
94
What organism causes leprosy?
Mycobacterium leprae.
95
What is unique about the cell wall of Mycobacterium leprae?
Contains mycolic acid.
96
How does Mycobacterium leprae grow?
Very slow-growing organism.
97
Can Mycobacterium leprae be stained with Gram stain?
No.
98
What stain must be used to identify Mycobacterium leprae?
Acid-fast stain.
99
Why does leprosy have a long incubation period?
Slow growth of the organism.
100
What is the incubation period for the mild form of leprosy?
2 to 5 years.
101
What is the incubation period for the severe form of leprosy?
9 to 12 years.
102
Where was leprosy first discovered?
Norway.
103
Who discovered leprosy?
Gerhard Hansen.
104
What is another name for leprosy?
Hansen’s disease.
105
How were leprosy patients treated historically?
Isolated and described as “unclean.”
106
What was done to leprosy patients in the past?
Made to live apart from others.
107
Is leprosy highly contagious in ordinary care settings?
No.
108
How is leprosy usually transmitted?
Prolonged close contact with nasal secretions.
109
Are healthcare workers at high risk of contracting leprosy?
No, they generally do not have that level of close contact.
110
What are the two main forms of leprosy?
Tuberculoid (paucibacillary) and lepromatous (multibacillary).
111
What is another name for the tuberculoid form of leprosy?
Skin form / paucibacillary form.
112
What is the incubation period for tuberculoid leprosy?
2 to 5 years.
113
What area of the body is mainly affected in tuberculoid leprosy?
Skin.
114
What happens to sensation in tuberculoid leprosy?
Skin loses sensitivity.
115
Where does the organism grow in tuberculoid leprosy?
Peripheral nerves.
116
What type of lesions are seen in tuberculoid leprosy?
Disfiguring nodules.
117
What happens to cell-mediated immunity in tuberculoid leprosy?
Weak, but not completely failed.
118
Can patients recover from tuberculoid leprosy?
Yes, with treatment.
119
What is the minimum treatment duration for tuberculoid leprosy?
At least 6 months.
120
What is another name for the lepromatous form of leprosy?
Progressive form / multibacillary form.
121
How is the lepromatous form described?
Progressive severe form.
122
What happens to the skin in lepromatous leprosy?
Becomes deformed and necrotic.
123
What happens to immunity in lepromatous leprosy?
Cell-mediated immunity has essentially failed.
124
What happens to the nose in lepromatous leprosy?
Structures begin to fall apart.
125
What is the characteristic facial appearance in lepromatous leprosy?
Lion-faced appearance.
126
What type of body areas does the organism prefer?
Cooler peripheral areas of the body.
127
What bodily fluid can carry the bacteria in lepromatous leprosy?
Nasal exudate.
128
What happens to fingers and toes in advanced lepromatous leprosy?
Become claw-like or reduced to stubs.
129
What happens to tissue in severe leprosy?
Becomes necrotic.
130
What happens to function in advanced leprosy?
Patient loses function.
131
Is death usually caused directly by leprosy?
No.
132
What is the common cause of death in leprosy patients?
Secondary infections like TB.
133
What is the minimum treatment duration for lepromatous leprosy?
2 years.
134
Can structural damage from leprosy be reversed?
No.
135
What drugs are used to treat leprosy?
Rifampin, sulfone (sulfa drugs), clofazimine.
136
What type of drug is clofazimine?
Antimycobacterial drug.
137
How does clofazimine function in treatment?
Complements rifampin and helps protect against resistance.
138
What is the relationship between rifampin and clofazimine?
They complement each other around DNA replication/transcription.
139
What do sulfa drugs target in leprosy treatment?
Enzyme activity.
140
How is leprosy diagnosed?
Skin scraping or scar tissue sample.
141
What test is used to confirm leprosy?
Acid-fast stain.
142
What causes polio?
Viral infection caused by poliovirus.
143
What cells does poliovirus attack?
Motor neurons.
144
What type of motor neurons are affected in polio?
Central nervous system motor neurons that supply muscles.
145
How is polio always acquired?
Ingestion.
146
What is the transmission route of polio?
Fecal-oral route.
147
What are common sources of polio infection?
Contaminated food and water.
148
What do early polio symptoms reflect?
GI/throat entry, not nervous system disease.
149
What are the first symptoms of polio?
Nausea and sore throat.
150
What happens after poliovirus enters the body?
Enters local lymph nodes.
151
What happens in lymph nodes?
Virus multiplies.
152
What happens after multiplication in lymph nodes?
Enters the blood.
153
What is the term for virus in the blood?
Viremia.
154
What happens in transient viremia?
Immune response is strong.
155
What type of immunity is especially important in transient viremia?
Cell-mediated immunity.
156
What immune cells destroy the virus in transient viremia?
T cells.
157
What is the outcome of transient viremia?
No progression of disease.
158
Which group most commonly experiences transient viremia?
Immunized people.
159
What happens in persistent viremia?
Immunity is not strong enough.
160
Who is most at risk for persistent viremia?
Unimmunized individuals.
161
Where does the virus go in persistent viremia?
Motor neurons.
162
What happens in motor neuron cell bodies?
Virus grows.
163
What is the result of poliovirus infection of motor neurons?
Death of motor neurons.
164
What can result from motor neuron death?
Paralysis.
165
What percentage of polio cases result in paralysis today?
Less than 1%.
166
What is the historical name for polio?
Infantile paralysis disease.
167
What concept does polio strongly demonstrate?
Social determinants of health.
168
What country was highlighted as a major example of polio control?
India.
169
When was India declared polio-free?
2012.
170
What contributed to polio control in India?
Government resources, education, and mass immunization efforts.
171
Can polio still reappear in some areas?
Yes, in rural areas.
172
What regions are currently at risk for polio?
Syria, Afghanistan, Pakistan, sub-Saharan Africa.
173
What factors contribute to polio spread in these regions?
Poor sanitation, contaminated water, lack of clean food, disrupted vaccination systems.
174
Who developed the Salk vaccine?
Jonas Salk.
175
What type of vaccine is the Salk vaccine?
Inactivated virus.
176
How is the Salk vaccine administered?
Injection.
177
Does the Salk vaccine require boosters?
Yes.
178
When was the Salk vaccine introduced?
Early 1950s (around 1954).
179
Who developed the Sabin vaccine?
Albert Sabin.
180
What type of vaccine is the Sabin vaccine?
Attenuated live virus.
181
How is the Sabin vaccine administered?
Oral drops (OPV).
182
What is an advantage of the Sabin vaccine?
Easy to give, no injections.
183
Does the Sabin vaccine usually require boosters?
No.
184
What is a rare risk of the Sabin vaccine?
Reversion back to disease.
185
What is the approximate risk of reversion with the Sabin vaccine?
About 1 in 750,000.
186
What was the relationship between Salk and Sabin?
Bitter rivals.
187
Were Salk and Sabin awarded the Nobel Prize?
No, according to the professor.
188
What is the correct scientific term for “blood poisoning”?
Septicemia.
189
What does septicemia mean?
Bacterial pathogen in the blood or toxins in the blood.
190
What proportion of septicemia cases are hospital-acquired?
About one-third.
191
What are common hospital sources of septicemia?
Catheter, urinary bag, IV sites.
192
What should you do if tubing or fluid looks cloudy or suspicious?
Think septicemia and report it.
193
What are general symptoms of septicemia?
Fever with chills, breathing difficulty.
194
What is the key sign of septicemia?
Lymphangitis.
195
What is lymphangitis?
Inflamed lymph vessels.
196
How does lymphangitis appear clinically?
Streaking along an arm or leg.
197
Where do lymphangitis streaks typically stop?
At the lymph node.
198
What later symptom may indicate worsening septicemia?
Decreased urinary output.
199
What can septicemia progress into?
Sepsis.
200
What term is used in hospitals for sepsis progression?
SIRS (systemic inflammatory response syndrome).
201
What does SIRS stand for?
Systemic inflammatory response syndrome.
202
What is the end stage of septicemia/sepsis progression?
Shock.
203
What does “puerperal” refer to?
Child.
204
What is puerperal sepsis?
Childbirth fever.
205
What organism commonly causes puerperal sepsis?
GAS (Streptococcus pyogenes).
206
How can puerperal sepsis be introduced?
During childbirth by healthcare contact.
207
What type of infection does puerperal sepsis become?
Uterine sepsis.
208
Can puerperal sepsis become systemic?
Yes, can become systemic and fatal.
209
What are symptoms of puerperal sepsis?
Pelvic distension, bloody discharge, fever, severe illness after childbirth.
210
What is the treatment for puerperal sepsis?
Penicillin.
211
When is treatment most effective for puerperal sepsis?
If recognized early.
212
What is rheumatic fever associated with?
Sequel to strep throat.
213
What organism is linked to rheumatic fever?
GAS / Streptococcus pyogenes.
214
How does strep throat lead to rheumatic fever?
When strep throat becomes septicemic, organisms can reach the heart.
215
Are the exact causes of rheumatic fever fully known?
No.
216
What is rheumatic fever thought to be a reaction to?
Reaction to organisms entering the blood.
217
What part of the heart is affected in rheumatic fever?
Heart valves.
218
Which valve is especially affected?
Mitral valve (left side).
219
How does rheumatic fever begin?
Insidiously with fever.
220
What joint-related symptom occurs in rheumatic fever?
Arthritis.
221
How may arthritis present externally?
Nodules near joints (e.g., elbow).
222
What cardiac symptoms occur in rheumatic fever?
Chest pain, palpitations, heart murmur.
223
What general symptom is common in rheumatic fever?
Fatigue.
224
How can rheumatic fever progress over time?
Mild/subacute → acute.
225
How long may it take before severe heart damage occurs?
Years.
226
What long-term complication may be required?
Valve replacement.
227
What serious outcomes can rheumatic fever lead to?
Heart attack, heart failure, death without warning.
228
Is rheumatic fever preventable?
Yes, if strep throat is treated properly with antibiotics.
229
Where is rheumatic fever reappearing according to the professor?
Some Indigenous communities.
230
What factors are linked to its reappearance?
Socioeconomic factors.
231
What is the treatment for rheumatic fever if caught early?
Penicillin.
232
Can penicillin reverse heart valve damage?
No, once damage has occurred it cannot be reversed.
233
Why is anthrax considered important?
It is very deadly.
234
What historical event did the professor reference for anthrax?
2001 anthrax attacks in the U.S.
235
Why is anthrax a major concern biologically?
It forms endospores.
236
How many exotoxins does anthrax produce?
Three.
237
What are the three anthrax exotoxins?
Lethal toxin, protective toxin, edema toxin.
238
What does lethal toxin do?
Destroys phagocytes / evades and destroys phagocytes.
239
What does protective toxin do?
Permits entry.
240
What does edema toxin do?
Causes swelling of infected area.
241
How were anthrax spores spread in 2001?
Mailed in packages.
242
What media organization was mentioned in the anthrax case?
NBC / Tom Brokaw case
243
Who was mentioned as being exposed to anthrax?
Erin O’Connor opened a contaminated package
244
What symptom did Erin O'Connor develop?
Lesion on left collarbone.
245
What form of anthrax did this represent?
Skin form.
246
What are the three forms of anthrax based on entry?
GI tract form, skin form, pulmonary form.
247
What is the mortality rate of skin anthrax?
About 20%.
248
How do spores enter in skin anthrax?
Through minute openings in skin.
249
What lesion is characteristic of skin anthrax?
Black lesion called Eschar.
250
How is an eschar described?
Black, charcoal-like lesion.
251
What is the treatment for skin anthrax?
Ciprofloxacin (Cipro) or penicillin if caught early.
252
How is pulmonary anthrax acquired?
Spores inhaled into lungs.
253
What is the mortality rate of pulmonary anthrax?
Almost 100%.
254
What severe condition can pulmonary anthrax cause?
Severe septicemia.
255
What can happen to survivors of pulmonary anthrax?
Permanent disability.
256
How is GI anthrax acquired?
Contaminated meat/food.
257
What is the mortality rate of GI anthrax?
About 50%.
258
What symptoms occur in GI anthrax?
Intestinal hemorrhage, diarrhea, breakdown of intestinal lining.
259
What is the go-to drug for anthrax?
Ciprofloxacin (Cipro).
260
What alternative drug can be used if caught early?
Penicillin.
261
Is there a vaccine for anthrax?
Yes.
262
Who is the anthrax vaccine mainly reserved for?
Military, frontline workers, high-risk individuals.
263
What is a limitation of the anthrax vaccine schedule?
Requires 6 doses over 18 months plus yearly boosters.
264
Why is the anthrax vaccine impractical for the general public?
Complex dosing schedule.
265
What is the anthrax vaccine based on?
Inactivated bacterial material.
266
Why is anthrax feared as a biological warfare weapon?
Spores are highly durable.
267
What organism causes gangrene?
Clostridium perfringens.
268
What two major virulence features are involved in gangrene?
Endospores and powerful alpha exotoxin.
269
What is the main effect of gangrene on tissue?
Death of tissue.
270
How does the alpha toxin affect blood supply?
Destroys blood supply to tissue.
271
What part of blood vessels does the toxin destroy?
Endothelial membranes.
272
What blood cells are destroyed in gangrene?
RBCs and WBCs.
273
What is the overall effect on the patient on Gangrene?
Patient becomes severely compromised.
274
What enzymes are produced by Clostridium perfringens?
Hyaluronidase and collagenase.
275
What is the role of hyaluronidase and collagenase in Gangrene?
Contribute to tissue destruction and necrosis.
276
What are early symptoms of gangrene?
Abrupt fever and pain at infected region.
277
What type of fluid may ooze from infected tissue in Gangrene?
Thin bloody fluid / pus mixed with blood.
278
What happens to the skin over the infected area in Gangrene?
Blackening of overlying skin.
279
What causes the blackening of tissue in Gangrene?
Hyaluronidase and necrosis.
280
What contributes to deeper tissue destruction in Gangrene?
Collagenase.
281
What happens to the infected area in terms of size in Gangrene?
Swelling/foul odour
282
Why does swelling occur in gangrene?
Gas accumulation in dead tissue.
283
What gases are involved in gangrene?
Hydrogen and carbon dioxide.
284
What odor is associated with gangrene?
Foul odor.
285
What unique sound is associated with gangrene?
“Snap, crackle, pop.”
286
What causes this sound in gangrene?
Gas bubbles in tissue.
287
When might this sound be noticed in Gangrene?
While moving or handling the patient.
288
What is the treatment for gangrene if caught early?
Penicillin.
289
What is required if tissue death is advanced gangrene?
Amputation.
290
In what situations can gangrene develop?
Wound infection, diabetic toe, injection site, compound fracture, gunshot wound, poorly performed abortion with contaminated instruments.
291
What organism causes spotted fever?
Rickettsia rickettsii.
292
How is spotted fever transmitted?
Spread by insects and ticks.
293
Is spotted fever exotoxin-mediated?
No.
294
Why is spotted fever included in this chapter?
Can cause heart complications.
295
What type of rash does spotted fever cause?
Macular rash.
296
What disease can spotted fever rash be mistaken for?
Measles.
297
What is a key difference between measles rash and spotted fever rash?
Measles rash does not occur on palms and soles, spotted fever rash does.
298
What is another name for spotted fever?
Rocky Mountain spotted fever.
299
What are other names for Epstein-Barr virus?
EB virus, human herpes virus 4.
300
What type of cancer can Epstein-Barr virus cause in the jaw?
Burkitt’s lymphoma.
301
What type of tumor is Burkitt’s lymphoma?
Fast-growing tumor of the jaw.
302
What carcinoma is associated with Epstein-Barr virus?
Nasopharyngeal carcinoma.
303
What oral condition is associated with EBV, especially in HIV patients?
Oral hairy leukoplakia - very contagious
304
What does oral hairy leukoplakia look like?
Whitish patches on sides of tongue.
305
What common disease is caused by EBV?
Infectious mononucleosis.
306
What chronic condition is EBV possibly linked to?
Chronic fatigue syndrome.
307
What neurological disease did the professor mention EBV may be implicated in?
Multiple sclerosis.
308
What cells does Epstein-Barr virus target?
B lymphocytes.
309
What happens to B cells during EBV infection?
Vigorous B-cell proliferation.
310
Where does EBV become latent?
In B cells.
311
What happens after EBV becomes latent?
It can reactivate.
312
How is infectious mononucleosis spread?
Contaminated saliva.
313
How long can EBV be shed in saliva?
Up to 18 months.
314
What are common symptoms of infectious mononucleosis?
Fever, sore throat with pus, swollen lymph nodes, enlarged spleen, extreme fatigue.
315
What is a rare fatal complication of mono?
Rupture of enlarged spleen.
316
Why is EBV linked to chronic fatigue syndrome?
Long-lasting fatigue, swollen lymph nodes, muscle pain, memory loss, higher EBV blood titers.
317
What does the professor suggest chronic fatigue syndrome may represent?
Prior mono becoming chronic.
318
What names did the professor mention for chronic fatigue syndrome?
“Yuppie flu” or “midlife flu.”
319
What are other names for Cytomegalovirus?
CMV, human herpes virus 5.
320
How is cytomegalovirus transmitted?
Saliva, blood/blood products, sexual transmission, placenta.
321
What cells does CMV target according to the professor?
T cells.
322
What happens to infected cells in CMV infection?
Cells become very large.
323
What does “megalo” refer to in cytomegalovirus?
Swelling.
324
How large do infected T cells become?
2–3 times larger.
325
What is the characteristic microscopic appearance of CMV-infected cells?
Owl’s eye appearance.
326
Where does CMV remain latent?
In T cells.
327
Can CMV reactivate after latency?
Yes, recurrent.
328
How can CMV affect a fetus?
Can infect through placenta.
329
What can CMV cause in fetal development?
Severe developmental problems.
330
What eye condition is caused by CMV in HIV/AIDS patients?
CMV retinitis.
331
What is a major cause of blindness in AIDS patients?
CMV retinitis (not directly HIV itself).
332
What causes malaria?
Protozoan disease caused by Plasmodium.
333
What is the most common example of Plasmodium mentioned?
Plasmodium vivax.
334
How is malaria transmitted?
Anopheles mosquito.
335
How many people are affected by malaria worldwide?
About 300 million.
336
Where do many malaria deaths occur?
Africa.
337
What is the definitive host in malaria?
Mosquito.
338
What type of reproduction occurs in the mosquito?
Sexual reproduction.
339
What is the intermediate host in malaria?
Human.
340
What is the main fever pattern in malaria?
Very high fever with chills.
341
What are “paroxysms” of fever?
Cyclical fever pattern.
342
What happens in the cold phase of malaria?
Shivering and feeling extremely cold.
343
What happens in the hot phase of malaria?
Very high fever (39–40°C).
344
What happens in the wet phase of malaria?
Drenching sweating.
345
What additional symptoms occur in malaria?
Headache, muscle aches, vomiting.
346
What form does the mosquito inject into humans?
Sporozoites.
347
Where do sporozoites go first in the human body?
Liver.
348
What happens to sporozoites in the liver?
Reproduce asexually.
349
What do sporozoites become in the liver?
Merozoites.
350
What happens when liver cells rupture?
Release merozoites.
351
What do merozoites infect next?
Red blood cells (RBCs).
352
What happens to RBCs during infection?
Become engorged and rupture.
353
What condition results from RBC destruction?
Anemia.
354
What happens to the spleen in malaria?
Enlarges.
355
What stage is seen in RBCs on a blood smear?
Ring stage.
356
What happens after the ring stage matures?
Forms more merozoites.
357
What happens to the cycle after RBC rupture?
Continues.
358
What forms do some parasites differentiate into?
Male and female gametocytes.
359
How does the mosquito acquire the parasite?
Blood meal.
360
What forms after fertilization in the mosquito?
Zygote.
361
What does the zygote develop into?
New sporozoites.
362
What happens after new sporozoites form?
Cycle continues.
363
How can malaria be treated?
Stop the cycle at multiple points.
364
What drugs are used to treat malaria?
Quinine or newer related drugs.
365
What additional antibiotics may be used?
Tetracycline / doxycycline.
366
Do malaria treatments have adverse effects?
Yes.
367
What physical prevention method is recommended?
Bed nets.
368
When are mosquitoes most active?
Night feeder.
369
What prophylactic drug may be used for travel?
Chloroquine.
370
Who prescribes malaria prophylaxis?
Clinician.
371
What is rheumatic fever?
Inflammation of the heart and a sequel to strep throat.
372
What organism causes rheumatic fever?
GAS organisms / Streptococcus pyogenes.
373
How does strep throat lead to rheumatic fever?
Strep throat becomes septicemic and reaches the heart.
374
What part of the heart becomes infected in rheumatic fever?
Heart valves.
375
Does the professor say the exact reason for rheumatic fever is fully known?
No.
376
What does the professor say we do know about rheumatic fever?
It becomes septicemic and often starts insidiously.
377
What is usually the first sign of rheumatic fever?
Fever.
378
What other symptom commonly occurs early in rheumatic fever?
Arthritis.
379
How can arthritis appear externally in rheumatic fever?
External nodules form near joints.
380
What example of nodules did the professor give?
Elbow joint develops a growth that should not be there.
381
What happens after the organisms become septicemic?
Circulate everywhere and reach the heart.
382
What heart structure is attacked in rheumatic fever?
Heart valves.
383
Which valve is especially dangerous if affected?
Left Valve (mitral valve)
384
Why is the left side of the heart more serious?
It is the more powerful side.
385
Can the right side also be affected?
Yes, but the left side is worse.
386
What happens to circulation in rheumatic fever?
Person cannot circulate blood in a regular cardiac rhythm.
387
What cardiac symptoms occur in rheumatic fever?
Chest pain, palpitations, murmur.
388
How do patients sometimes describe the palpitations?
Feels like their heart is coming out of their chest.
389
What general symptom develops over time in rheumatic fever?
Fatigue.
390
How may rheumatic fever progress over time?
Subacute then acute.
391
When may rheumatic fever become especially serious?
By midlife.
392
What major procedure may be needed later in life?
Valve replacement.
393
What can happen if the heart stops functioning properly?
Heart attack, heart failure, death.
394
Can death occur suddenly in rheumatic fever?
Yes, without warning.
395
Should rheumatic fever still be common in modern medicine?
No.
396
Why should rheumatic fever usually be preventable?
Treat strep throat properly with antibiotics.
397
Where is rheumatic fever reappearing according to the professor?
Indigenous communities.
398
What factor did the professor connect to its reappearance?
Socioeconomic conditions.
399
What does the professor say about patients complaining of symptoms?
Do not take it lightly.
400
What is the treatment for rheumatic fever before valve damage occurs?
Penicillin.
401
Is penicillin useful after valve damage has already happened?
No.
402
Why is anthrax considered such a dangerous disease?
It forms endospores and produces 3 powerful exotoxins.
403
What historical event did the professor connect to anthrax?
The September 2001 anthrax attacks in the United States.
404
About how many Americans took antibiotics during the 2001 anthrax attacks?
About 10,000.
405
What are the three exotoxins produced by anthrax?
Lethal toxin, protective toxin, edema toxin.
406
What does lethal toxin do?
Destroys phagocytes.
407
Why is destroying phagocytes dangerous?
It destroys the body's first line of defense.
408
What does protective toxin do?
Permits entry.
409
What does edema toxin do?
Causes swelling of the infected area.
410
What is one major reason anthrax is feared?
It can form durable endospores.
411
Where were anthrax endospores mailed during the 2001 attacks?
NBC headquarters.
412
Who was the package intended for?
Tom Brokaw.
413
Who actually opened the package?
Erin O'Connor.
414
What symptom did Erin O'Connor develop?
A lesion on her left collarbone.
415
What are the three portals of entry for anthrax?
GI tract (initial way)
Skin (ERIC OCONNORS case)
Pulmonary (lung form, breathing in endospores)
416
What is the mortality rate of skin anthrax?
About 20%.
417
How do skin anthrax spores enter the body?
Through minute openings in the skin.
418
What classic lesion forms in skin anthrax?
Eschar.
419
What does eschar look like?
Charcoal-colored black lesion.
420
Which anthrax case is used as the example of eschar?
Erin O'Connor's case.
421
How does pulmonary anthrax enter the body?
By inhaling endospores into the lungs.
422
What is the fatality rate of pulmonary anthrax?
Almost 100%.
423
What happens after spores enter the lungs?
They germinate and lead to severe septicemia.
424
Even if people survive pulmonary anthrax, what can happen?
Permanent disability.
425
Which group was especially affected by inhalational anthrax during the 2001 attacks?
Postal workers.
426
What is the mortality rate of GI anthrax?
About 50%.
427
How does GI anthrax enter the body?
Through contaminated food, especially meat.
428
What GI symptoms can anthrax cause?
Intestinal hemorrhaging, diarrhea, breakdown of intestinal lining.
429
What food-related factor increases the risk of GI anthrax?
Undercooked contaminated food.
430
What is the main antibiotic used for anthrax today?
Ciprofloxacin.
431
What group of antibiotics does ciprofloxacin belong to?
Quinolones / fluoroquinolones.
432
What naming pattern often identifies quinolone antibiotics?
Ending in “-floxacin”.
433
Can penicillin treat anthrax?
Yes, if caught early.
434
Which anthrax drug does the professor describe as the best among the floxacins?
Ciprofloxacin.
435
Is there a vaccine for anthrax?
Yes.
436
Who usually receives the anthrax vaccine?
Military, frontline workers, and people at highest risk.
437
Why is the anthrax vaccine not practical for the general public?
It requires 6 doses over 18 months plus yearly boosters.
438
What is the anthrax vaccine made from?
Inactivated bacterial material.
439
What future improvement does the professor hope for in the anthrax vaccine?
One dose or one booster every 10 years.
440
Why is anthrax considered a biological warfare threat?
Its endospores are highly durable and can survive for long periods.
441
Why is the anthrax vaccine not given to the general public?
It requires 6 doses over 18 months.
442
How is the current anthrax vaccine described?
Very mild.
443
Who is the anthrax vaccine usually reserved for?
Frontline workers, soldiers, navy, and people entering danger zones.
444
What is required after the initial anthrax vaccine series?
Yearly booster doses.
445
What future improvement is hoped for with the anthrax vaccine?
One vaccine dose or one booster every 10 years.
446
Is a single-dose anthrax vaccine currently available?
No.
447
What is the current anthrax vaccine made from?
Inactivated bacterial pathogens.
448
Why is the anthrax vaccine considered impractical for the general public?
It requires multiple doses and yearly boosters.
449
Why can anthrax be used as a biological warfare weapon?
Anthrax endospores are highly durable.
450
What makes anthrax theoretically effective for biological warfare?
The enduring nature of its endospores.
451
What organism causes gangrene?
Clostridium perfringens.
452
What two major virulence factors are associated with gangrene?
Endospores and alpha exotoxin.
453
What exotoxin is especially important in gangrene?
Alpha toxin / alpha exotoxin.
454
How does gangrene enter the body?
Through small wounds.
455
Is it difficult for gangrene organisms to enter tissue?
No, entry is very easy.
456
What does gangrene always cause?
Death of tissue.
457
How does gangrene cause tissue death?
It destroys the blood supply to tissue.
458
What destroys the blood supply in gangrene?
Alpha exotoxin.
459
What structures does alpha exotoxin destroy?
Endothelial membranes of blood vessels, red blood cells, and white blood cells.
460
Why does the patient become severely compromised in gangrene?
Blood vessels, RBCs, and WBCs are destroyed.
461
What two enzymes are also produced by gangrene bacteria?
Hyaluronidase and collagenase.
462
What does hyaluronidase contribute to in gangrene?
Blackening of the skin.
463
What does collagenase do in gangrene?
Breaks apart collagen and contributes to necrosis.
464
What fever pattern is seen in gangrene?
Abrupt fever.
465
What happens at the infection site in gangrene?
Abrupt pain develops.
466
What kind of fluid may ooze from gangrene?
Thin bloody fluid, almost like pus mixed with blood.
467
Why does the fluid contain blood?
Blood cells are dying as blood supply is destroyed.
468
What happens to the overlying skin in gangrene?
It blackens due to hyaluronidase
469
Why does the skin blacken in gangrene?
Due to hyaluronidase and tissue death.
470
What happens to the tissue as collagen is broken down?
It becomes necrotic.
471
What causes swelling in gangrene?
Gas accumulation in dead tissue.
472
Which gases commonly accumulate in gangrene tissue?
Hydrogen and carbon dioxide.
473
What smell is associated with gangrene?
Foul, putrid odor.
474
Why is the odor of gangrene so strong?
Gases accumulate in dead tissue.
475
What special sound can gangrene make?
Snap, crackle, pop sound.
476
What does the snap, crackle, pop sound resemble?
Bubble wrap popping.
477
When might a nurse hear the gangrene sound?
While turning the patient, changing the patient, taking blood pressure, or moving them.
478
Why do these sounds occur in gangrene?
Gas bubbles are trapped in the tissue.
479
What is the treatment for gangrene if caught early?
Penicillin.
480
Why is penicillin effective against gangrene?
Clostridium perfringens is gram-positive.
Clostridium perfringens endospores germinate in tissue
481
What may be required if gangrene is not treated early enough?
Amputation.
482
Why may amputation be necessary in gangrene?
To prevent spread to the next region.
483
What are common situations where gangrene can occur?
Wounds, compound fractures, gunshot wounds, old diabetic patients, accidents, injection sites, and ill-performed abortions with unclean utensils.
484
Why are diabetic toes a common example of gangrene?
Poor circulation and infection risk.
485
What happens when Clostridium perfringens endospores germinate in tissue?
Tissue becomes necrotic.
486
How does GI anthrax enter the body?
Through contaminated food products like meat.
487
What type of food can lead to GI anthrax?
Undercooked contaminated food.
488
What GI symptoms can anthrax cause?
Intestinal hemorrhaging, diarrhea, and breakdown of the intestinal epithelial lining.
489
Can GI anthrax be fatal?
Yes.
490
What is the worst form of anthrax?
Pulmonary anthrax.
491
Why is pulmonary anthrax considered the worst form?
It is almost always fatal or can leave the person permanently disabled.
492
What fever pattern is seen in gangrene?
Abrupt fever.
493
What happens in the infected area in gangrene?
Abrupt pain develops.
494
Where can gangrene pain occur?
In the region of infection.
495
What are some common body sites where gangrene may develop?
Injection sites and toes.
496
Why are toes a common site for gangrene?
Especially in diabetic patients.
497
What type of patient is at higher risk for gangrene because they cannot clean an area properly?
Older patients.
498
What causes spotted fever?
Rickettsia rickettsii.
499
Is spotted fever exotoxin-mediated?
No.
500
How is spotted fever spread?
By insects and ticks.
501
What type of rash occurs in spotted fever?
Macular rash.
502
Why can spotted fever be confused with measles?
Both can cause a macular rash.
503
How can you tell spotted fever rash apart from measles rash?
Spotted fever rash occurs on the palms and soles.
504
Should measles rash occur on the palms and soles?
No.
505
What is the specific name of this spotted fever?
Rocky Mountain spotted fever.
506
What serious complication can spotted fever cause?
Heart failure.
507
What type of heart issue may develop with spotted fever?
Heart complications.
508
What organism causes Rocky Mountain spotted fever?
Rickettsia rickettsii.
509
How does a person usually get Rocky Mountain spotted fever?
From an insect or tick bite.
510
What organism is linked to rheumatic fever?
GAS / Streptococcus pyogenes.
511
What are the main symptoms of rheumatic fever?
Fever, arthritis, chest pain, palpitations, and murmur.
512
What part of the heart is especially affected in rheumatic fever?
Heart valves, especially the mitral valve on the left side.
513
What may happen by midlife in severe rheumatic fever?
Valve replacement may be needed.
514
What serious outcomes can rheumatic fever cause?
Heart failure and death.
515
What is the treatment for rheumatic fever if caught early?
Penicillin.
516
Why is anthrax especially dangerous?
It forms endospores and produces 3 powerful exotoxins.
517
What are the 3 exotoxins of anthrax?
Lethal toxin, protective toxin, edema toxin.
518
What does lethal toxin do in anthrax?
Destroys phagocytes and evades them.
519
Why is destroying phagocytes dangerous?
It destroys the body's first line of defense.
520
What does protective toxin do?
Permits entry.
521
What does edema toxin do?
Causes swelling.
522
What is the mortality rate of GI anthrax?
About 50%.
523
How does GI anthrax enter the body?
Through contaminated meat or undercooked food containing endospores.
524
What GI symptoms can anthrax cause?
Diarrhea, hemorrhaging, and breakdown of the intestinal lining.
525
What is the skin lesion seen in skin anthrax called?
Eschar.
526
What is the worst form of anthrax?
Pulmonary anthrax.
527
What is the best antibiotic for anthrax?
Ciprofloxacin.
528
What antibiotic can work if anthrax is caught early?
Penicillin.
529
Who usually gets the anthrax vaccine?
Frontline workers.
530
How many doses are required for the anthrax vaccine?
6 doses over 18 months.
531
What is required after the anthrax vaccine series?
Yearly boosters.
532
What organism causes gangrene?
Clostridium perfringens.
533
What are the major virulence factors in gangrene?
Endospores and alpha exotoxin.
534
How does gangrene enter the body?
Through any small wound.
535
What does gangrene always cause?
Death of tissue.
536
How does alpha exotoxin damage tissue?
Destroys blood supply and damages endothelial membranes of blood vessels.
537
What other enzymes are produced in gangrene?
Hyaluronidase and collagenase.
538
What does hyaluronidase cause in gangrene?
Blackening of the skin.
539
What does collagenase contribute to in gangrene?
Necrosis.
540
What symptoms occur in gangrene?
Abrupt fever, pain, and bloody fluid oozing from the infection site.
541
Why does swelling occur in gangrene?
Due to gas buildup, especially hydrogen and carbon dioxide.
542
What special sound may be heard in gangrene?
Snap, crackle, pop.
543
What disease can spotted fever be mistaken for?
Measles.
544
How can you tell spotted fever apart from measles?
Spotted fever rash occurs on the palms and soles.
545
Does measles rash occur on the palms and soles?
No.
546
herpes virus number four
Epstein-Barr virus (EBV).
547
other names for EBV
Epstein-Barr virus, EB virus, herpes virus number four.
548
Who discovered EBV
Michael Epstein and Yvonne Barr.
549
What family does EBV belong to
Herpes virus family.
550
What neurological disease is EBV implicated in
Multiple Sclerosis.
551
What cancers are associated with EBV
Burkitt's lymphoma and nasopharyngeal cancer.
552
What oral condition is associated with EBV
Oral hairy leukoplakia.
553
What common viral illness is associated with EBV
Infectious mononucleosis.
554
What syndrome is commonly tied to EBV
Chronic fatigue syndrome.
555
What is the underlying common link between EBV diseases
Abnormal B lymphocytes.
556
What happens to B lymphocytes in EBV infection
They become enlarged and proliferate abnormally.
557
Where does EBV become latent
B lymphocytes.
558
Why can EBV keep causing disease over time
It becomes latent and reactivates again and again.
559
What is Burkitt's lymphoma
Fast-growing lymphoma tumor.
560
Where does Burkitt's lymphoma commonly occur
Jaw region.
561
How does EBV contribute to nasopharyngeal cancer
Converts nasopharyngeal cells into cancer cells.
562
In what patients is oral hairy leukoplakia often seen
HIV patients, infection of oral mucosa
563
What does oral hairy leukoplakia look like
Whitish patches on the sides of the tongue.
564
Is oral hairy leukoplakia contagious
Yes.
565
How is infectious mononucleosis spread
By contaminated saliva.
566
How long can EBV be shed in saliva
Up to 18 months.
567
What are the symptoms of infectious mononucleosis
Fever, sore throat with pus, swollen lymph nodes, enlarged spleen, extreme fatigue.
568
What is the rare fatal complication of mononucleosis
Burst spleen.
569
Why does the professor connect EBV to chronic fatigue syndrome
Enlarged lymph nodes and higher EBV titers in blood.
570
What symptoms are linked to chronic fatigue syndrome in EBV
Long-lasting fatigue, muscle soreness, memory loss, swollen lymph nodes.
571
What blood finding supports the EBV-chronic fatigue connection
Higher EBV titers.
572
What does the professor think chronic fatigue syndrome may actually represent in some people
Prior mononucleosis becoming chronic.
573
What nicknames were given to chronic fatigue syndrome in the lecture
Yuppie flu and midlife flu.
574
What symptoms do “yuppie flu” patients often show later in life
Memory loss, severe muscle symptoms, long-term fatigue.
575
What does the professor think links chronic fatigue syndrome and EBV?
Abnormal B lymphocytes and latency in B lymphocytes.
576
Why is chronic fatigue syndrome linked to EBV?
Enlarged lymph nodes and higher EBV titers in the blood.
577
What blood finding is commonly seen in chronic fatigue syndrome linked to EBV?
Higher EBV titers over time.
578
What muscle-related symptom is common in chronic fatigue syndrome?
Debilitating muscle fatigue.
579
What other muscle symptom can occur in chronic fatigue syndrome?
Muscle soreness.
580
What memory-related symptom is associated with chronic fatigue syndrome?
Memory loss.
581
According to the professor, what might chronic fatigue syndrome show on blood work?
Similar blood work to mononucleosis.
582
What does the professor think may have happened in some people with chronic fatigue syndrome?
They had mononucleosis earlier in life and it became chronic.
583
What nicknames are sometimes used for chronic fatigue syndrome?
Yuppie flu and midlife flu.
584
What symptoms may young professionals later develop if they have chronic EBV-related illness?
Memory loss, severe muscle symptoms, and long-term fatigue.
585
What symptoms together may suggest EBV as the cause of chronic fatigue syndrome?
Long-lasting fatigue, swollen lymph nodes, muscle pain, memory loss, and higher EBV titers.
586
Why can EBV continue to cause chronic symptoms over time?
B lymphocytes remain latently infected.
587
How is CMV spread?
Saliva.
588
What blood-related route can spread CMV?
Blood / blood products
Sexual Transmission
Can go through placenta
589
What does CMV stand for?
Cytomegalovirus.
590
What is the official name of CMV in the herpes family?
Human herpes number five.
591
What is the main effect of CMV according to the professor?
The effect is on the blood cells.
592
Where does CMV hide in the body?
In the T cells.
593
What analogy did the professor use to compare EBV and CMV?
EBV in B cells was one thing; CMV in T cells is like a civil war.
594
How did the professor describe CMV in T cells with that analogy?
The commander itself is ill.
595
What does CMV do to T cells?
Makes T cells very large.
596
What word was used to describe the enlargement caused by CMV?
Megalo.
597
What does megalo mean?
Swelling.
598
How large do CMV-infected T cells become?
Two to three times larger than a normal T cell.
599
What is the characteristic appearance of CMV-infected cells on a smear?
Owl’s eye.
600
What did the professor say about recognizing owl’s eye appearance?
You cannot miss it on a smear.
601
How did the professor describe the look of owl’s eye cells?
Looks like eyes gleaming out.
602
What is the mechanism of CMV infection in the cell?
CMV grows in the cell and becomes latent.
603
Where is CMV latency located?
In T cells.
604
What did the professor say about latency in T cells?
Latency in T cells is a mark of herpes viruses.
605
Does CMV recur after latency?
Yes, recurrent / reoccurring.
606
What is the transmission summary for CMV?
Saliva, blood, sexual, placenta.
607
What can happen if CMV goes through the placenta?
Baby gets ill.
608
What severe fetal effect did the professor mention for CMV?
Severe mental retardation.
609
What body system is affected in congenital CMV according to the lecture wording?
Blood cells affected.
610
What important HIV/AIDS connection was emphasized for CMV?
Fully developed AIDS patients often have severe blindness due to CMV retinitis.
611
Is retinitis in an HIV patient caused directly by HIV itself?
No.
612
What actually causes retinitis and blindness in these AIDS patients?
CMV.
613
What type of organism causes malaria?
Protozoan / eukaryotic parasite
It is not caused by a virus or bacteria
614
Is malaria caused by bacteria or viruses?
No.
615
What kind of disease is malaria?
Protozoan disease and cardiovascular disease.
616
What protozoan causes malaria?
Plasmodium.
617
What is the most common species discussed?
Plasmodium vivax.
618
How is malaria spread?
By the Anopheles mosquito.
619
How should Plasmodium vivax be written?
Plasmodium with a capital P, vivax as the species.
620
About how many people worldwide suffer from malaria?
About 300 million
5k deaths
621
Where do about 90% of malaria deaths occur?
Africa or related regions.
622
Why is malaria considered such an important disease?
It causes a major global burden and many deaths.
623
How many hosts does Plasmodium have?
Two.
624
What is the definitive host of malaria?
Mosquito.
625
What happens in the mosquito host?
Sexual reproduction.
626
What forms in the mosquito?
Zygote
Sexual conjugation happens here
627
What is the intermediate host of malaria?
Human.
628
What happens when the mosquito takes a blood meal?
It injects sporozoites into the human.
629
What is the main symptom picture of malaria?
Very high fever with chills, cyclical fever
630
What term did the professor use for cyclical fever in malaria?
Paroxysm of fever
paroxysm = cyclical fever demonstration
631
What happens in the cold phase of malaria?
Shivering and feeling extremely cold.
632
What happens in the hot phase of malaria?
High fever, often 39–40°C.
633
What happens in the wet phase of malaria?
Drenching sweating.
634
What other symptoms can occur early in malaria?
Muscle aches, body aches, headaches, vomiting.
635
Why does vomiting seem unusual in malaria?
Malaria is mainly a cardiovascular disease, but vomiting still occurs.
636
What is the starting infective form injected by the mosquito?
Sporozoites.
Step 1:
mosquito comes for a blood meal
injects sporozoites into blood
637
Where do sporozoites travel first?
Liver.
Step 2:
sporozoites travel through blood to the liver
638
What happens to sporozoites in the liver?
They reproduce asexually.
639
What form is produced in the liver after sporozoites divide?
Merozoites.
divide quickly
no conjugation
form second stage called merozoites
640
How many merozoites can form in the liver?
Several hundred.
641
What happens when liver cells rupture?
Merozoites are released into the blood.
642
Why may the liver enlarge in malaria?
Liver cells rupture and release many merozoites.
643
What other organ enlarges in malaria?
Spleen.
644
Why does the spleen enlarge in malaria?
It tries to make more blood cells.
645
What do merozoites infect after leaving the liver?
Red blood cells.
646
What happens to RBCs in malaria?
They become engorged and rupture.
647
What happens when RBCs are repeatedly destroyed?
Patient becomes anemic.
648
What stage is seen inside RBCs on blood smear?
Ring stage.
649
What happens during the ring stage?
Ring grows, divides, forms more merozoites,bRBCs rupture
more merozoites released
650
What happens after the RBC ruptures?
More merozoites are released.
651
Why can malaria continue for a long time?
Merozoites keep infecting RBCs.
652
At what point can malaria be stopped?
At any point in the cycle.
653
What is the classic treatment for malaria?
Quinine.
654
What antibiotic can be combined with quinine?
Doxycycline.
655
What class of antibiotic is doxycycline?
Tetracycline.
656
Why did the professor not discuss antimalarial drugs in detail?
They have many adverse effects.
657
What happens if malaria is not stopped in the human body?
Merozoites start forming male and female gametes.
658
Can male and female gametes conjugate in the human body?
No.
659
What must happen for gametes to continue the life cycle?
Another mosquito must take a blood meal.
660
What does the mosquito pick up during a blood meal?
Male and female gametocytes.
661
What happens to gametocytes in the mosquito?
They conjugate.
662
What forms after gametocytes conjugate?
Zygote.
663
What does the zygote become in the mosquito?
Sporozoites.
Zygote:
differentiates into sporozoites
ready for next blood meal
cycle continues
664
What are the summary mosquito steps in malaria?
Mosquito ingests gametocytes → sexual reproduction → zygote → sporozoites.
665
What physical prevention method is recommended for malaria?
Bed nets.
666
Why are bed nets useful?
Mosquitoes are night feeders.
667
What prophylactic drug may be taken before travel?
Chloroquine.
668
What is chloroquine?
Semi-synthetic modification of quinine.
669
Does chloroquine require a prescription?
Yes.
670
What important warning did the professor give about quinine?
It has many side effects.
671
What virus is associated with Burkitt’s lymphoma?
Epstein-Barr virus (herpes virus #4).
672
What is Burkitt’s lymphoma?
Fast-growing lymphoma cancer of the jaw region.
673
What other cancer can EBV cause?
Nasopharyngeal carcinoma.
674
How does EBV contribute to nasopharyngeal carcinoma?
It can convert nasopharyngeal cells into cancer cells.
675
What common illness is caused by EBV?
Infectious mononucleosis.
676
What syndrome is often tied to mononucleosis?
Chronic fatigue syndrome.
677
Where does EBV remain latent?
B lymphocytes.
678
Why can EBV keep causing problems over time?
It remains latent and reactivates again and again.
679
How is infectious mononucleosis spread?
By saliva.
680
How long can EBV be spread in saliva?
Up to 18 months.
681
What are the symptoms of infectious mononucleosis?
Fever, sore throat with pus, swollen lymph nodes, enlarged spleen, extreme fatigue.
682
Is mononucleosis usually fatal?
No.
683
What rare complication can make mononucleosis fatal?
Burst spleen.
684
What symptoms are linked to EBV-related chronic fatigue syndrome?
Muscle fatigue, muscle soreness, memory loss.
685
What blood finding may be elevated in chronic fatigue syndrome?
EBV titers.
686
What nickname is sometimes used for chronic fatigue syndrome?
Yuppie flu.
687
What symptoms together suggest chronic EBV infection?
Swollen lymph nodes, memory loss, muscle fatigue, high EBV titers.
688
What does CMV stand for?
Cytomegalovirus.
689
How is CMV transmitted?
Saliva, blood products, sexual transmission.
690
Where does CMV hide in the body?
T cells.
691
What does “megalo” mean in cytomegalovirus?
Swelling.
692
How large do CMV-infected T cells become?
Two to three times larger than normal.
693
What is the classic appearance of CMV-infected cells?
Owl’s eye cells.
694
Does CMV become latent?
Yes.
695
Can CMV recur after latency?
Yes.
696
What eye condition in HIV/AIDS patients is caused by CMV?
Retinitis.
697
What causes retinitis in HIV/AIDS patients?
CMV.
698
Is malaria caused by a virus or bacteria?
No.
699
What causes malaria?
Protozoa.
700
What protozoan commonly causes malaria?
Plasmodium vivax.
701
How is malaria spread?
Mosquitoes.
702
What is the intermediate host in malaria?
Human.
703
What is the definitive host in malaria?
Mosquito.
704
What happens in the mosquito host?
Sexual reproduction and zygote formation.
705
What are the three fever phases of malaria?
Cold phase, hot phase, wet phase.
706
What happens in the cold phase?
Shivering.
707
What happens in the hot phase?
Fever rises to around 39°C.
708
What other symptoms occur in malaria?
Muscle aches, headaches, vomiting.
709
What is the first infective stage injected by the mosquito?
Sporozoites.
710
Where do sporozoites go after entering the blood?
Liver.
711
What happens in the liver during malaria infection?
Asexual reproduction.
712
What are the next forms produced in the liver?
Merozoites.
713
What can happen to the liver in malaria?
Enlargement.
714
What do merozoites infect?
Red blood cells.
715
What blood problem develops in malaria?
Anemia.
716
Why does the spleen enlarge in malaria?
It tries to make more blood cells.
717
What drug is commonly used to treat malaria?
Quinine.
718
What forms are picked up by the mosquito during the blood meal?
Gametocytes.
719
What forms in the mosquito after gametes combine?
Zygote.
Microbiology
flashcards
Decks in class (20)
# Cards
