1
Q
Plague epidemics contributed to devastating morbidity and mortality preceding the 19th century, causing widespread panic. Where are these places?
A
- Asia
- Europe
- North Africa
2
Q
How did plague epidemics affect the world?
A
- there was death on a global scale
- referenced in art and music, literature, the horrors of death
- most impactful disease in the world, black plague
- before people could properly develop antibodies
3
Q
There are 3 major plagues during this period. What are they?
A
- the Justinian plague
- the black plague, bubonic plague
- the modern plague
4
Q
What are some defining features of the Justinian plague?
A
- 541 AD
- most characterized by waves of pandemicity for hundreds of years
- estimated to have killed 15% of the worlds population (>25 million)
5
Q
What are some defining features of the Black death?
A
- started in the 14th century
- originated in China
- spread throughout trade routes to Europe
- estimated to have killed nearly 60% of the European population at the time (>100 million)
6
Q
What are some distinguishing features about the Modern plague?
A
- started in China in the 1860’s
- spread around the world from ships
- caused an estimated 10 million deaths
7
Q
State some facts about Alexander Yersin.
A
- french physician, pasture institute
- discovered the causative agent of the plague during the modern pandemic
- called it Pasteurella pestis at first, then later named Yersinia
8
Q
Plague is spread by the bite of____.
A
-Oriental Rat Fleas
9
Q
What was one of the ways the spread of the plague would be mitigated?
A
- known that humans with close contact with rats are more likely to get the plague
- the infection rate increases with increased contact with rats
- For, example rat catchers were tasked with executing rats in mostly urban areas, which brought the populations down
- live were spared and infection rated decreased
- control of a reservoir is important in controlling a disease
10
Q
Y.pestis has a broad host range. What are these animals that carry the plague?
A
- squirrel
- chipmunks
- rats
- mouse
11
Q
Reservoirs in squirrels , and other rodents allow plague to become______- including western U.S.
A
-endemic in many rural areas
12
Q
Why is the plague prominent in the western U.S.?
A
- plague in the west, reported cause of human plague in the western United States
- 1970-2012, predominately in the western part of the U.S.
- wild squirrels, wild rats, prairie dogs
13
Q
What can change the outcome of the plague in the U.S.?
A
-improved rodent control, insecticides for insect control
14
Q
Yersinia is divided into at least 11 different species. What are the ones significant to this lecture?
A
- Y.pestis
- Y.enterocolitica
- Y.pseudotuberculosis
- the pathogenic potential of the other species is unknown
15
Q
Describe the Morphology of Yersinia.
A
- gram-negative
- cocobacilli
- small bipolar staining “safety pin” pattern of staining by Wayson’s Method
- capsular heat envelope antigen, heat liable
- Stomatic V/W antigen associated with virulence
16
Q
Describe the epidemiology of Y.pestis.
A
- primary a rat pathogen (sepsis)
- maintains its primary reservoir in rats and other rodents
- is able to be indirectly transmitted to humans by the bite if the rat flea, parenteral
17
Q
Both Y.enterocolitica and Y.psudotuberculosis cause yersiniosis. What is this?
A
- generalized infection of the small/large bowl
- usually self limiting, diarrehagenic, gastrointestinal disease
- sometimes can progress to a abscess stage and gut proliferation, results in life threatening sequelae paratinitis
18
Q
What is a popular diagnostic method used for direct examination of a specimen suspected to be Y.pestis?
A
- Wayson’s method
- stained, Y.pestis will appear purple with a safety pin appearance
19
Q
Y,pestis, as well as other species of Yersinia, have the intrinsic ability to survive in immune cells. What type of strategy is this?
A
- pathogenic strategy
- are able to infect lymphatic tissue
- they are also able to colonize the gut, have a broad host range, species of yersinea in general
20
Q
Answer these questions about Y.pestis:
- In its bubonic form, can there be direct transmission between humans?
- What does Y.pestis have to do in order to become highly contagious?
A
- In its bubonic form, Y.pestis does not have any way of direct transmission, contained within the individual
- The bubonic form of the disease has to progress to pneumonia, that way there can be direct transmission via aerosolization, spreads easily
- pnumonic form of the disease can be a complication of the bubonic form
21
Q
Answer these questions about Y.enterocolitia:
- Y.enterocolitica is enteropathogenic to what two organisms?
- How is it transmitted?
- What type of disease does it cause if it invades M-cells?
A
- Ungulates ( cattle and deer), humans, also pigs
- transmitted by fecal-oral route
- causes diarrhea disease, result from the invasion of these pathogens into basil membranes through M-cells through the process of transcytosis
22
Q
What are these three bacterium mode of transmission?
- Y.pestis?
- Y.enterocolitus?
- Y.psudotuberculosis?
A
- through vectors
- fecal-oral transmission
- fecal-oral transmission
23
Q
Fill in the blank:
Bubonic plague is to _____, while _____ is to lungs.
A
- lymph nodes
2. Pnumonic Plague
24
Q
State some facts about Pasteurella:
- What was it later called?
- What is the morphology of Pasteurella?
- Where does it largely cause disease?
- What type of infection does it cause in humans?
A
- later called Yersinea
- Morphology: Non-motile, gram-negative coccobacilli, retain their bipolar stain, most disease caused by P.multocida
- causes disease in animals (domestic/wild), cattle, sheep, rodents, fowl, rabbits
- causes integumental (abscess) infection in humans, there can be exposure to infected animals from arthropod vectors (deerfly/ticks)
25
What 2 ailments are associated with P.multocida?
1. "Snuffles" in rabbits
2. Hemorrhagic pneumonia in lagomorphs
3. the disease progresses to snuffles to HP, the mortality rate is over 50%
4. associated with inner ear infection that produces pus
26
Answer these questions about Y.pestis vector transmission:
1. What type of transmission (chain of infection) is essential for Y.pestis to infect humans and what must it do first in order to achieve this?
1. transmission form rat fleas to humans, for this to occur Y.pestis must infect rat fleas
27
Explain how flea colonization occurs with Y.pestis
-in general, Y.pestis must multiply int he flea, this leads to the formation of a mass that is able to block the proventricular valve
28
What are the steps that usually happen when Y.Pestis colonizes a flea in order infect it?
1. Pestis is ingested by the flea when it takes a blood meal from a septic rodent
2. Multiplies in the foregut of the flea, blocking the valve, proventriculus
2. 5 What is the Proventriculus? It is the gateway organ that separates the esophagus from the midgut
3. Blockage of the proventriculus is lethal to the flea as it will starve to death, if the blockage is not removed
- note: green florescent protein can make the obstruction more prominent
29
Answer these questions about rat fleas:
1. Y.pestis blocked fleas are defective at what?
2. What happens if blocked fleas attempt to take blood from a rat?
3. What can happen if fleas are desperate for blood fleas?
1. defective in ingesting blood
2. fleas attempting to take a blood meal will regurgitate blood mixed with Y.pestis into the host dermis, transmitting the pathogen
3. the fleas will increase their reservoir
30
State some of the steps that need to happen in order for a flea to be desperate enough to get a blood meal from an human.
1. Healthy flea bites septic rat, Y.pestis is in the blood meal of the rat
2. Y.pestis will colonize the proventriculus of the flea and block the organ, flea can not properly eat blood meals
3. infected flea will attempt to take a blood meal from the healthy rat
4. there is a blockage however, so the flea can not properly ingest the blood, the blood meal will mix together in the proventriculus, regenerated by the flea into the host, healthy rat, in this way it is transmitted prenatally
5. the flea will start to starve ;(((. the flea becomes desperate for blood :)) its host range increases and it goes for humans, in this way the flea is a bridging vector
- to summarize, primary reservoir=rats, secondary reservoir=humans
31
Answer these questions about the capsular antigen of Y.pestis:
1. In Y.pestis what doe the capsular antigen, F1 (Caf1) do during dissemination?
2. What is another purpose of F1?
3. F1 capsule is needed for dissemination and systemic illness, but not for what?
1. the expression of the capsular antigen is able to protect Y.pestis from innate immunity and phagocytosis
2. it prevents adhesion to the phagocytic cells, therefore it prevent phagocytosis, allows for survival in immune tissues
- y.pestis is a disseminate type of disease
3. intracellular survival
- y.pestis is in the cells, invades the lungs and tissues
32
Name the 3 clinical presentations of Y.pestis.
1. bubonic, lymph nodes, idiopathic
2. septicemic, blood, blood infection
3. pnumonic, lungs, respiratory
33
1. What is the most common presentation of Y.pestis?
2. What can this presentation eventually lead to?
3. Hematogenous dissemination (in Y.pestis) can lead to what?
1. the most common presentation is the bubonic form, it replicated in the lymphatic tissue (nodes), pelvic and cervical, inflammation
2. this can eventually lead to immunopathologic damage and eventually to hemorrhage
3. can lead to sepsis or hemorrhagic pneumonia, highly communicable
34
Mortality in Y.pestis:
1. What tend to be the mortality rates in the clinical forms of the plague?
2. Which forms of plague tend to be 100% fatal without medical intervention?
1. In bubonic plague= 50% mortality rate
- in septicemic plague= 90% mortality rate
- pnumonic plague= 100% mortality rate
2. septicemic and pnumonic forms will be 100% fatal without medical intervention
35
Answer these questions about the infection Strategy of Y.pestis part 1:
1. During the initial stages of infection, Y.pestis is able to survive in phagocytic immune cells, targeting cells through interaction with various adherence factors. What are those factors?
2. Y.pestis survives and does what in the macrophage? Once it is in the macrophage what does it synthesize?
1. Pla (plasminogen activator) and Ali (attachment invasion locus), may also be considered as invasions
2. replicated in the macrophage, it synthesized F1 antigen (fraction 1)
36
Answer these questions about the infection Strategy of Y.pestis part 2:
3. What happens after F1 antigen is synthesized?
4. F1 is opsonophagocytic. What does this allow?
3. Y.pestis destroys the macrophage
| 4. this allows for the F1 antigen to allow for dissemination
37
Answer these questions about the infection Strategy of Y.pestis part 3:
1. In later stages of infection, what strategy does Y.pestis utilize?
2. What does it do once at this late stage?
1. Immune subversion
2. uses immune subversion to replicate int he nodes (bubonic) and disseminates in the blood and invades the lungs (pnumonic), in later stages it is anti-pathogenic
38
Answer these questions about Y.pestis, invasion strategy:
1. What does dissemination of the disease require?
2. What is involved in both adherence and immune masking?
3. How does immune masking work?
4. What are Yops?
1. requires F1, Psa, and Yops (yersinea outer protein)
2. pH 6 antigen, Psa, pilus
3. It binds to host low density lipoprotein (LDL) in blood, is able to mask itself from immune effectors
4. Yops, protein effectors of the YSC (yersinea secretion complex)
39
Answer these questions about Yersinea Secretion Complex (YSC):
1. What type of secretion system is it?
2. What is the function of the YSC?
3. What are the 3 components of the YSC?
1. Type 3 secretion system
2. secretes Yops into target cells, altering normal cell function
3. [top-middle-bottom], Pore complex--Needle--Basal Body
40
Answer these questions about the YSC:
1. What is the YSC encoded on?
2. Is the plasmid highly conserved?
3. Is it essential for Y.pestis virulence?
1. it is encoded on a 70-kb virulence plasmid
2. pYV, the plasmid is highly conserved among the pathogenic species of Yersinea
3. pYV is essential for Y.pestis virulence
41
1. What is the YSC regulated by?
2. What does the v-antigen do?
3. What is another part of its purpose?
1. it is regulated by V-antigen
2. the v-antigen (LcrV) is able to oligomerize to form part of the YSC pore structure
3. it also serves as a regulator of YSC
42
1. What does LcrV activate?
2. Before YSC contacts the cell, what happens?
3. What does Y.pestis do during dissemination using the YSC?
4. What does Yop do during this stage?
5. After question 4 what does Yops do this via?
6. What does these steps allow for?
1. it activates the secretion Yop effectors
2. sealed by the LcrG- contact by YSC with the cell leads to binding of LcrG by LcrV- unsealing the YSC
3. it attacks immune cella and epithelial cells
4. Yops blocks phagocytosis and alters cell signal events and physiology
5. It does this via Rho, Rac, Cdc42 (YopE/T)
6. It allows for extracellular survival and replication in lymphatic/pleural tissues
43
Answer these questions regarding Parthenogenesis, postscript:
1. What putative adherence factors does Y.pestis express?
2. What do they induce?
3. What is the late stage of the disease associated with?
1. several factors, Ali, YadBC
2. they induce invasion by zippering into lymphatic and pleural tissues
3. associated with high CFRs unless treated promptly
- replication in lymph, lung or blood occludes vital passages and is highly prion-inflammatory
3. 5 also associated with significant tissue destruction, edema, hemorrhage
44
Answer these questions regarding diagnosis:
1. Yersinea must be diagnosed quickly because?
2. What types places can yersinea present itself?
3. What are some tests that can be used as diagnostic tools to find yersinea in a bacterium culture?
1. must be diagnosed quickly because of its extraordinary virulence and dissipate clinical presentations
2. can be found in sputum specimens, blood cultures, lymph node biopsies
3. DFA stain (direct florescence antibody against F1 capsule and urease production
45
Explain How a DFA stain works:
1. works by targeting direct florescent antibody in the F1 capsule
- purified antibodies to F1, high sensitivity for bubonic and sputum
46
Explain how a Urease production test works:
1. What does it test for?
2. Why does the reaction happen?
3. What is a positive and negative test and what type of bacteria can it differentiate?
1. it tests for the production of urease
2. this happens because of catalyzing hydrolysis of urea to ammonia and CO2
3. Positive=pink, Negative=yellow/orange, Y.pestis will appear negative and Y.enterocolitica and Y.pusdotuberculosis will appear pink
47
Yersinea regarding prevention:
1. Is there a vaccine for Yersinea?
2. What can help with reducing infections to humans?
1. no there is no vaccine
| 2. Control of domestic reservoirs (rats) and bridge-vectors (fleas) in endemic regions will mitigate epidemics
48
Therapy for Yersinea:
1. How would you treat patients with early stages of Yersinea?
2. What are the first line of drugs used?
1. with early stages the disease responds well to antibiotic chemotherapy
2. first line of drugs= aminoglycosides, gentamicin and streptomycin, trimethorprim
Med Bacc
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