Lecture Final- new info Flashcards
(81 cards)
1
Q
Infection
A
A parasite growing and multiplying within or on a host. May or may not result in overt infectious disease
2
Q
Pathogen
A
any parasitic organism that causes infectious disease
3
Q
primary (frank) pathogen
A
causes disease by direct interaction with healthy host
4
Q
opportunistic pathogen
A
may be part of normal flora and causes disease when it has gained access to other tissue sites or host is immunocompomised
5
Q
pathogenicity
A
ability of parasite to cause disease
6
Q
Robert Koch
A
- identified the causative egen of anthrax with the help of his wife and daughter
- Developed the tuberculin test, formulated four postulates for definitively linking a specific microorganism to a specific disease, and use agar as a solidifying agent in growth media
7
Q
Koch’s 4 Postulates
A
- The microorganism must be found in abundance in diseased individuals
- The microorganism much be isolated from the diseased individual and grown in pure culture
- That cultured microorganism must cause disease when re-introduced inot a healthy organism (animal model)
- The microorganism must be re-isolated from that animal model
8
Q
infectious disease
A
infection with viruses, bacteria, fungi, protozoa
9
Q
order of the course of an infection
A
- incubation periods: period after pathogen entry but before signs and symptoms appear
- prodromal stage: onset of signs and symptoms. not clear enough for diagnosis
- period of illness: disease is most severe and has characteristic signs and sympotoms
- covalescence: signs and symptoms begin to disappear
10
Q
Neissera gonorrhoeae
A
- Gram-negative, diplococcus
- Aka: gonocci (plural), gonococcus (singular)
11
Q
where does N. gonorrhoeae exist in the male and female?
A
Men: colonizes the urethra
Women: Most commonly in the cervix (can lead to pelvic inflammatory disease)
More rare in the Fallopian Tubes, Uterus, and Urethra
12
Q
What is “super” gonorrhoae resistant to?
A
azithromycin (a macrolide)
13
Q
what can be used to treat “super” gonorrhoea?
A
Ceftiaxone (third generation cephalorsporin)
14
Q
What’s the difference between Genetic Variation and Gene Regulation?
A
In genetic variation there is a trigger and the antibodies randomly switch, resulting in a heterogeneous population. (can invade adaptive immune system)
In Gene Regulation there is an environmental stimulus that reustls in a homogeneous population.
15
Q
Gonococcal surface molecules involved in adhesion as well as invasion or transcytosis. What does thea antibody recognize?
A
PiliE
16
Q
Pilin phase variation, how can some N. gonorrhoeae esape the adiaptive immune response?
A
By varying the pilin amino acid sequence
17
Q
What are treatments no longer used for N. gonorrhoeae due ot drug resisitance?
A
Penicillin, tetracuclines, and fluoroquinolones are no longer used
18
Q
Staphylococcus aureus
A
- Gram-positive cocci
- Latin: straphyle (bunch of grapes) Aureus (gold coin in ancient Rome)
- major nosocomial pathogen (originating in hospital)
- cause of several disease
- opportunistic pathogen
19
Q
Staphylococcus aureus symptomes
A
- staphycoccal folliculitis
- staphycoccal abess
- staphylococcal osteomyelitis
- staphlococcal scalded skin symdrom
- stye
20
Q
Expression of S. aureus hemolysin is controlled by ___ ______
A
cell density
21
Q
waht is the accessory gene regulator of virulence gene regulation?
A
agr
22
Q
two component system of virulence gene regulation
A
Histidine Kinase + Response Regulator
23
Q
Quorum sensing system
A
a mechanism where a bacterial population can determine the abundance of itself and others in an environment
24
Q
WHere can quorum sensing be found?
A
Originally discovered in Vibrio fischeri
- lives in most oceans (very low abundance)
- lives in the light organ of the Hawaiian bobtail squid (very high abundance)
- makes autoinducing peptide (AIP) to sense the levels to itself
- High AIP -> makes luciferase
25
Sortase
* membrane protein conserved in Gram-positive bacteria
* attaches proteins to the cell wall
- uses another "zip code" termed a "sorting signal"
- attaches many virulence determinats to the cell wall
26
Methicillin Resistance. What is it mediated by?
Mediated by mecA
- encodes MecA
- penicllin binding protein- (PBPa)
- normal cellular PBPs have a high affinity for methicillin
- MecA has a low affinity for methicllin
27
Vibrio cholerae
gram negative
Vibrio
concentrated in Africa, russia, asia
came to new york from Dominican Republic
28
Cholera historical impact with cystic fibrosis
Thought to be the reason for the mutation that gives rise to Cystic Fibrosis
- CF patients have an increased resistance to Cholera
29
Cholera pathogenesis
Cholera toxin - encoded by a phage
30
Cholera symptoms
* Infection of the samm intestines with Vibrio
* servere diarrhea (rice-water stool) (250 ml/kg per day)
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Cholera Toxin
* works in small intestinal epithelial cells
* 2 subunits
- 2 molecules of the A subunit (trigger fluid release)
- 5 molecules of the B subunit
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Cholera Toxin mechanism of action
* cAMP production increases significantly
* Results in protein kinase A phosphorylating the CFTR channel
* Chloride is secreted into the lumen of the gut (results in osmotic movement of water in the gut)
33
Toxin-corregulated pilus (TCP)
* Expressed in a host
* Pili self-aggregate
- Forms microcolonies of V. cholerae
- concentrates toxin to a partcular location
* Receptor for CTX Phage
34
Cholera treatments
* Oral/IV rehydration salts
* salt & water are the best
* antibiotics are not productive
35
Mycobacterium tuberculosis
* not a rewuired vaccine in the US
* acid-fast gram postive
* obligate aerobe
* disovered by Robert Koch
* instead of OM, M. tuberculosis has an outer layer of mycolic acids
* unique becuase its a gram + with an outer membrane of mycolic aicds
36
Mycolic acids vs. phospholipids
phospholipids have a shorter FA chain
37
Why wont Mycolic acids cell wall gram stain?
mycolic acids wont stain with gram stain bc mycotic acid layer
38
Mechanism of Tuberculosis disease
* enters alveolar macrophages by phagocytosis
* secretes virulence factors:
- KatG (catalase-peroxidase) & SodA (superoxide dismutase)
- Esat6/CF-10
- Co-transcribed and form a tight 1:1 complex
39
What is the host strategy Granuloma?
strategy a host uses to wall-off a foreign substance that it cannot eliminate
(TB granuloma)
an inflammatory mononuclear cell infiltrate that, while capable of limiting growth of Mycobacterium tuberculosis, also provides a survival niche from which the bacteria may disseminate
contains microbacteria inside in a dorminate stage
TB- your a systematic carrier for life
40
Treatment for Tuberculosis
* Latent Infection: isoniazid (medicine) - 9 months
* Active infection: 2 months
- Isoniazid
- Rifampin
- Ethambutol
- Pyrazinamide
41
What activated isoniazid?
KatG
42
Malaria
* *Plasmodium falciparum*
* Arthropod Borne Disease
* caused by 4 species of *Plasmodium*
* transmitted by bite of an infected female mosquito
43
What is the life cycle of *Plasmodial* protists?
1. sporozite injected with mosquito bite
2. replicates as merozoite in hepatic cells
3. released, enters erythrocytes and replicates
4. lyses erythrocytes - correlates with fever
44
Whete country is Maleria most prominate?
Africa
45
How prominate in Maleria in Africa?
* could get maleria every other year in Africa
* half of the population is highly effected
* its an epidmeic
46
What indaves the hepatocytes cells first in malaria process?
sporozoites
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What hides and replicates in the red blood cells for the maleria process?
Merozoites
48
# Maleria
Once sporozoites are relased by a mosquito bite what is formed in the exorythrocytic state?
formation of schixont and merozoites in the liver
49
Whart happend with the schizont breaks?
infects the red blood cells and the liver. Leading to the development of maleria in the human
50
How does maleria reproduce in the human?
In the Erythrocytic stage the Meroxoites infect and repordude in the red blood cells sexually. Leads to symptoms of malaria
51
What are symptoms of Malaria?
* periodic attacks of chills and fever
* anemia can result and the spleen and liver often hypertophy
* can cause cerebral maleria in children and nonimmune individuals (reaches the brain, brain blood barrier)
52
How can Maleria be diagnosied? Lab testing?
demonstration of parasites withiin Write- or Giemsa-stained red blood cells and serological tests (look at a syrum similarly to how you would for an antigen)
53
Malaria Treatment
antimalerial drugs
- resistance has been observed
- chemoprophylaxis for individuals traveling to endemic areas
54
Malaria prevention and control
- prevention by use of bed netting and insecticides to control mosquitoes
- new vaccine shows promise
55
What are ways to break the cycle of Malaria with vaccines?
* Pre-erthrocytic vaccines -in the liver
* Bloodstage vaccines -in the bloodstream
* Transmission blocking vaccines- inside the mosquito
56
Sickle-Cell diseases importance to human evolution
Human evolution to fight malaria
the malaria parasite acts as a selective pressure to maintain the high frequency of the sickle cell allele in a population. If the heterozygous (AS) condition no longer provides any selective advantage, the frequency of the sickle cell allele will gradually decrease.
57
Causes of sickle-cell disease
* Abnormal hemaglobin (codon mutation)
* under low oxygen, hemaglobin forms polymers and the red blood cell elongates
- RBCs are noramlly elastic, sickle-cel disease prevetns elasticity
58
What type of mutation is sicke-cell disease?
point mutation
* 6th codon mutation from the codon GAG -> GUG
* amino acid change from glutamate -> valine
59
What who disease have an overlap of distribution (correlated in Africa)?
sickle-cell disease and maleria
60
Why is sickle-cell bad for malaria? good for people?
* cells aren't elastic anymore b/c of sickle-cell
* cells lyse before the parasite can replicate to high numbers (malaria cannot replicate)
* allows the immune system to play catch-up. Keeps the parasite from causing major problems for the patient. Patients are 'resistant' to disease NOT immune
61
Why does someone without sickle-cell disease want to marry someone with sickle-cell disease in Africa?
This results in an offpsring with the sickle strait (carrier- hetero). People with normal hemaglobin are susceptibleto death form maleria. People with sickle cell disease are susceptible to death from the complications of sicke cell disease. People with sickle cell trait, hetero, have each type of hemoglobin have a great chance of surviving malaria and do not suffer the consequences from sickle-cell.
62
Do atheltes with sicke-cell perform better at high or low altitudes?
at high altitudes they cannot perform well, feel tired and slow
63
Malaria treatment
* quinine
* chloroquine
* atovaquone/proguanil
64
what does Atovaquone/proquanil do for malaria treatment?
inhibits plasmodium's electron transport chain/ DHFR
65
What causes Leishmaniasis?
* caused by many different *Leishmania* species
* spread form host-to-host through a sand fly vector - tropical regions
66
Promastigote parasite form of Leishmaniasis
- in the fly
- oblong, flagellated
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Amastigote parasite form of Leishmaniasis
- in people
- orval, rudimentary flagella
68
What are teh two forms of Leishmaniasis
- Cutaneous
- Visceral
69
Cutaneous Leishmaniasis
* lesions of mouth, nose, throat, skin that cuase extensive scarring and disfigurement
* papules that develop into curstanted ulcers
* healing occurs with scarring and permanent immunity (can healt w/o tratment but can take weeks to years)
70
Visceral Leishmaniasis (kala-azar)
* involves monocyte-macrophage sytem
* clinical manifestations: fever, weight loss, elarged speen/liver
* without treatment portaility rateis near 100%
* recovery provides permanent immunity
71
Leishmaniasis diagnosis, lab testing?
observation of parasites within infected macrophages, cultural and serological tests
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Leishmaniasis treatment, prevention, and control
- antiparasite therapy
- vector and reservior control, and epidemiological surveillance
73
Chagas disease: location and bug
Caused by Trypanosoma cruzi
-present in tropical Latin American regions
- Also has an insect vector: kissing/ assassin bugs (Triatomine bugs)
74
How does Chagas disease infect a person?
* Triatome big takes blood meal, defecates in wound, and is scratched into body
* acute diease
- rapid onset, trypanosome moves through bloodstream, enters cells and becomes amastigote, replicates (change in morphotype that allows it to replicate more rapidly)
- may be cleared or develop chronic form
- treatment may be effective at this stage
75
Acute Chagas disease symptoms
* may have no/mild initial symptoms (swelling/reddening of the bite site)
* futher symptoms develop
- eye swelling
- lymph node infections
- fever
- malaise
- speen/liver may enlarge
76
Chagas Chronic disease, where does it go?
* amastigotes reach heart, gastrointestial and other cells
* replite casuing heat disease and other disorders due to destruction of papastized cells in the liver, spleen, lymph nodes, GI, and central nervous system
* no treatment available at chronic stage
* vaccines not effective due to antigenic carision of trypanosome
77
Chagas Disease treatment
* Benznidazole
* Nifurtimox
78
African sleeping sickness, what is it caused by?
caused by Trypanosoma brucei
spread through the Tsetse fly vector
epidmeic/endemic in africa
79
What are the two types of African sleeping sickness? Which is more servere?
East African: casued by *T. brucei rhodesiense* (more servere)
West African: caused by* T. brucei gambiense *(sleepy symptoms)
80
Symptoms of African sleeping sickness
- spreads through the blood: fever, headache, sweating & swelling of the lymph nodes
- spread to CNS (central nervous system): Behavior changes, Drowsiness during the day (insomnia at night)
- Coma
81
African sleeping sickness treatment
- suramin: 6 weeks of therapy
- melarsoprol: VERY toxic and can itself be fatal (Arsenic compount- causes poisoning)
- pentamidine
