Final Extra Details Flashcards
(164 cards)
1
Q
What does “pneumonia” mean?
A
Lungs have fluid in them.
2
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.
A lot of gram negs can case it. Actually basically any bacteria can.
3
Q
What is the case fatality rate of pneumonia with antibiotics?
A
5-10%
4
Q
About ___% of preschool age children carry S. pneumo
A
40%
5
Q
What area of the body does S. pneumo usually colonize?
A
nasopharynx, may be displaced and move lower over time
6
Q
In what situations is S. pneumo more virulent
A
if you have asthma, smoke, or have another bacterial infection
7
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
8
Q
How do you treat pneumonia?
A
penicillin G erythromycin (azithromycin, clarithromycin) ceftriaxone vancomycin (usually only for HAP)
9
Q
Until recently ____ was the drug of choice for pneumonia (usually S. pneumo caused). What do we use now and why?
A
Penicillin G. Now there is widespread resistance, so we use clarithromycin
10
Q
What happens during stage 1 of pneumonia?
A
bacteria stimulate flow of fluid into alveoli fluid promotes growth of the bacteria fluid spills into other alveoli and allows spread of bacteria to other alveoli and lobes loss of air exchange capacity due to fluid
11
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
12
Q
Describe stage 4 of pneumonia and what is special about pneumonia?
A
neutrophils leave macrophage clean up debris Pneumonia lack of permanent damage very little fibrous scar tissue
13
Q
What are some potential complications associated with pneumonia infection?
A
Bacteria enter bloodstream - septicaemia. heart valve inection, meningitis, trouble breathing
14
Q
What bacteria (other than S. pneumo and TB) cause most upper RT infections?
A
H. influenzae, M. pneumoniae, K. pneumoniae, N. meningitidis
15
Q
What bacteria causes epiglotittis?
A
epiglottitis is nearly always caused by H. influenzae B
16
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
17
Q
How are M. pneumoniae specimens collected?
A
Biphasic medim - which is an agarslant covered in broth. When broth becomes turbid from growth it is plated on a solid medium
18
Q
What must the media 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
19
Q
What are “transport media”?
A
USed when a doctor takes a sample from a patient and needs to transfer it to a lab (usually just a tbe with a small amount of agar and a cotton swab)
20
Q
Describe the symptoms and incubation period of a M. pneumoniae infection. How does this differ from S. pneumoniae?
A
Mild-asymptomatic with 2-3 weeks incubation. Fever, sore throt, headache, non-productive cough.
S. pneumo has much more severe symptoms and a shorter incubation period (rapid onset)
21
Q
How does one treat M. pneumoniae?
A
Tetracyclie/macrolides since B-lactams don’t work
22
Q
Give me some characteristics of Klebsiella pnuemoniae. APPARENTLY I WROTE THAT THIS IS FOR SURE ON THE EXAM
A
Gram-negative bacillus, lactose positive with gas production MR-VP (- +) Indole negative, citrate positive (E. coli is MR-VP + - and indole +, citrate -)
23
Q
The symptoms of K. pneumoniae are often described as “distinctive”, explain them. What is the primary difference in symptoms between this and S. pneumo?
A
Thick, bright red sputum, chest pain, rapid breathing, cavities and abscesses in lungs, necrotization of tisse.
Primary difference is S. pneumo has frothy pink sputum
24
Q
Haemophilus influenzae infections are most common in ____
A
BABIES
25
The ___ serotype is the most virlent form of H. influenzae. How do we deal with this? What are the consequences?
B serotype. We made a vaccine, but now a bunch of new strains are popping up
26
Describe H. influenzae
Small gram neg bacillus, found naturally in the human oro/nasopharynx. 6 serotypes exist
27
What are some characteristics of the Influenza virus?
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
28
The spikes found on the influenza virus are called \_\_\_\_\_. What are their names?
Peplomers. Hemagglutinin and neuraminidase
29
What does it mean if a virus is "negative sense"?
NEgative stranded nucleic acid. Mst be converted to positive before replication can occur
30
In the influenza virus, how many genomes are produced and what are the proteins produced as a result?
8 RNA segments coding for 10 total proteins
HA – hemagglutinin and NA – neuraminidase
Matrix protein-1, M-2
Nucleoprotein
Polymerase B1, B2 and A
Non-structural-1 and NS-2
31
Most anti-influenza drugs target which protein?
M2
32
How does the influenza virus escape the host cell?
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
33
Where are the matrix proteins found in the influenza virus and which is the most important?
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
34
Briefly describe the purpose of Influenza virus nucleoprotein, Polymerase, and NS1 and NS2
Nucleoprotein - Associates with RNA segments
Poylmerase B1, B2, A - Transcribe/replicate viral genome.
NS1/NS2 - Regulate replication
35
What are the symptoms of influenza virus and how is it transmitted?
fever/chills headache, muscle aches and pains malaise cough lasting 3 - 7 days Through water droplets spread by coughing and sneezing
36
How does the influenza virus enter the cell?
The influenza hemagglutinin binds to sialic acid containing receptor on epithelial cells.
Viral particles are taken up by receptor-mediated endocytosis and fuse with a lysosome. the drop in pH of the endosome causes a change in hemagglutinin.
Part of the hemagglutinin is now exposed and fusion of lysosome membrane and virus membrane occurs, allowing virus to escape into cytoplasm
37
How does the Influenza virus replicate in the host cell?
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
38
The natural host for Influenza A is \_\_\_\_
wild birds
39
There are ____ different combinations of Hemagglutinin and Neuraminidase
82
40
How many types of influenza H and N are found in humans? List them
3 HA types (H1, H2, H3), 2 NA types (N1 and N2)
41
\_\_\_\_\_\_\_ flu and _____ flu had the same HA and NA proteins
Spanish flu and swine flu
42
How do recombinants with different HA and NA form?
When two flu viruses affect the same cell, the genome segments could mix into the new virus.
43
New recombinant flu viruses tend to cause \_\_\_\_\_
pandemics!
44
How does the yearly influenza virus usually spread? (geographically speaking)
Starts in rural china, spreads to south east asia, australia, then to us by winter
45
How areinfluenza strains identified?
TYPE/ HOST SPECIES/ GEOGRAPHIC SITE OF ISOLATION / NUMBER / YEAR
46
How is the influenza vaccine made?
Injected into chicken eggs to replicate, separated from eggs and purified. The purified HA and NA proteins are used to make the vaccine.
47
What is the causative agent of Typhoid?
Salmonella Typhi (
48
The fatality rate of Typhoid is \_\_\_\_
10%
49
How is Typhoid spread?
Usually food or water borne, but mostly food borne in developed countries
50
What organisms cause symptoms extremely similar to Typhoid?
Salmonella Paratyphi A, B, C and S. Typhimurium
51
S. Typhi and S. Typhimurium share \_\_\_% of their genes. How do they differ? Why is this relationship interesting?
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.
52
What is it called when one of two closely related organisms has genes that are inactive, causing the differences between the two
Reductive evolution
53
What countries are hot spots for Typhoid?
South east asia is main hotspot, then rest of Asia, Africa,and South America
54
What was the most important health advancement affecting Typhoid rates in North America? What were typhoid rates like before this?
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.
55
Who gave us the idea of an asymptomatic carrier?
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
56
Describe the advent of Typhoid in Winnipeg
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
57
Describe the symptoms of typhoid fever
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.
58
What is the most common cause of death with Typhoid?
Perforated intestine or intestinal hemorrhaging
59
How is typhoid treated?
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
60
What types of typhoid vaccines exist?
An oral attenuated vaccine and a Vi (capsule) antigen vaccine
61
How is Typhoid diagnosed
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
62
How does one determine if a bacterial species is in fact S. Typhi in a clinical lab setting?
Slide agglutination with anti-O antiserum.
63
How to the bacteria causing Typhoid infect you
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.
64
What other organs to S. Typhi bacteria like to infect
Gallbladder - Causes leakage of more bacteria into intestines
65
What can happen when the Gallbladder is infected during Typhoid?
Can become permanent. The person may be a permanent shedder and carrier of S. Typhi. Like Typhoid Mary
66
What other organs to S. Typhi bacteria like to infect
Gallbladder - Causes leakage of more bacteria into intestines Liver
67
How is Salmonella taxonomized? IT MAKES NO SENSE
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).
68
Distinguish between innate and adaptive immunity
Innate - first line of defense. IT is a permanent part of your body, does not change with repeated exposure to a pathogen, recognizes classes of pathogenic molecules
Adaptive immunity - can recognize different forms fo the same molecule. Has memory, will respond to second exposure with increased activity, can differentiate between self and non self, resting state when not responding to a pathogen
69
How specific is the specificity in the adaptive immune system?
It can figure out one amino acid substitution in a protein
70
If a virus manages to get past the epidermal layer of the skin, what is it hit by?
SALT: Skin associated lymphoidal tissue.
71
If a virus/bacteria makes it past the SALT layer, what is the next obstacle for the bacteria?
MALT or Mucosal associated lymphoid tissue. It traps microorganisms and removes them
72
Why are mucous membranes a major route of entry for pathogens?
BEcause mucousal epithelium often passes viruses and bacteria through it :(
73
What are antimicrobial peptides? Describe the 3 families we have!!!
They are short peptides that protect usss
Defensins - Membrane-actvie and bactericidal, stimulate immune system changes.
Cathelicidins - Secreted as a precursor protein before it is cleaved for use. Is antimicrobial, can neutralize lipopolysaccharides
Histatins - large peptides, repeating amino acids. Antimicrobial and found in saliva
74
What is the purpose of the immune "Complement system"
"tags" bacteria so macrophage can detect them - can also be directly bactericidal
75
Why is the complement system so effective?
Involves a sequence of protealysis. If one protein is cleaved then it activates another step of the sequence. No matter which route it takes, the result is always the same.
76
Describe some of the ways complement can be activated
Classic pathway - involving antibodies
Lectin pathway - lectin binds to carbohydrates such as bacterial capsule
Alternative pathway
77
What are some of the functions of the complement system? Describe each
Antimicrobial - "Membrane attack complex" punches holes in bacterial membranes.
Opsonization - Stimulates phagocytosis by allowing macrophage to bind to bacteria. Can also activate the processes WITHIN macrophage that kill bacteria
Chemotaxis - Attracts neutrophils
Agglutination - Viruses themselves are too small for macrophage to phagocytose, so antibodies canbind viruses to each other until they clump up
Neutralizes toxins - yeah
78
Early in an infection the liver produces proteins known as _____ that function similarly to complement
"acute-phase proteins"
79
What is inflammation called and what actually happens to cause the swelling and redness?
"Anything its affecting"-itis.
Fluid from the blood leaves capillaries (become more permeable) and enters tissue. Blood follows bringing neutrophils and leukocytes.
80
What is a common term for chronic inflammation
Arthritis
81
What are some effects of long term swelling?
Scar tissue formation,
fibrosis
82
What are leukocytes?
"White blood cells", responsible for immune functions - types variable dependent on infection
83
What are the 3 types of Granulocytes? Howdoes one distinguish between them in a lab setting? Do they function differently?
Neutrophils -don't stain with super acidic or basic stains
basophils - stain with basic stain
eosinophils - stain with eosin
Basophils and eosinophils are part of the immune response to multicellular parasites such as tapeworms
84
What are some characteristics for neutrophils? How do they kill bacteria?
multilobed, irregular nuleus.
short lived, stay in circulation until they die
move to tissue when cued by chemicals
Are phagocytic. The granules inside the cell have lytic enzymes, lysozyme (breaks down peptidoglycan), defensins (anti microbial peptide) that can all be used to kill bacteria.
85
How is the destructive nature of neutrophils controlled? CAN WE STOP THEM?!?!?
Yes. In order for neutrophils to do potentially harmful things like creating reactive oxygen species and nitric oxide, they must be activated by something like complement
86
BActeria that live and grow in neutrophils livein the \_\_\_\_
Endosome
87
Why do neutrophil levels in the blood go down during an infection?
Neutrophil production is increased when you have an infection/inflammatory response. Neutrophils will move out of your blood stream during infection as you wait for more neutrophils to be matured - this leads to low levels of neutrophils in blood for a short time
88
What is that cool thing Neutrophils can do with their DNA?
Expel it to create a net, straining the capillaries and catching only bacteria
89
If neutrophils are phagocytic, what are basophils and eosinophils?
Baso: release histamine (cause allergic reactions) and other effector compounds
Eosino: Defense against protozoa AND PLATYHELMINTHES
90
Differentiate between macrophage and monocytes
Macrophage are just monocytes that have taken up residence in a tissue and matured. They have names like "alveolar macrophage".
Monocytes are undifferentiated and come from the bone marrow, circulating in the blood.
91
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.
They are named depending on where they are located and will thus have different names They must be activated
92
Can macrophage live outside the body?
Yeah, like on alveoli. Problem is they can also bring disease back in (I'm looking at you, *Legionella*)
93
Describe Dendritic cells. How do they go about their bidness
Live in places where bacteria can enter the body, or where blood/lymph fluid is (ex. skin, respiratory tract, GI tract). When they find their permanent home, they develop spikes to increase surface area. Form a network that picks antigens off of bacteria.
After that, they move to lymph nodes, and tell the T and B cells of the adaptive immune system about the bad guys
94
\_\_\_\_\_ are specialized Dendritic cells that function in detecting intracellular viruses. How do they do this?
Plasmacytoid dendritic cells. They take up viruses, carry them to dendritic cells, and the interferon in dendritic cells prevents the virus from replicating. Effectively killing it
95
What is Holloway's favorite cell and what are they the first line of defense against?
Natural Killer Cells
Viruses
96
What is an NK cell?
Do not have the receptors seen on T and B cells, but are still lymphocytes. Do not need activation, allowing them to act quickly.
97
How do NK cells attack intracellularly infected cells?
by releasing a granzyme that forces the cell to undergo apoptosis. They also activate macrophage
98
Briefly describe what makes lymphocytes so cool
Recognize a SPECIFIC antigen, are small cells that circulate in the blood. When they encounter an antigen along with another signal like cytokines they become activated
99
What do activated lymphocytes do?
Form large lymphoblasts which differentiated into effector cells that can then produce memory cells.
100
What is the purpose of memory cells?
Help the body respond better to an antigen the next time it is encountered
101
Distinguish between the two types of lymphocytes
B lymphocytes - mature in bone marrow, express antibody molecule on cell surface.
T lymphocytes - formed in bone marrow, mature in thymus. have non-antibody antigen receptors (do not produce antibodies).
102
What are the two types of T cells
helper T cells - produce cytokines (help activate lymphocytes) and CD4+
cytolytic T cells - express CD8 and kill your own fucking cells (HIV MOTHAFUCKA), either virus or bacteria infected
103
Which of the lymphocytes produce antibodies and which produce cytokines?
B = antibodies T = Cytokines
104
Since both B and T cells produce memory cells, what is the resulting lifespan?
20 years
105
How do antibodies affect bacteria?
They specifically and non-covalently bind to antigens. This binding prevents attachment of the pathogens, neutralizes toxins, stimulates opsonization, and serves as a signal to the immune system.
106
Where are antibodies found in the body?
Circulating in blood and lymph, secreted out onto mucosal membranes. Present on the cell surfaceof B cells
107
What is the typical structure of an antibody?
IgG - 4 individual polypeptide cells: 2 long or heavy, 2 short or light
108
Give me some facts about antibodies binding to antigens. Like about the bonding itself.
1 Antibody = 2 Antigens.
both of the binding sites are identical to each other
They are composed of both light and heavy chains (both of which contribute to binding) and even though the actual antibody molecule is the same, the binding site differs between specific antibodies.
109
What is a "clonal population" of antibodies?
Those in which all daugters came from one cell. Every clone creates a specific antibody. A polyclonal system develops when these clones spread through the body
110
How many types of heavy chains/immunoglobulin types are there?
5.
alpha - IgA
delta - IgD
epsilon - IgE
gamma - IgG (with 4 subclasses)
mu - IgM
111
Which of the antibodies is produced during the initial (1o) response?
IgM.
IgG also appears but it isn't major
112
Describe IgM antibodies
IgMs circulate in the blood all the time but still form the first immune response. it is usually a pentamer of antibodies, creating a star shape. Can be utilized by B cells in a singular form,
113
Describe IgG antibodies
Not a major player in primary immune response, increases over time and is the primary Ab in secondary response. Can cross placenta.
Binds to Fcgamma receptors on macrophage, increasing efficiency of phagcytosis and activating complement
114
What is the structure of IgG?
a monomer of 2 light and 2 heavy g chains
115
Which of the antibodies is very efficient at agglutination reactions?
IgM It can bind 10 small antigens but usually only 5 because of steric interference
116
What do T cell receptors respond to? (TCR = T cell receptor)
They respond to protein antigens. TCR only response to a peptide on the MHC protein complex
117
How are T-cells restricted in what they can bind to?
Can only bind to antigens as a peptide and only when attached to another cell
118
Which of the MHC-restricted T cells recognize intracellular and extracellular proteins?
CD4+ class II (TH cells) = extracellular
CD8+ class I (CTLs) = intracellular proteins
119
What are cytokines responsible for and describe in vague general terms to their concentration in the body?
They signal between different types of cells and regulate immune reactions and inflammation
They are produced mostly by immune system cells (usually helper T cells)
they are active at extremely low concentrations
120
What does TNF stand for and give me some facts about it (like what it does and shit)?
Tumour Necrosis Factor - the cytokine responsible for inflammatory effect of gram negs.
Produced primarily by activated Macrophage. Recruits and activates monocytes and neutrophils by inducing endothelial cells to secretechemokines. 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).
121
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-gamma which activates macrophage.
IL-10: inhibits macrophage function by downregulating IL-12 into IFN-g.
122
What is the definition of epidemiology?
the science that studies the occurrence and reasons for health and disease in popilation
123
What are the different levels of epidemiology? Briefly describe each
In order of severity:
sporadic - Doesn't happen often
endemic - confined to one area, steady, low-level
outbreak - localised sudden increase (ex. food poisoning)
epidemic - sudden increase on a large scale (basically a big outbreak)
pandemic - super crazy increase over several continents
124
A ____ is a animal diseases which can be transmitted to humans. Does this happen often? At what scale?
Zoonosis/zoonotic. Happens all the time, human is just usually a dead end host.
125
Differentiate between morbidity rate, mortality rate, prevalence rate
Morbidity - number of individuals who become sick over a period of time
Mortality - number of people who died as a proportion of total people with disease
Prevalence - total cumulative number of people suffering from disease over a time period, usually in \_\_\_/100 000/year
126
What is an infectious disease? A communicable disease? A dead-end host?
1. Infectious: a disease caused by bacterium, fungi, protozoan, or living creature, may not be communicable 2. Communicable: person-to person 3. Dead-end: Cannot be spread
127
What is the difference between sign, symptom, and a syndrome?
sign: What you can observe
symptom: what they complain about
syndrome: combination of all that plus scientific data
128
Distinguish between incubation time, prodromal stage, illness period, and decline
Incubation time - time between infection and start of symptoms
Prodromal stage - Indication of disease present but symptoms undiagnostic
Illness period - definite, diagnostic signs and symptoms
Decline - patient survives, develops antibodies to a disease. Seroconversion of IgM to IgG.
129
Distinguish between a common source epidemic and a propogated epidemic
Common source - short time, limited number of patients, all got infected by same thing (restaurant, water, etc.)
Propagated - Slow increase in infected, long time span, may have originated from one person
130
What is herd immunity and why is it so effective?
When a susceptible person does not become sick even though the bacteria is in the population. \>80% must be non-susceptible. Small probability of the susceptible person catching it. BUT GUESS WHAT. ANTIVAXXERS ARE RUINING THIS FOR ALL THE GOOD PEOPLE WHO SIMPLY CAN'T GET VACCINES FOR HEALTH REASONS
131
How can you determine if the bacteria is actually causing the infection?
Koch's postulates
132
What is the difference between source and reservoir in regards to bacterial infection?
source: immediate object or organism from which the pathogen is passed
reservoir: the natural environmental location of the pathogen
ex. reservoir of influenza is birds, your source will probably not be birds
133
Most diseases are ____ in their reservoir organism. Why?
Benign.
Because each reservoir organism carries a different strain, way more variety and years and years of evolution to make the organism less susceptible
134
Distinguish between incubatory carriers, active carriers, and convalescent carriers of disease
Incubatory - shows no signs of disease but is infected and infectious
active - shows signs of disease but is still infectious
convalescent - has recovered from disease but still infected with pathogen
135
What are the major routes of transmission. Briefly describe them
Airborne - very small, suspended water droplets, usually from upper RT. From sneezing, coughing, oil, dust. Usually leeds to RT infections. Ex. most forms of pneumonia
Contact - contact with a surface someone sneezed/coughed on (indirect contact), direct contact (sex, kissing, intimate hugs). Ex. leprosy, gonorrhea.
Vehicle - Physical contactwith contaminated inanimate objects. Food/water, medical devices. Ex. E. coli.
Vector-borne - Usually biting animals.
136
Give examples of times where airborne transmission is an alternate form
Bubonic plague can infect the lungs and become an airborne "pneumonic bubonic plague", Hanta virus is transmitted to humans by mouse poop instead of the common biting transmission seen in mice
137
Distinguish between endogenous and exogenous nosocomial infections. where can nosocomial infections come from?
Endogenous - patient's own bacteriasource of infection
Exogenous - pathogen transmitted while in hospital.
Can come from direct contact, medical devices, airborne
138
Burn victims in hospitals are often colonized by \_\_\_\_
P. aeruginosa
139
Most hospitals have a _______ to help monitor the spread of (esp. antibiotic resistant) nosocomial infection
"infection control committees"
140
What is the name of the bacteria that causes cholera?
Vibrio cholerae
141
Why is cholera more common in tropical areas?
Does not grow bellow 18degrees
142
Untreated cholera has a casefatality rate of \_\_\_\_\_
60%
143
What are the geographical reservoirs for Cholera?
Bengal basin, ganges-brahmaputra delta. Cholera likes estuaries because it prefers a large amount of salt
144
What seemed to stop the first pandemic of cholera? How did it initially spread?
the extreme cold winter of 1823/24. Spread from north east india to nepal and afganistan by English troops. They spread it all across the middle east and eastern africa, as well as southern russia. By sea they spread it to the Philippines, Japan, China
145
Which of the cholera pandemics affected Canada?
The 3rd and 4th. No others because of strict quarantine
146
How did Canada react during the second cholera pandemic
Health board were set up in Quebec City and Montreal, citieswere divided into wards to enforce health regulations and cleaning. We prepared a quarantine station and were ready for immigrants to arrive there.
But there were too many. We couldn't hold them back. Not all ships were inspected, and it resulted in a major epidemic. 43% case fatality rate. People fled to thecountry, businesses closed down, everyone was scared to use the river, and immigrants were shunned.
147
What did John Snow discover about cholera? In this regard he actually knew something ba dum tsss
He practiced during the 1st and 2nd pandemics and during the third he spoke up. 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
148
What did Pasteur and Koch determine during the 5th cholera pandemic
Pasteur had this crazy notion that not only did bacteria cause disease, but some didn't, and they differed. Both believed in thegerm theory of disease, and Koch examined dead people for vibrio shaped bacteria.
149
Give me some characterisitics for vibrio cholerae.
Gram neg, motile, comma shaped, oxidase pos, glucose fermenter, require or grow better in 1% NaCl, acid sensitive
150
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?
O1 El Tor.
El Tor but isolates have been found in Sulawesi, Indonesia
151
How does one grow cholera in a lab
TCBS agar. pH is higher than 8, has bile salts, basically everything chlera wants. V. cholerae appear yellow on it
152
What antigen components comprise the Inaba serotype of O1 Cholera? Ogawa?
Inaba - A and C components
Ogawa - A and B with a little bit of C
153
How many V. cholerae cells are needed to infect a healthy fasting person? A fasting person taking sodium bicarbonate?
1011 cells
106 cells
154
Which blood type is most likely to give you worse cholera symptoms?
Type O
155
What is the pathogenesis of V. cholera?
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
156
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.
You die of dehydration because their is not enough water in your body. You show symptoms of dehydration at 5% water loss
157
In order for cholera bacteria to inhabit the large intestine, what must they first produce?
Pili which they do
They produce Toxin co-regulated pilus
158
What is V. cholerae associated with?
Phytoplankton and marine invertebrates
159
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?
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.
160
In this crazy world, could lake Winnipeg harbor V. cholerae?
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.
161
If the amount of algal blooms increase in a lake, why would a increase in cholera be possible?
Basically, algal blooms lead to an increase in the population of copepods which harbour V. cholerae.
162
Say people don't drink from a lake but from the clean river, are they safe from Cholera? What about if a monsoon hits?
Hypothetically yes. Probably not as the mixing would have driven some the cholera laden copepodes into the river exposing people to them.
163
Describe the shit caused by cholera?
rice water stool
164
How do you treat a cholera infection?
Intravenous electrolyte solution
oral rehydration therapy with glucose-balanced salts solution
homemade sugar-salt water solution
