Final Flashcards

1
Q

Since 60% of pneumonia is caused by S. pnuemoniae, what are the other bacteria that cause it?

A

Chlamydophila (Chlamydia) pneumoniae Mycoplasma pneumoniae Haemophilus influenzae Pneumocystis carinii

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2
Q

What are some symptoms of pneumonia and whats its incubation period?

A

abrupt onset fever, chills chest pain difficulty in breathing productive cough rust coloured sputum incubation: 1 - 3 days

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3
Q

How do you treat pneumonia?

A

penicillin G erythromycin (azithromycin, clarithromycin) ceftriaxone vancomycin (usually only for HAP)

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4
Q

What happens during stage 1 of pneumonia?

A

bacteria stimulate flow of fluid into alveoli fluid promotes growth of the bacteria fluid allows spread of bacteria to other alveoli and lobes loss of air exchange capacity due to fluid

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5
Q

What happens during stage 2 and 3 of pneumonia?

A

second stage (early consolidation) infiltration of the alveoli by neutrophils and red blood cells phagocytosis of bacteria the point where infection brought under control third stage (late consolidation) alveoli are packed full of neutrophils with ingested bacteria clearance of bacteria from the lungs occurs “hepatization” of lungs, alveoli look like hepatocytes

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6
Q

Describe stage 4 and what is special about pneumonia?

A

neutrophils leave macrophage clean up debris Pneumonia lack of permanent damage very little fibrous scar tissue

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7
Q

What bacteria causes epiglotittis?

A

epiglottitis is nearly always caused by H. influenzae B

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8
Q

Give me some characteristics for Mycoplasma pneumoniae?

A

the mycoplasma are the smallest free-living bacteria they do not produce peptidoglycan not sensitive to b-lactams and vancomycin membranes contain sterols can take up to 3 weeks to grow colonies

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9
Q

What must the mdeia contain in order to grow M. pnuemoniae?

A

isolation media contain peptone enriched with yeast extract and serum to provide cholesterol also b-lactam antibiotics to suppress other bacterial contaminants methylene blue can be added to suppress all other Mycoplasma species and/or glucose as M. pneumoniae is the only species which ferments glucose to acid

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10
Q

Give me some characteristics of Klebsiella pnuemoniae.

A

Gram-negative bacillus, lactose positive with gas production MR-VP (- +) Indole negative, citrate positive (E. coli is MR-VP + - and indole +, citrate -)

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11
Q

What are some characteristics of the Influenza virus?

A

member of the Orthomyxoviridae a single-stranded, negative sense RNA virus with a segmented genome enveloped virus (host cell membrane) the surface of the virus is covered with spikes called peplomers there are two types of spikes, one is the hemagglutinin and the other is the neuraminidase

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12
Q

In the influenza virus, how many genomes are produced and what are the proteins produced as a result?

A

8 RNA segments each codes for one or more proteins, 10 in total HA – hemagglutinin and NA – neuraminidase Matrix protein-1, M-2 Nucleoprotein Polymerase B1, B2 and A Non-structural-1 and NS-2

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13
Q

How does the influenza virus escape the host cell?

A

HA binds the virus to its receptor sialic acid tipped galactose carbohydrates NA cleaves sialic acid from the end of the receptor to allow the newly formed virus to escape

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14
Q

Where are the matrix proteins found in the influenza virus and which is the most important?

A

M1 coats the inside of the envelope M1 is the most important protein for the structure, assembly and budding of the virus M2 is found in small amounts in the envelope

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15
Q

What are the symptoms of influenza virus and how is it transmitted?

A

fever/chills headache, muscle aches and pains malaise cough lasting 3 - 7 days Through water droplets spread by coughing and sneezing

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16
Q

How does the influenza virus enter the cell?

A

the influenza hemagglutinin binds to sialic acid containing glycolipid/glycoprotein receptor on epithelial cells viral particles are taken up by receptor-mediated endocytosis and fuse with a lysosome the drop in pH in the virus containing endosome causes a conformational change in hemagglutinin. Part of the hemagglutinin is now exposed and can mediate fusion between the viral envelope and the endosome membrane nucleocapsids are then liberated into cytoplasm and move to the nucleus

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17
Q

How does the Influenza virus replicate in the host cell?

A

viral RNA is replicated in cell nucleus using viral encoded RNA-dependent RNA polymerase 10 transcripts produced (+ sense mRNA) viral mRNAs “steal” the 5’ cap and 3’ polyA tail from preformed cellular mRNAs viral proteins are synthesised nuclear replication of the original 8 (-) strand RNAs

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18
Q

What is the causative agent of Typhoid?

A

Salmonella Typhi (

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19
Q

The fatality rate of Typhoid is ____

A

10%

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20
Q

How is Typhoid spread?

A

Usually food or water borne, but mostly food borne in developed countries

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21
Q

What organisms cause symptoms extremely similar to Typhoid?

A

Salmonella Paratyphi A, B, C and S. Typhimurium

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22
Q

S. Typhi and S. Typhimurium share ___% of their genes. How do they differ? Why is this relationship interesting?

A

89%. S. Typhi affects only humans whereas S. Typhimurium affects lots of mammals and even reptiles. S. Typhi evolved relatively recently and has a large amount of genes that are “turned off”, probably resulting in the limited host range.

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23
Q

What is it called when one of two closely related organisms has genes that are inactive, causing the differences between the two

A

Reductive evolution

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24
Q

What countries are hot spots for Typhoid?

A

South east asia is main hotspot, then rest of Asia, Africa,and South America

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25
Q

What was the most important health advancement affecting Typhoid rates in North America? What were typhoid rates like before this?

A

Water treatment. introduction of filtration and chlorination reduced mortality by 50%, and infant mortality by 75%. Typhoid death rates in 1900-1920 varied from 20 - 100 per 100 000 per year. After treatment it fell to 2 per 100 000 per year.

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26
Q

Who gave us the idea of an asymptomatic carrier?

A

TYPHOID MARY!!! she worked in a restaurant and had some mad dank typhoid, which was aymptomatic but she was shedding cells like nobody’s business. Then she was basically locked up forever

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27
Q

Describe the advent of Typhoid in Winnipeg

A

Winnipeg was at one point named the Typhoid capital. The lack of sewers and the fact that drinking water was drawn straight from rivers or wells led quickly to the spread of Typhoid (duh, there are two rivers in the middle of the city and everyone is dumping their shit in them). So in the 1880s the city made all new properties use the new sewer system, but they didn’t force old properties to change, which was dumb. Then they started drinking more from wells (which are partially filtered, since aquifers are usually under sand). FINALLY, in 1904 sewer connections were made mandatory. They city made most outhouses illegal. Typhoid rates finally decreased

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28
Q

Describe the symptoms of typhoid fever

A

Fevers spike quickly reaching 40degrees over 2-3 days. Headaches, pain, lethargy, anorexia, abdominal pain and constipation are common. In the 2nd week as fever dies down a bit the bloody diarrhea appears. Can develop rosy spots on chest and abdomen.

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29
Q

What is the most common cause of death with Typhoid?

A

Perforated intestine or intestinal hemorrhaging

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30
Q

How is typhoid treated?

A

Used to be treated with toxic Chloramphenicol. Then we moved to ampicillin and contrimoxazole, which S. Typhi quickly became resistant to. Now we use a 3rd gen cephalosporin or a fluoroquinolone. If the strain is resistant to many antibiotic we use azithromycin

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31
Q

What types of typhoid vaccines exist?

A

An oral attenuated vaccine and a Vi (capsule) antigen vaccine

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32
Q

How is Typhoid diagnosed

A

Blood cultures, sometimes stool (can also look for neutrophils in stool) or rose spot culture, bone marrow culture (best and most inconvenient diagnostic tool). Cultures plated on a selective medium like Salmonella-Shigella

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33
Q

How does one determine if a bacterial species is in fact S. Typhi in a clinical lab setting?

A

Slide agglutination with anti-O antiserum.

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34
Q

S. Typhi and S. Typhimurium share ___% of their genes. How do they differ? Why is this relationship interesting?

A

89%. S. Typhi affects only humans whereas S. Typhimurium affects lots of mammals and even reptiles. S. Typhi evolved relatively recently and has a large amount of genes that are “turned off”, probably resulting in the limited host range. S. Typhimurium infections can also be killed by macrophage.

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35
Q

How does one determine if a bacterial species is in fact S. Typhi in a clinical lab setting?

A

Slide agglutination with anti-O antiserum.

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36
Q

How to the bacteria causing Typhoid infect you

A

Pass through intestinal epithelium through a process called “ruffling”, convincing microvilli to phagocytize themselves, forming a small vacuole around the bacterium. Can also enter by breaking the junctions of the columnar cells. Some escape into blood stream, other organs such as the liver. The bacteria live inside of macrophage, replicating until they burst forth and cause secondary bacteremia. The bacteria then REINFECT the intestine, necrotizing tissue and causing bloody diarrhea.

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37
Q

What other organs to S. Typhi bacteria like to infect

A

Gallbladder - Causes leakage of more bacteria into intestines

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38
Q

What can happen when the Gallbladder is infected during Typhoid?

A

Can become permanent. The person may be a permanent shedder and carrier of S. Typhi. Like Typhoid Mary

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39
Q

What other organs to S. Typhi bacteria like to infect

A

Gallbladder - Causes leakage of more bacteria into intestines Liver

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40
Q

How is Salmonella taxonomized? IT MAKES NO SENSE

A

Basically there are several (well, technically >2400) serovars, but there are 7 GENETIC variants (I, II, IIIa, IIIb, IV, V, VI). There are only two species but Salmonella enterica is divided into those 7 “subspecies”. The serovars are determined based on antigens (somatic, flagella, capsular). These help us identify paratyphi, typhimurium and typhi).

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41
Q

Which of the lymphocytes produce antibodies and which produce cytokines?

A

B = antibodies T = Cytokines

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42
Q

Since both B and T cells produce memory cells, what is the resulting lifespan?

A

20 years

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43
Q

How do antibodies affect bacteria?

A

They specifically and non-covalently bind to antigens. This binding prevent attachment of the pathogens, neutralizes toxins, opsonization, and serves as a signal to the immune system.

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44
Q

What is the typical structure of an antibody?

A

4 individual polypeptide cells 2 long or heavy 2 short or light

45
Q

Give me some facts about antibodies binding to antigens. Like about the bonding itself.

A

1 Ab = 2 Ag both of the binding sites are identical to each other They are composed of both light and heavy chains and even though the actual antibody molecule is the same, the binding site differs between antibodies.

46
Q

How many types of heavy chains are there?

A

5 alpha IgA delta IgD epsilon IgE gamma IgG mu IgM

47
Q

Which of the antibodies is produced during the initial (1o) response?

A

IgM IgG also appears but it isn’t major

48
Q

Which of the antibodies is produced during the initial (1o) response?

A

IgM IgG also appears but it isn’t major

49
Q

Which of the antibodies is found in the mucosal surfaces and in titty juice (ie breast milk)?

A

IgA

50
Q

What is the structure of IgG?

A

a monomer of 2 light and 2 heavy g chains

51
Q

What is the monomer form and serum form of IgM?

A

M: 2 light, 2 heavy S: Pentamer, 10 light, 10 heavy and 1 joining polypeptide

52
Q

Which of the antibodies is very efficient at agglutination reactions?

A

IgM It can bind 10 small antigens but usually only 5 because of steric interference

53
Q

Which of the 5 antibodies only appears only slightly in serums, like its really only a minor?

A

IgE and IgD

54
Q

What do T cell receptors respond to? (TCR = T cell receptor)

A

They respond to protein antigens

55
Q

Which of the MHC-restricted T cells recognize intracellular and extracellular proteins?

A

CD4+ class II MHC-restricted T cells (or THs) = extracellular proteins “ “ class I “ “ = intracellular proteins

56
Q

Which of the MHC-restricted T cells recognize intracellular and extracellular proteins?

A

CD4+ class II MHC-restricted T cells (or THs) = extracellular proteins “ “ class I “ “ = intracellular proteins

57
Q

What are cytokines responsible for and describe in vague general terms to their concentration in the body?

A

They are polypeptide signaling molecules that regulate immune reactions and inflammation active in low concentrations

58
Q

What does TNF stand for and give me some facts about it (like what it does and shit)?

A

Tumour Necrosis Factor Recruit and activate monocytes and neutrophils. Causes vascular endothelial cells to secrete chemokines which recruit said monocytes etc. Activates antibacterial properties of monocytes and neutrophils If the levels of TNF get to high, you experience a fatal fall of blood glucose and get fucked up the ass by the grim reaper (ie death).

59
Q

What are interleukins and what are the most common ones (or most important)?

A

subclass of cytokines IL 12: causes NK and T cells to produce IFN-g which actiavtes macrophage IL-10: inhibits macrophage function by downregulating IL-12 into IFN-g

60
Q

How many parts can we divide the immune system into?

A

2 innate and adaptive

61
Q

Why is the innate immune system our first line of defense?

A

It’s immediate and permanent. Doesn’t change over time and only recognizes classes of molecules not found in the human boy.

62
Q

Why is the adaptive immune system so cool?

A

It has specificity (it’ll attack different forms of the same molecule) It has memory meaning it won’t forget it knowd the difference between us and them and it’ll go back to resting state once the threat has bee cleared

63
Q

How specific is the specificity in the adaptive immune system?

A

It can figure out one amino acid substitution in a protein

64
Q

If a virus manages to get past the epidermal layer of the skin, what is it hit by?

A

SALT Skin associated lymphoidal tissue.

65
Q

If it makes it past the SALT layer, what is the next obstacle for the bacteria?

A

MALT or Mucosal associated lymphoid tissue

66
Q

Why is the innate system so effective?

A

Because of it’s complement system. If one protein is cleaved then another step of the sequence is started. No matter which route it takes, the result is always the same.

67
Q

What are some of the functions of the complement system?

A

Antimicrobial Opsonization Chemotaxis Agglutination Neutralizes toxins

68
Q

What is inflammation called and what actually happens to cause the swelling and redness?

A

anything its affecting-itis Fluid from the blood leaves capillaries and enters tissue. Blood follows bringing neutrophils and leukocytes.

69
Q

What are some effects of long term swelling?

A

scar tissue fibrosis

70
Q

What are leukocytes?

A

“White blood cells”

71
Q

What are the 3 types of Granulocytes?

A

Neutrophils basophils eosiniphils

72
Q

What are some characteristics for neutrophils?

A

multilobed, irregular short lived move to tissue when cued by chemicals

73
Q

What do neutrophils contain how do they fuck up bacteria?

A

lytic enzymes, lysozyme, defensins generate reactive oxygen and nitrogen intracellularly

74
Q

If neutrophils are phagocytic, what are basophils and eosinophils?

A

Baso: release histamine and other effector compounds Eosino: Defense against protozoa

75
Q

Macrophages are pretty cool with some pretty cool names; what is the reasoning for these names and in order for them to reach their maximum killing potential, what must happen.

A

They are named depending on where they are located and will thus have different names They must be activated

76
Q

What is Holloway’s favorite cell and what are they the first line of defense against?

A

Natural Killer Cells Viruses

77
Q

How do NK cells attack viruses?

A

They kill virally infected cells by releasing a granzyme that force the cell to undergo apoptosis. They also activate macrophage

78
Q

What is the definition of epidemiology?

A

the science that studies the occurrence and reasons for health and disease in popilation

79
Q

What are the different levels of epidemiology?

A

In order of severity: sporadic endemic outbreak epidemic pandemic

80
Q

What is an infectious disease? A communicable disease? A dead-end host?

A
  1. a disease caused by bacterium, fungi, protozoan, or living creature 2. person-to person 3. Cannot be spread
81
Q

What is the difference between sign and symptom?

A

sign: What you can observe symptom: what they complain about

82
Q

What is herd immunity and why is it so effective?

A

When a susceptible person does not become sick even though the bacteria is in the population. >80% are not affected by it. Small probability of the person catching it

83
Q

How can you determine if the bacteria is actually causing the infection?

A

Koch’s postulates

84
Q

What is the difference between source and reservoir in regards to bacterial infection?

A

source: immediate object or organism from which the pathogen is passed reservoir: the natural environmental location of the pathogen

85
Q

What are the major routes of transmission?

A

Airborne Contact Vehicle Vector-borne

86
Q

What is vector-borne transmission?

A

From animal to person

87
Q

What is the name of the bacteria that causes cholera?

A

Vibrio cholerae

88
Q

What are the geographical reservoirs for Cholera?

A

Bengal basin ganges-brahmaputra delta

89
Q

What seemed to stop the first pandemic of cholera?

A

the extreme cold winter of 1823/24

90
Q

Which of the cholera pandemics affected Canada?

A

The 3rd and 4th No others because of strict quarantine

91
Q

What did John Snow discover about cholera? In this regard he actually knew something ba dum tsss

A

He believed that cholera was being spread by a waterborne pathogen because of the irregularly high amount of cholera victims near a certain water pump. He convinced the municipality to do it and low and behold, the endemic stopped

92
Q

Give me some characterisitics for vibrio cholerae.

A

G - motile, comma shaped oxidase + glucose fermenter require or grow better in 1% NaCl

93
Q

Up until the 6th pandemic of cholera, there was only 1 type of it (O1) but during the 7th pandemic, a second one emerged. Whats the name of the second strain and where is it from?

A

O1 El Tor El Tor but isolates have been found in Sulawesi, Indonesia

94
Q

What antigen components comprise the Inaba serotype of O1 Cholera? Ogawa?

A

A and C components A and B with a little bit of B

95
Q

How many V. cholerae cells are needed to infect a healthy fasting person? A fasting person taking sodium bicarbonate?

A

1011 cells 106 cells

96
Q

Which blood type is most likely to give you worse cholera symptoms?

A

Type O

97
Q

What is the pathogenesis of V. cholera?

A

Ingestine where it colonizes the large intestine but remains in lumen (not invasive) Produces cholera toxin (CT). The body responds by pumping in water. Symptoms show 24-72 hours after infection

98
Q

Why do you kick the shit bucket because of cholera? Get it…like kick the bucket but with poop…because of the constant need to poop…so I’ll just go drink bleach.

A

You die of dehydration because their is not enough water in your body. You show symptoms of dehydration at 5% water loss

99
Q

In order for the bacteria to inhabit the large intestine, what must they first produce?

A

Pili which they do They produce Toxin co-regulated pilus

100
Q

About ____% of preschool children are carriers of S. pneumoniae

A

40%

101
Q

What is V. cholerae associated with?

A

Phytoplakton and marine invertabrates

102
Q

If I were to take my cotton shirt and fold in about 7 times and filter cholera laced water with it, would it be safe to drink?

A

Yes, hypothetically You haven’t filter the bacteria as the bacteria is so small it can move through the cross-sections of thread. It’s safe to drink because you filtered the organisms that allow the bacteria to grow outside of your body.

103
Q

In this crazy world, could lake Winnipeg harbor V.cholerae?

A

Possibly. The lakes temperature would need to increase, the surface height would need to rise and the amount of algal blooms would need to increase.

104
Q

If the amount of algal blooms increase in a lake, why would a increase in cholera be possible?

A

Basically, algal blooms lead to an increase in the population of copepods which harbour V. cholerae.

105
Q

Say people don’t drink from a lake but from the clean river, are they safe from Cholera? What about if a monsoon hits?

A

Hypothetically yes. Probably not as the mixing would have driven some the cholera laden copepodes into the river exposing people to them.

106
Q

Describe the shit caused by cholera?

A

rice water stool

107
Q

How do you treat a cholera infection?

A

Intravenous electrolyte solution oral rehydration therapy with glucose-balanced salts solution homemade sugar-salt water solution

108
Q

How do you treat a cholera infection?

A

Intravenous electrolyte solution oral rehydration therapy with glucose-balanced salts solution homemade sugar-salt water solution

109
Q

What type of bacterial toxin is the Cholera Toxin?

A

AB5 A is the toxin B is the receptor 5 is the amount of copies of a protein that can bind to a receptor