1
Q
What is meningitis?
A
Inflammation of the three layers covering nerve tissue.
2
Q
What system does meningitis involve?
A
The coverings of the nervous system.
3
Q
What is the critical clinical rule for meningitis management?
A
DO NOT wait for confirmation before treatment.
4
Q
When should treatment for suspected meningitis be started?
A
Start treatment immediately.
5
Q
Why must treatment be started immediately in meningitis?
A
Very short clinical window.
6
Q
What can happen if treatment is delayed in meningitis?
A
It can become fatal quickly.
7
Q
What is the first-line approach in suspected meningitis?
A
Start empiric treatment immediately.
8
Q
What antibiotics are used as the best initial choice for meningitis?
A
3rd generation cephalosporins.
9
Q
Why are 3rd generation cephalosporins used initially for meningitis?
A
Broad coverage.
10
Q
Why else are 3rd generation cephalosporins effective in meningitis?
A
Effective for major organisms.
11
Q
What important property must meningitis antibiotics have?
A
Ability to cross into CSF.
12
Q
Why is crossing into CSF important for meningitis treatment?
A
Because the infection is in the coverings of the nervous system.
13
Q
After starting empiric treatment for meningitis, what procedure should be done?
A
Lumbar puncture (CSF sample).
14
Q
What is collected during a lumbar puncture?
A
CSF sample.
15
Q
What is done with the CSF sample after collection?
A
Culture.
16
Q
What is the purpose of culturing the CSF sample?
A
To identify the organism causing meningitis.
17
Q
What should be done after culture results are available?
A
Adjust antibiotics.
18
Q
What is another diagnostic option mentioned besides culture?
A
Serology testing.
19
Q
What does serology testing use?
A
Known antibodies.
20
Q
What does serology testing help identify?
A
Specific strains (e.g., streptococcus).
21
Q
What age group does Haemophilus influenzae commonly cause meningitis in?
A
Young children (6 months – 4 years).
22
Q
Why is the 6 months – 4 years age group especially vulnerable to Haemophilus influenzae meningitis?
A
Around 6 months maternal antibodies decline and the child’s immune system is still developing.
23
Q
How many strains of Haemophilus influenzae are there?
A
6 types (A–F).
24
Q
Which strain of Haemophilus influenzae causes most meningitis cases?
A
Type B (Hib).
25
Approximately what percentage of cases does Hib cause?
~95% of cases.
26
How is Haemophilus influenzae type B prevented?
Hib vaccine.
27
What does the Hib vaccine specifically target?
Type B.
28
What organism is considered the most dangerous type among the BIG 3 causes of meningitis?
Neisseria meningitidis.
29
What diseases does Neisseria meningitidis cause?
Meningococcal meningitis and meningococcal septicemia.
30
What percentage of people are healthy carriers of Neisseria meningitidis?
~40% of people.
31
Where does Neisseria meningitidis live in carriers?
Nasopharynx.
32
What age group is at high risk for Neisseria meningitidis infection?
Children (especially <5).
33
What lifestyle groups are at higher risk for Neisseria meningitidis?
College students, soldiers, prisoners, anyone in close-contact environments.
34
How is Neisseria meningitidis transmitted?
Saliva contact.
35
What are examples of transmission through saliva contact?
Sharing drinks, chapstick, utensils.
36
How easily does Neisseria meningitidis spread?
Very easy to spread.
37
How do early symptoms of meningococcal infection begin?
Starts like sore throat.
38
Why are early symptoms of meningococcal disease often missed?
Because they resemble a sore throat.
39
What severe symptom follows the early stage?
Severe throbbing headache (migraine level)
40
What happens after the headache stage in meningococcal disease?
It spreads into blood → septicemia.
41
What skin sign appears in severe meningococcal infection?
Petechiae (purplish skin lesions).
42
What type of skin damage can occur?
Hemorrhagic skin damage.
43
What happens to tissue in severe meningococcal infection?
Tissue becomes non-functional.
44
What are possible severe outcomes of meningococcal disease?
Amputation, paralysis, deafness (partial or complete), high fatality risk.
45
What key concept did the professor emphasize about meningococcal disease?
24-hour window disease.
46
What does “24-hour window disease” mean?
Must treat immediately.
47
What strains of Neisseria meningitidis were listed against the vaccine
A, B, C, W-135, Y.
48
What is the most common strain in Edmonton according to the lecture?
C strain.
49
What vaccine is used for the most common strain in Edmonton?
Meningococcal C vaccine.
50
What are the BIG 3 major causes of bacterial meningitis?
Haemophilus influenzae
Neisseria meningitidis
Streptococcus pneumoniae
51
What diseases are caused by Streptococcus pneumoniae?
Meningitis and pneumonia.
52
What percentage of people are carriers of Streptococcus pneumoniae?
~70% of people.
53
What age group of children is at risk for Streptococcus pneumoniae meningitis?
Children (1 month – 4 years).
54
What other population is at high risk for Streptococcus pneumoniae infection?
Elderly.
55
What is the mortality rate in children with Streptococcus pneumoniae meningitis?
~8%.
56
What is the mortality rate in elderly patients with Streptococcus pneumoniae meningitis?
Up to 22%.
57
How can Streptococcus pneumoniae infection be prevented?
Pneumococcal vaccine.
58
What is a key distinguishing structural feature of Streptococcus pneumoniae?
Has a capsule.
59
What does the capsule allow Streptococcus pneumoniae to do?
Helps it attach and invade.
60
What is the first major entry route for Streptococcus pneumoniae to cause meningitis?
From pneumonia (lung infection spreads to brain).
61
What is the second entry route for Streptococcus pneumoniae?
Head/neck injury.
62
Why does head/neck injury increase risk of meningitis?
Opens subarachnoid space.
63
What happens when the subarachnoid space is opened?
Bacteria enters CSF.
64
What is the third entry route for Streptococcus pneumoniae meningitis?
Surgery.
65
What type of infection can occur after head/neck surgery?
Nosocomial infection.
66
What is the fourth entry route for Streptococcus pneumoniae?
Other infections.
67
What examples of other infections can lead to Streptococcus pneumoniae meningitis?
Otitis media (ear infection) and sinusitis.
68
What is the main cause of neonatal meningitis?
E. coli.
69
Why do newborns get E. coli meningitis?
During birth, baby passes through birth canal and is exposed to mother’s E. coli.
70
Do newborns typically get the “big 3” causes of meningitis?
No.
71
What organism should you think of for meningitis in newborns?
E. coli.
72
What organism causes listeriosis?
Listeria monocytogenes.
73
How is listeriosis transmitted?
Food-borne.
74
What examples of foods were mentioned for listeriosis transmission?
Milk, cheese, contaminated food.
75
What unique feature does Listeria monocytogenes have?
Can move cell → cell (phagocyte to phagocyte).
76
What are the high-risk groups for listeriosis?
Pregnant women and immunocompromised patients.
77
What can listeriosis cause in pregnant women?
Miscarriage, stillbirth, very ill newborn.
78
What is the key mechanism that allows Listeria to infect the fetus?
Can cross the placenta → infect fetus.
79
What is the treatment for listeriosis?
Penicillin.
80
What is the alternative treatment for listeriosis, especially in pregnancy?
Erythromycin (safer in pregnancy).
81
What is the most important clinical rule for meningitis treatment?
Treat meningitis immediately, do NOT wait for confirmation.
82
What are the BIG 3 causes of meningitis in children and general population?
Haemophilus influenzae (Hib), Neisseria meningitidis, Streptococcus pneumoniae.
83
What is the most common cause of meningitis in newborns?
E. coli.
84
What organism causes food-borne meningitis?
Listeria monocytogenes.
85
What vaccines should be remembered for meningitis prevention?
Hib (type B), meningococcal (especially C), pneumococcal.
86
What does “Cause (Etiology)” refer to?
What organism causes the disease.
87
What examples were given for causes of meningitis?
Haemophilus influenzae (Hib), Neisseria meningitidis, Streptococcus pneumoniae, E. coli (newborns), Listeria monocytogenes (food-borne).
88
According to the professor, what is always your starting point when answering a meningitis question?
Cause (organism).
89
What does “Pathogenesis” refer to?
How the organism enters the body, spreads, and damages tissues.
90
What examples of pathogenesis were given?
bloodstream → brain (septicemia)
toxins (exotoxins)
capsule → helps attachment (S. pneumoniae)
food → placenta → fetus (Listeria)
91
What does “Symptoms (Clinical Presentation)” refer to?
What the patient looks like.
91
What are the common signs of meningitis?
Stiff neck (Kernig sign), headache (severe), fever, nausea/vomiting, confusion.
92
What unique symptom is associated with Neisseria meningitidis?
Petechiae (purplish rash).
93
What unique feature is associated with Listeria infection?
Pregnancy complications.
94
What is the general rule for meningitis treatment?
Start immediately (don’t wait).
95
What is the first-line treatment for meningitis?
3rd generation cephalosporins.
96
What alternative treatments were mentioned for meningitis?
Penicillin, erythromycin (if allergy/pregnancy).
97
What does “Prevention” refer to in meningitis?
How we stop it.
98
What vaccines were mentioned for meningitis prevention?
Hib vaccine, meningococcal vaccine (C strain), pneumococcal vaccine.
99
What non-vaccine prevention methods were mentioned?
Hygiene, avoid saliva sharing, food safety (Listeria).
100
What special points were mentioned for Neisseria meningitidis?
40% carriers, spreads via saliva, 24-hour disease → EMERGENCY.
101
What special points were mentioned for Haemophilus influenzae?
6 months–4 years, type B = 95%.
102
What special points were mentioned for Streptococcus pneumoniae?
Capsule, multiple entry routes (lungs, surgery, ear).
103
What special point was mentioned for E. coli meningitis?
Newborns only.
104
What special points were mentioned for Listeria monocytogenes?
Food-borne, crosses placenta, dangerous in pregnancy.
105
What are the “5 big agents” of meningitis you must know?
Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae, Listeria monocytogenes, E. coli.
106
What is the key diagnostic test for meningitis?
CSF (cerebrospinal fluid).
107
Why is CSF used for meningitis diagnosis?
It bathes the entire nervous system.
108
Where is CSF collected from?
Lumbar region (lower spine).
109
What is the FIRST step in analyzing CSF?
Gram stain (MOST important).
110
If a question asks “Which meningitis is spread by food?” what is the answer?
Listeria monocytogenes.
111
What must you know about meningitis treatment?
Drug choice and reasoning.
112
Why is chloramphenicol NOT the preferred treatment?
Because of adverse effects.
113
What is the correct first-line treatment for meningitis?
3rd generation cephalosporins.
114
What is a key prevention strategy for meningitis transmission?
Do NOT share items.
115
Why is sharing items a risk factor for meningitis?
Because of saliva transmission.
116
Where do meningitis organisms commonly live in carriers?
Nasopharyngeal region.
117
What key concept explains how meningitis spreads between people?
Healthy carriers spread via saliva.
118
What causes tetanus?
Produces powerful exotoxin.
119
What is the mechanism of tetanus toxin?
Blocks GABA (inhibitory neurotransmitter).
120
What is the result of blocking GABA in tetanus?
No relaxation → continuous contraction.
121
What are early symptoms of tetanus?
Restlessness/grouchiness, drooling, lockjaw, stiff neck.
122
What is the KEY early symptom of tetanus?
Lockjaw.
123
What are later symptoms of tetanus?
Muscle spasms, opisthotonos (severe back arching).
Can cause spinal fracture
124
What is opisthotonos?
Severe back arching.
125
What serious complication can result from severe muscle spasms in tetanus?
Spinal fracture.
126
What does NOT cause death in tetanus?
Fracture.
127
What is the actual cause of death in tetanus?
Respiratory and cardiovascular failure.
128
How is tetanus prevented?
DTaP vaccine.
129
How often is the tetanus booster required?
Every 10 years.
130
What organism causes botulism?
Clostridium botulinum.
131
What type of toxin causes botulism?
Foodborne toxin.
132
What type of foods are commonly associated with botulism?
Low-acid canned foods.
133
What examples of foods were mentioned for botulism risk?
Beans, corn, mushrooms.
134
Which food was specifically noted as safer and why?
Tomatoes (acidic → safer).
135
What toxin types are associated with Clostridium botulinum?
A, B, E, F.
136
Which botulinum toxin type is the most lethal?
Type A
Most lethal = 70% mortality
137
What is the mortality rate for toxin A?
~70%.
138
What is the mortality rate for toxin B and E?
~25%.
139
What neurotransmitter is blocked in botulism?
Acetylcholine (excitatory neurotransmitter).
140
What is the result of blocking acetylcholine?
Flaccid paralysis.
141
How does botulism paralysis compare to tetanus?
Opposite of tetanus.
142
What are early symptoms of botulism?
Dizziness, abdominal cramps, nausea.
143
What GI symptom is seen in infants with botulism?
Constipation (“floppy baby”).
144
What GI symptom is seen in adults with botulism?
Diarrhea.
145
What is a KEY neurological sign of botulism?
Dilated pupils.
146
What visual symptoms occur in botulism?
Blurred/double vision.
147
What happens as botulism progresses?
Paralysis.
148
What causes death in botulism?
Respiratory and cardiac failure.
149
How might contaminated food appear in botulism cases?
Look normal and smell normal.
150
What is the danger despite normal appearance of food?
It contains toxin.
151
What organism causes leprosy?
Mycobacterium leprae.
152
What is a key structural feature of Mycobacterium leprae?
Mycolic acid cell wall.
153
What type of stain is required for Mycobacterium leprae?
Acid-fast stain.
154
How does Mycobacterium leprae grow?
VERY slow growth.
155
What is the incubation period for mild leprosy?
2–5 years.
156
What is the incubation period for severe leprosy?
Up to 9–12 years.
157
How is leprosy transmitted?
Prolonged contact and nasal secretions.
158
Is leprosy highly contagious in healthcare settings?
No.
159
What are the two forms of leprosy?
Tuberculoid (paucibacillary) and lepromatous (multibacillary).
160
Where is tuberculoid leprosy typically limited?
Skin.
161
What lesions are seen in tuberculoid leprosy?
Nodules.
162
What sensory change occurs in tuberculoid leprosy?
Loss of sensation.
163
Can tuberculoid leprosy be treated successfully?
Yes, can recover with treatment.
164
How does lepromatous leprosy progress?
Severe progression with immune failure.
165
What facial feature is seen in lepromatous leprosy?
Lion face appearance.
166
What happens to the nose in lepromatous leprosy?
Nose destruction.
167
What type of tissue damage occurs in lepromatous leprosy?
Necrosis.
168
What happens to fingers and toes in severe lepromatous leprosy?
Become stubs.
169
What is the cause of death in lepromatous leprosy?
Secondary infections (TB).
170
What drugs are used to treat leprosy?
Rifampin, sulfa drugs, clofazimine.
171
How long is treatment for mild leprosy?
6 months.
172
How long is treatment for severe leprosy?
2 years.
173
Is the damage from leprosy reversible?
No, damage is irreversible.
174
What causes polio?
Poliovirus.
175
How is polio transmitted?
Fecal-oral route.
176
What are common sources of polio transmission?
Contaminated food/water.
177
What happens in Stage 1 of polio infection?
Virus infects throat + intestine.
178
What symptoms occur in Stage 1 of polio?
Nausea and sore throat.
179
What happens in Stage 2 of polio infection?
Spreads to blood → viremia.
180
What happens in transient viremia?
Strong immunity, no disease progression.
181
What happens in persistent viremia?
Weak immunity.
182
Where does the virus go in persistent viremia?
Motor neurons.
183
What does poliovirus do to motor neurons?
Causes neuron death = paralysis
184
What is the result of motor neuron damage in polio?
Paralysis.
185
What percentage of polio cases result in paralysis?
<1%.
186
What is polio still called despite low paralysis rates?
Infantile paralysis.
187
What are the two main polio vaccines?
Salk and Sabin (OPV).
188
What type of vaccine is the Salk vaccine?
Killed virus.
189
How is the Salk vaccine administered?
Injection.
190
Does the Salk vaccine require boosters?
Yes.
191
What type of vaccine is the Sabin (OPV) vaccine?
Live attenuated.
192
How is the Sabin vaccine administered?
Oral drops.
193
Does the Sabin vaccine require boosters?
No.
194
What is a rare risk of the Sabin vaccine?
Reversion → disease.
195
What conditions contribute to polio spread?
Poor sanitation, war zones, lack of vaccination.
196
What examples were given of regions affected by polio?
Syria, Afghanistan, Sub-Saharan Africa.
197
What is septicemia?
Pathogen in blood.
198
What term should NOT be used for septicemia?
“Blood poisoning.”
199
What term should be used instead?
Septicemia.
200
What proportion of septicemia cases are hospital-acquired?
1/3 cases.
201
What hospital-related sources can cause septicemia?
Catheters, IV lines, urinary bags.
202
What are early symptoms of septicemia?
Fever + chills, breathing difficulty.
203
What is the KEY sign of septicemia?
Lymphangitis.
204
What is lymphangitis?
Red streaks along limb.
205
Where do the red streaks stop in lymphangitis?
At lymph node.
206
What happens early in septicemia progression related to kidneys?
↓ urine output.
207
What stage follows septicemia?
Sepsis.
208
What stage follows sepsis?
SIRS.
209
What is the final stage of septicemia progression?
Shock.
210
What is puerperal sepsis?
Childbirth infection.
211
What organism causes puerperal sepsis?
Streptococcus pyogenes (GAS).
212
What are symptoms of puerperal sepsis?
Pelvic distension, fever, bloody discharge.
213
What is the treatment for puerperal sepsis?
Penicillin (effective).
214
How quickly do bacterial meningitis symptoms progress?
Very quickly, within 24 hours.
215
What are the initial symptoms of bacterial meningitis?
Fever, headache, stiff neck.
216
Why can stiff neck be difficult to assess in children?
Difficult for kids to express stiff neck.
217
What clinical test can be used to assess meningitis stiffness?
Kernig’s sign.
218
What is Kernig’s sign?
Severe stiffness of hamstrings and inability to straighten the leg.
219
What symptoms follow the initial stage of meningitis?
Nausea and vomiting.
220
What are late-stage symptoms of meningitis?
Convulsions and coma.
221
How does the professor emphasize the progression of meningitis?
Happens very quickly.
222
What procedure is used to diagnose meningitis?
Spinal tap (lumbar puncture).
223
What fluid is collected during a lumbar puncture?
CSF (cerebrospinal fluid).
224
What is the KEY diagnostic test performed on CSF?
Gram stain.
225
What other tests can be done on CSF?
Culture and serology.
226
What age group does Haemophilus influenzae affect?
Children (6 months – 4 years).
227
How many strains of Haemophilus influenzae are there?
6 (A–F).
228
Which strain is most common in meningitis?
Type B.
229
What vaccine prevents Haemophilus influenzae meningitis?
Hib vaccine
targets group B
230
What type of meningitis does Neisseria meningitidis cause?
Meningococcal meningitis.
231
Who are the most vulnerable groups for Neisseria meningitidis?
Children, college students, prisoners, soldiers (close-contact groups).
232
What percentage of people are carriers of Neisseria meningitidis?
40%.
233
Where does Neisseria meningitidis reside in carriers?
Nasopharynx.
234
What are early symptoms of meningococcal disease?
Sore throat.
235
What severe symptom follows early meningococcal infection?
Throbbing headache (migraine-like).
236
What happens when Neisseria meningitidis spreads to blood?
Septicemia.
237
What severe skin sign is associated with meningococcal septicemia?
Petechiae.
238
What are possible severe outcomes of meningococcal infection?
Amputation, paralysis, deafness, possible fatality.
239
What is the key treatment principle for meningococcal meningitis?
Start treatment immediately.
240
What strains of Neisseria meningitidis are listed?
A, B, C, W-135, Y
C is most common
241
Which strain is most common?
C.
242
How can Streptococcus pneumoniae enter to cause meningitis?
Multiple routes.
243
How can pneumonia lead to meningitis?
Lung infection spreads to brain.
244
How can injury lead to Streptococcus pneumoniae meningitis?
Head or neck injury opens subarachnoid space where CSF dwells.
245
What medical procedures can lead to Streptococcus pneumoniae meningitis?
Head and neck surgery.
246
What infections can lead to Streptococcus pneumoniae meningitis?
Otitis media and sinusitis.
247
Who does E. coli meningitis typically affect?
Newborns.
248
How do newborns acquire E. coli meningitis?
Passing through birth canal and exposure to mother’s bacteria.
249
How is Listeria monocytogenes transmitted?
Through food.
250
What disease is caused by Listeria monocytogenes?
Listeriosis.
251
Why is Listeria dangerous in pregnancy?
Very dangerous for fetus.
252
What groups are at high risk for Listeria infection?
Pregnant and immunocompromised patients.
253
What food sources were mentioned for Listeria?
Milk and cheese.
254
What is the key diagnostic test for meningitis?
Gram stain.
255
What is the best initial treatment for meningitis?
Third generation cephalosporins.
256
What key prevention concept should you argue for meningitis?
Do not share items (saliva transmission).
257
Where are meningitis organisms commonly carried?
Nasal (nasopharyngeal) region.
258
How are meningitis organisms commonly spread between people?
Sharing → saliva.
259
What is the key mechanism of tetanus?
Blocks GABA (GABA = relaxation of muscles).
260
What is the result of blocking GABA in tetanus?
Continuous muscle contraction.
261
What are early symptoms of tetanus?
Restlessness, grouchiness, drooling.
262
What is the first key symptom of tetanus?
Lockjaw.
263
What other early symptom occurs with lockjaw?
Stiff neck.
264
What happens later in tetanus progression?
Back spasms.
265
What causes death in tetanus?
Cardiovascular failure.
266
How is tetanus prevented?
DTaP vaccine.
267
How often is the tetanus booster required?
Every 10 years.
268
What is botulism associated with?
Canned food, ultra processed food.
269
What type of foods are safer from botulism?
Acidic foods like tomatoes.
270
How is botulism described in terms of severity?
Lethal food poisoning.
271
What toxin types are associated with botulism?
A, B, E, F.
272
Which botulinum toxin types do NOT affect humans?
C, D, F (affects birds, other animals).
273
Which toxin type is most lethal?
Type A.
274
What are early symptoms of botulism?
Dizziness, abdominal cramps, nausea.
275
What symptom occurs in children with botulism?
Floppy baby syndrome (constipation).
276
What GI symptom occurs in adults with botulism?
Diarrhea.
277
What happens to the pupils in botulism?
Dilated pupils.
278
What visual symptoms occur in botulism?
Double and blurred vision.
279
What is the role of the pupil mentioned in lecture?
Pupil is where light enters.
280
What type of paralysis occurs in botulism?
Flaccid paralysis.
281
What does flaccid paralysis mean?
Muscle tone is lacking.
282
What neurotransmitter is blocked in botulism?
Acetylcholine.
283
What body systems are affected in severe botulism?
Cardiovascular and respiratory systems.
284
What can result from severe botulism (especially toxin A)?
Fatality.
285
What organism causes leprosy?
Mycobacterium leprae.
286
What is unique about the cell wall of Mycobacterium leprae?
Contains mycolic acid.
287
What type of stain is required for leprosy diagnosis?
Acid-fast stain.
288
What is the incubation period for mild leprosy?
2–5 years.
289
What is the incubation period for severe leprosy?
9–12 years.
290
What is a key feature of leprosy incubation?
Longer incubation period.
291
What is the mild form of leprosy called?
Paucibacillary (tuberculoid).
292
What is the incubation range for the paucibacillary form?
2–5 years.
293
Where does the paucibacillary form mainly affect?
Skin.
294
What happens to immunity in the paucibacillary form?
Immunity present (can control infection).
295
How long is treatment for the mild form?
6 months.
296
What is the total treatment duration mentioned?
2 years.
297
What drugs are used for leprosy treatment?
Rifampin, sulfone, clofazimine.
298
What is the severe form of leprosy called?
Multibacillary (lepromatous).
299
What happens to immunity in the multibacillary form?
Immunity failed.
300
What happens to facial features in multibacillary leprosy?
Lion face appearance.
301
What happens to the nose in severe leprosy?
Structure starts to fall apart (eaten away).
302
What type of discharge is associated with severe leprosy?
Nasal exudate.
303
What happens to fingers and toes in advanced leprosy?
Become stubs.
304
What type of tissue damage occurs in severe leprosy?
Necrosis.
305
What is the cause of death in leprosy?
Secondary infections like TB.
306
What causes poliomyelitis (infantile paralysis)?
Virus.
307
What type of transmission does polio use?
Fecal-oral route.
308
What are common sources of polio transmission?
Contaminated food and water.
309
What does ingestion of the virus determine in polio?
Symptoms reflect where infection starts.
310
What are the first symptoms of polio?
Nausea (small intestine) and sore throat.
311
Are early polio symptoms related to the nervous system?
No.
312
Where does the virus go after initial infection?
Lymph nodes, makes it way to blood
313
What happens after the virus reaches lymph nodes?
Makes way to blood → viremia.
314
What is viremia?
Virus present in blood.
315
What happens in transient viremia?
Immunity is strong that there is no symptoms
316
What are the symptoms in transient viremia?
No symptoms.
317
What happens in persistent viremia?
Immunity is not present.
318
What type of individuals are at risk for persistent viremia?
Those not immunized.
319
Where does the virus go in persistent viremia?
Nervous system.
320
What specific neurons does poliovirus target?
Motor neurons.
321
What type of muscles are affected by these neurons?
Skeletal muscles (not ANS).
322
What happens when motor neurons are infected?
Death of motor neurons.
323
What is the result of motor neuron death in polio?
Paralysis.
324
What is another name for poliomyelitis?
Infantile paralysis.
325
What social factors affect polio spread?
War and sanitation (SDOH).
326
What example was given of a country becoming polio-free?
India (Feb 2012).
327
Why is war significant in polio spread?
Disrupts vaccination and sanitation (example: Serbia).
328
What happens in persistent viremia in polio?
Immunity not there, person has never been immunized.
329
Where does the virus go in persistent viremia?
Disease progresses into nervous system, reaches motor neurons
330
What type of neurons are affected in polio?
Motor neurons.
331
What type of muscles do these neurons control?
Skeletal muscles (not ANS).
332
What type of motor neurons are affected?
Motor somatic neurons.
333
What happens when poliovirus reaches motor neurons?
Starts to grow there.
334
What is the result of poliovirus infection of motor neurons?
Death of motor neurons.
335
What is the final outcome of motor neuron death in polio?
Paralysis.
336
What was the first polio vaccine developed?
Jonas Salk vaccine (1954).
337
What type of vaccine is the Salk vaccine?
Inactivated virus.
338
How is the Salk vaccine administered?
Injection.
339
What is the abbreviation for the Salk vaccine?
IPV (Inactivated Polio Vaccine).
340
Does the Salk vaccine require boosters?
Yes, boosters are very important.
341
What was the second polio vaccine developed?
Sabin vaccine (1963).
342
What type of vaccine is the Sabin vaccine?
Live attenuated (weakened virus).
343
How is the Sabin vaccine administered?
Orally (drops in child’s mouth).
344
What is the abbreviation for the Sabin vaccine?
OPV (Oral Polio Vaccine).
345
Does the Sabin vaccine require boosters?
No.
346
What is a key advantage of the Sabin vaccine?
No injections, very easy.
347
What is a rare risk associated with the Sabin vaccine?
Reversion → disease (1 in 750,000).
Microbiology
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