Chapters 22 And 23 For Final Flashcards
(125 cards)
1
Q
What is the word for a parasite growing and multiplying within or on a host that may or may not result in overt infectious disease?
A
Infection
2
Q
What is a pathogen?
A
Any parasitic organism that causes infectious disease
3
Q
What is a primary (frank) pathogen?
A
Causes disease by direct interaction with healthy host
4
Q
What is an opportunistic pathogen?
A
May be part of normal flora and causes disease when it has gained access to other tissue sites or host is immunocompromised
5
Q
What is Pathogenicity?
A
The ability of a parasite to cause disease
6
Q
Who was Robert Koch?
A
The father of immunology that identified the causative agent of anthrax
7
Q
What are Koch’s Postulates?
A
- The microorganism must be found in abundance in diseased individuals
- The microorganisms must be isolated from the diseased individual and grown in pure culture
- The cultured microorganisms must causes disease when re-introduced into a healthy organism (animal model)
- The microorganism must be re-isolated from that animal model
8
Q
An infection with viruses, bacteria, fungi, or Protozoa is called what?
A
An infectious disease
9
Q
What are signs (aka “read outs” of a patient)?
A
Objective changes in body that can be directly observed
10
Q
What is the definition of symptoms?
A
Subjective changes experienced by patient
11
Q
Disease syndrome definition
A
Set of characteristic signs and symptoms
12
Q
Incubation period definition
A
Period after pathogen entry but before signs and symptoms appear
13
Q
What is the prodromal stage?
A
- the onset of signs and symptoms
- not clear enough for diagnosis
14
Q
What is the period of illness?
A
Disease is most severe and has characteristic signs and symptoms
15
Q
What type of immunity is activated during the “period of illness”?
A
Adaptive immunity
16
Q
What is convalescence?
A
When signs and symptoms begin to disappear
17
Q
After which event does convalescence appear?
A
After class switching from IgM to IgG
18
Q
What are the direct modes of spread of communicable infectious disease?
A
- Horizontal contact (kissing, sex)
- airborne droplets
- Vertical contact (mother to child)
- Vector ( flies and mosquitos)
19
Q
What are examples of indirect (vehicles) of communicable infectious disease?
A
- contact fomites (solid surfaces)
- food, water, biological products (ex: Typhoid Mary)
- Airborne
20
Q
What is the stain and shape of Neisseria gonorrhoeae?
A
Gram-negative diplococcus
21
Q
What type of disease is N. gonorroeae?
A
An STD
22
Q
Where does N. gonorhoeae colonize most commonly in males vs females?
A
Males: colonizes the urethra
Females: colonizes the cervix
23
Q
Why is N. gonorrhoea called a superbug?
A
It is called “super” because of its resistance to azithromycin
24
Q
What is a third generation cephalosporin that can be still be used to treat N. gonorrhoeae despite it being a superbug?
A
Ceftriaxone
25
What is the difference between Genetic Variation and Gene Regulation?
Genetic Variation -> Random switching -> Heterogeneous Population
Genetic Regulation -> Environmental stimulus -> Homogeneous population
26
In Pilin phase variation, which genes does the promotor control: PilE, pilS1, pilS2, or pil3?
PilE
27
What do pilS1, pilS2, and pilS3 have the tendency to do? What does this lead to?
They have the genetic tendency to recombine. This leads to mixed genes and Variability
28
By varying the pilin amino acid sequence, some N. gonorrhoeae can _______ the adaptive immune response.
Escape
29
What used to be used to treat gonorrhea that can no longer be used due to resistance?
- Penicillin (targets cell wal)
- Tetracyclines (targets ribosomes)
- Fluoroquinolones
30
What is the now recommended treatment for gonorrhea?
Ceftriaxone
31
What is the stain and shape of Staphylococcus aureus?
Gram-positive cocci
32
Where is staphylococcus aureus a huge threat since it is a major nosocomial pathogen?
Hospitals
33
What is the percentage of commensalism/Nasal carraiage of S. aureus?
20% stably colonized
60% intermittent carriers
(If you are in this 20% don’t handle for for others)
34
What type of pathogen is S. aureus?
An opportunistic pathogen
35
What are the features of S. aureus toxins?
- Apoptotic induction/Nutrient acquisition
- Resistance to oxidative burst killing
- Binding to host tissues
- Superantigens
- Cloaking of opsonins
- Host cell lysis
- Impairment of phagocyte recruitment
- Biofilm
36
Apoptotic induction/nutrient acquisition:
What three types of enzymes can cause cell degradation via apoptosis?
protease, nuclease, and lipase
37
resistance to oxidative burst killing: ______ catalase is resistant to hydrogen peroxide in the phagosome and has burst protection.
SodA
38
What does binding to host tissues in S. aureus?
MSCRAMMs are surface proteins for binding
39
What do Superantigens do in S. aureus?
They can make the immune system go crazy. an example is TSST-1
40
What is an IgG binding protein that can bind to flip antibody to the outside?
Protein A~
41
What accomplishes the cloaking of opsonins in S. aureus?
Capsules
42
What are capable of Host cell lysis for S. aureus? What symdrome toxin occurs as a result?
- alpha-toxin
- delta-toxin
- beta-toxin
scalded skin syndrome toxin
43
Impairment of phagocyte recruitment: impairs the recruitment of antibodies through ____, ____, and ____.
CHIPS, Sak, and Efb
44
What does biofilm allow?
It allows it to be resistant to antibiotics (like a little shield of protection)
45
Expression of S aureus hemolysis is controlled by what?
Cell density
46
What are the two components of the Two Component System?
Histidine Kinase + Response Regulator
47
What is Quorum sensing?
A mechanism where a bacterial population can determine the abundance of itself and others in an environment
48
Where was Quroum sensing originally discovered?
Vibrio fischeri
49
What does vibrio fischeri make to sense the levels of itself?
Autoinducing Peptide (AIP)
High AIP -> makes luciferase
50
how does Quorum sensing work?
When sufficient cells accumulate in an environment, they trigger gene expression and transmission of AIPs
51
What attaches to the cell wall and uses another “zip code” termed a “sorting signal” and attaches many virulence determinants to the cell wall?
Sortase
52
Sortase is a membrane protein conserved in Gram- __________ bacteria?
Positive
53
Methicillin resistance is mediated by what?
mecA
54
MecA has a _____ affinity for methicillin
Low
55
What is the stain and shape of vibrio cholerae?
Gram-negative Vibrio
56
what condition is cholera thought to cause the mutation for?
Cystic Fibrosis
57
Because cholera is thought to be the reason for the mutation that causes CF, what do CF patients have increased resistance to?
Cholera
58
What are Cholera toxins encoded by?
A phage
59
What are the symptoms of infection of the small intestine with Vibrio cholera?
- rice water stool
- severe diarrhea
60
What are the two subunits of the Cholera toxin? how many molecules do each have?
- Subunit A: 2 molecules
- Subunit B: 5 molecules
61
When the cholera toxin mechanism is in action, does the production of cAMP increase or decrease significantly?
Increase
62
During cholera toxin mechanisms of action, the increase of cAMP leads to protein kinase A phosphorylating the CFTR channel. What is the next step in this pathway?
Chloride is secreted into the lumen of the gut
63
What do the following characteristics describe?
- expressed in a host
- Pili self-aggregate
- receptor for CTX Phage
Toxin-corregulated pilus (TCP)
64
What
- forms microcolonies of V. cholerae
- concentrates toxin to a particular location
Pili self-aggregate
65
What are the treatments for cholera?
Oral/IV rehydration salts
66
What disease do these characteristics describe?
- Acid-fast gram-positive
- Obligate aerobe
- Discovered by Robert Koch
Mycobacterium tuberculosis
67
What does M. tuberculosis have instead of an outer membrane?
An outer layer of mycolic acids
68
How do Mycolic Acids differ from from phospholipids?
- normal phospholipids has 13-18 carbons
- This has. Variable region
- phospholipids have phosphate region
69
how does M. tuberculosis differ from other gram-positives?
It has a layer with Mycolic acids that makes it waxy
70
What virulence factors does M. tuberculosis secrete?
- KatG ( catalase-peroxidase) and SodA (superoxide dismutase)
- Esat6/CF-10
71
What dos the virulence factor Esat6/CF-10?
- Co-transcribed and form a tight 1:1 complex
- immunodominant antigen
72
What is Granuloma?
Strategy a host uses to wall-off a foreign substance that it cannot eliminate
73
Tuberculosis can remain a persistent cell for years which means what?
Once you are infected, you become a carrier for life
74
What is the treatment for the TB Latent Infection?
Isoniazid (9 months)
75
When does isoniazid become activated?
It can only become activated in the presence of KatG because the active drug form inhibits the synthesis of Mycolic acid
76
What are these treatments for?
- Isoniazid
- Rifampin
- Ethambutol
- Pyrazinamide
TB Active Infection
77
What is Malaria caused by?
Four species of Plasmodium
78
How is malaria transmitted?
By the bite of a female mosquito
79
What is the life cycle of plasmodia protists?
- sporozoite injected with mosquito bite
- replicates as merozoite in hepatic cells
- released, enters erythrocytes and replicates
- lyses erythrocytes- correlated with fever
80
What happens when the schizont breaks?
It releases merozoites and infect the liver cells
81
Where do sporozites relicate?
Schizont
82
What are the clinical manifestations of malaria?
- chills and fever
- anemia
- hypertrophy of the spleen and liver
- can cause cerebral malaria in children and non immune individuals
83
How is Malaria diagnosed?
Uses the Wright or Giemsa-stained red blood cells and serological tests to see the demonstration of parasites
84
treatment, prevention, and control of Malaria
- antimalarial drugs
- prevention by use of bed netting and insecticides to control mosquitos
- new vaccine shows promise
85
Why might malaria vaccines not always work?
Depending on the stage of the disease, the surface proteins completely change and therefore changes the antigens. Vaccines are surface protein specific, so if the vaccine is distributed at the wrong stage in the cycle, it might be ineffective
86
What percent of 5-7 month olds who received the malaria vaccine were Protected?
40%
87
The _____ vaccine trains the immune system to attack the malaria parasite, which is spread by mosquito bites.
RTS,S
88
What is sickle-cell disease?
An endemic in Africa that is a human evaluation to fight Malaria
89
What is thought to be the most pressure on human evolution in recent history?
Sickle-cell disease
90
What are the causes of Sickle-cell disease?
- Abnormal hemoglobin
- under low oxygen, hemoglobin forms polymers and the red blood cell elongates
91
RBCs are normally elastic. What disease prevents elasticity?
sickle-cell disease
92
Why is sickle-cell bad for malaria?
- the cels aren’t elastic anymore
- cells lose before the parasite can replicate to high numbers
93
In sickle-cell, are patients immune to malaria?
NO, they are resistant and NOT immune
94
What are treatments for malaria?
- Quinine
- Chloroquine
- Atovaquone/progunil
95
What does Atovaquone/proguanil do?
It inhibits plasmodium’s electron transport chain/ DHFR
96
What is Leishmaniasis caused by and how is it spread?
It is caused by different Leishmania species and it is spread from host-to-host through a sand fly vector
97
What are the two forms of Leishmaniasis?
- Cutaneous
- Visceral
98
What are the two forms of the Leishmaniasis parasite?
- Promastigote
- Amastigote
99
The Promastigote form of Leishmaniasis in (people/the fly)
In the fly
100
What is the difference in morphology between Promastigote and amstigote?
Promastigote is oblong and flagellated in the fly while the Amastigote is oval and has a rudimentary flagella in people
101
Where are the lesions of cutaneous leishmaniasis? what do they cause?
The mouth, nose, throat, and skin
they cause disfigurement and excessive scarring
102
True or False: people who have cutaneous leishmaniasis have permanent immunity after healing
True
103
Can cutaneous leishmaniasis heal without treatment?
Yes it can, but it can take weeks, months, or years and typically leaves a scar
104
What system does viscera Leishmaniasis (Kala-azar) involve?
The monocyte-macrophage system
105
What are the clinical manifestations of visceral Leishmaniasis?
- intermittent fever and enlargement of spleen and liver
- may be fatal
106
True or False: people that recover from Visceral Leishmaniasis get permanent immunity
True
107
What is the mortality rate of untreated Visceral leishmaniasis?
Nearly 100%
108
What is the treatment, prevention, and control for Leishmaniasis?
- anti parasite therapy
- vector and reservoir control
- epidemiological surveillance
109
What is the bacteria that causes Chagas’ disease? What is the vector?
Trypanosoma cruzi
“Kissing” bugs or “assassin” bugs
110
what regions is Chagas’ disease present in?
Tropical Latin American regions
111
What is acute Chagas’ disease?
Rapid onset, trypanosome moves through the bloodstream, enters cells and becomes Amastigote, replicates
112
At which stage of Chagas’ might treatment be effective?
The Acute stage
113
What are the symptoms of Chagas’ disease?
- May have no/mild symptoms (swelling/reddening of the bite site)
- further symptoms develop
- eye swelling
- lymph node infections
- fever
- malaise
- spleen/liver may enlarge
114
What happens in chronic Chagas’ disease?
- Amastigotes reach the heart, GI and other cells
- replicate causing heart disease and other disorders due to the destruction of parasitized cells in the liver, spleen, lymph nodes, GI, and central nervous system
115
Are there treatment options available at the chronic stage of Chagas’ disease? Why or why not?
No. Vaccines are not effective due to the antigenic variation of the trypanosome
116
How does chronic Chagas’ disease emerge?
- heart disease
- often leads to sudden death
- bowel abnormalities
- can lead to malnutrition
117
What are the two treatment drugs for Chagas’ disease?
- Benznidazole
- Nifurtimox
118
What bacteria causes African sleeping sickness? What is the vector?
Trypanosoma brucei
Tsetse fly vector
119
What are the two types of African sleeping sickness?
East African and West African
120
What causes East African sleeping sickness?
T. brucei rhodesiense
121
What causes West African sleeping sickness?
T. brucei gambiense
122
What are the symptoms of African sleeping sickness when it spreads through the blood?
Fever, headache, sweating, and swelling of the lymph nodes
123
What are the symptoms of African sleeping sickness when it spreads through the CNS?
Behavioral changes, drowsiness during the day (insomnia at night), coma
124
What are the treatment options for African sleeping sickness?
- Suramin (for 6 weeks)
- Melarsoprol (very toxic and can be fatal due to arsenic compound)
- Pentamidine
125
what is a side effect of treatment of Melarsoprol for African sleeping sickness?
Arsenic poisoning
