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510 Final > FInal > Flashcards

FInal Flashcards

1
Q

Principles of Treatment

A

Early diagnosing & complete treatment, rational use of antimalarial agents, combo therapy & weight based dosing

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2
Q

early diagnosis & complete treatment

A

○ All patients should have a parasitological diagnosis: Light microscopy or RDTs
Uncomplicated can progress to severe if untreated

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3
Q

Rational use of antimalarial agents

A

○ Limit unnecessary use
○ Identify other febrile illnesses better
Only those with malaria should get the medicine

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4
Q

Combo therapy

A

○ Treat with at least 2 effective meds with different MOA = much harder to mutate for both
○ Helps prevent & delay resistance
○ Choose ACT should be based on efficiency and adherence in that region
§ Fixed doses of combo ACT is preferred
§ Solid formulation > liquid
§ Fixed dose combos of all recommended ACT are available except artesunate + SP
Pediatric formulas are not available

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5
Q

Weight based dosing

A
  • Weight based dosing
    ○ Maximize rapid clinical and parasitological cure
    ○ Treatment should minimize transmission (and hypnozoites)
    ○ Need sufficient concentrations to eliminate the infection
    Clinical cure = symptoms go away
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6
Q

Clinical cure vs parasitological cure

A

symptoms go away; parasite is gone

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7
Q

Drug groups

A
  1. treat acute attack
  2. effect radical cure (cure + prevent relapse)
  3. chemoprophylaxis (kills sporozoites)
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8
Q

Chloroquine

A

works well against vivax; causes buildup of heme; was developed after quinine and last longer in blood. This caused quinine prices to drop but resistance has developed

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9
Q

Primaquine

A

Treats hepatic stages of all malaria (prevents recrudesence); hypnozoites of vivax/ovale (prevents relapse) - x14 days
Is the radical cure for vivax

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10
Q

Adverse effects of primaquine

A

GI, hemolysis with G6PD deficiency; can give low dose to avoid this

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11
Q

Artusenate & derivatives

A

ACT Therapy; uncomplicated malaria with SP; can cause delayed hemolysis

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12
Q

Artemesenin compound potential danger for:

A

reinfection as they clear from the blood rapidly and co-drug helps the rest. But window of time where artemesinin is gone and only have co-drug, reinfection means parasite will persist with co-drug = resistance developing

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13
Q

Primaquine MOA

A

Primaquine
• Inhibits ETC in plasmodium
• Active against hepatic stages of all malaria
• Active against hypnozoite stages of vivax/ovale
• Use for presumptive anti-relapse, prophylaxis for short duration travel & radical cure of vivax/ovale
Adverse effects: GI disturbances, methemoglobinemia, hemolysis in those with G6PD deficiency

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14
Q

G6PD Deficiency

A

G6PD deficiency: sex linked disorder with some protection to falciparum & vivax but susceptibility to oxidant hemolysis; rarely causes this issue without primaquine so most people don’t know they have it. Screening is not really available. Hemolysis will stop once the drug is stopped

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15
Q

Parenteral

A

administered anywhere besides oral

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16
Q

How do you treat uncomplicated falciparum?

A

ACT x 3 days; primiquine to decrease transmission

Artemether + L; Artesunate + A; Artesunate + M; Artesunate + SP; D+P

Risk groups: pregnant, obese, co-infection, non immune travel, uncomplicated hyperparasitemia

Avoid monotherapy; dose by weight; treat symptoms

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17
Q

How do you treat uncomplicated non falciparum?

A

Primiquine; low dose for those with G6PD deficiency

Not for pregnant women, infants <6 months

Radical cure for vivax/ovale; hemolysis will stop when drug is stopped

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18
Q

How do you treat severe malaria?

A

IV or IM artesunate for 24 hours; 3 days oral ACT; single primiquine

Parasite count; hematocrit; BGL

1st: prevent death
2nd: prevent disability & recrudescence

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19
Q

How do you treat severe malaria in pregnant women?

A

Parenteral artusenate full doses; artemether IM if unavailable; Parenteral quinine if unavailable

Those in 2nd or 3rd trimester are more likely to get severe malaria; 50% mortality with treatment

Severe malaria can present after delivery

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20
Q

How do you treat mixed infections?

A

ACT

Vivax is the most common complication of falciparum

Detect via PCR or microscopy and some RDT

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21
Q

Falsified medication

A 
Little to no active ingredient
Sometimes harmful substance
Intended to deceive
Hard to distinguish
Encourage resistance
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22
Q

Substandard medication

A

Incorrect amounts or stored incorrectly; artemisinin & derivatives have built in instability & are sensitive to heat; humidity and heat problems; sold past expiry date

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23
Q

How do you treat coma?

A

Maintain airway; R recovery side; exclude other causes; avoid harmful treatments; intubate if necessary

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24
Q

How do you treat hyperprexia?

A

Treat if fever > 38.5 with antipyretics; no NSAIDs; fanning; cooling blanket; ice packs

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25
Q

How do you treat convulsions?

A

Maintain airway; admin benzos; check BGL; >2/day is severe malaria

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26
Q

How do you treat hypoglycemia?

A

Check BGL; correct hypoglycemia; maintain with glucose infusion

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27
Q

How do you treat severe anemia?

A

Transfuse (<5 = high setting; <7 = low setting)

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28
Q

How do you treat acute pulmonary edema?

A

ARDS = prop to 45 angle; give O2 & diuretic; hypoxemia = stop IV; intubate; + pressure

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29
Q

How do you treat acute kidney injury?

A

Exclude causes; check fluids; hemofiltration, hemodialysis & peritoneal dialysis

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30
Q

How do you treat bleeding/coagulopathy?

A

Transfuse; vitamin K inj

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31
Q

How do you treat metabolic acidosis?

A

Exclude/treat hypoglycemia, hypovolemia or septicemia; add hemofiltration or hemodialysis; body INC lactic acid due to DEC Hb

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32
Q

How do you treat shock?

A

Suspect septicemia; blood culture; parenteral broad abx; correct hemodynamic disturbances

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33
Q

How do you treat vomiting?

A

Parenteral antimalarial treatment until oral is tolerated; then 3 day ACT; antiemetics are sedative and can confound severe malaria

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34
Q

List the special risk groups who may need chemo prevention

A

pregnant women, infants, seasonal children, non immune travelers

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35
Q

Describe IPTP

A

In endemic areas give IPT + SP in 1st or 2nd pregnancy; dose 1 month apart

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36
Q

Describe IPTI

A

<12 months in moderate-high transmission, give IPT + SP at 2nd/3rd DTP/MMR

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37
Q

Describe Seasonal chemo treatment

A

SMC + monthly amodiaquine + SP for children <6 months each season

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38
Q

Describe non immune traveler treatment

A

Start chemoprophylaxis before entering endemic area

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39
Q

How does chemoprevention work?

A

prevent malarial illness by maintaining therapeutic levels throughout the period of greatest risk

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40
Q

What are the 3 types of chemoprevention?

A

Causal prophylaxis: inhibit liver stage development (pre-erythrocytic); stop after leaving endemic area

Suppressive prophylaxis: kill asexual blood stages; taken at least 4 weeks after leaving the area

Disruptive prophylaxis: experimental; monoclonal antibodies disrupt malaria binding to host

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41
Q

What does the Mululaza plant do?

A

African shrub that reduces the level of parasites; chimpanzees chew on leaves when not feeling well

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42
Q

What does clove/nutmeg/basil/onion do?

A

reduce body’s repair of free radicals (which normally allow infected cells to be exposed longer)

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43
Q

What does the cinchona tree produce?

A

Adean (from the Andes) tree bark; Jesuit’s Bark; secondary compound is quinine which interferes with Hb digestion & parasite is poisoned by toxic residue; can’t prevent but can treat
Cinchona is difficult to cultivate; doesn’t produce quinine for 5 years and cant harvest bark for 15 years

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44
Q

Describe British India’s issues

A

Segregation like in Africa; built dams across riverways making miles of irrigation canals; irrigation canals disrupted drainage = rain bogs; 2x more swollen spleens than in non-irrigated villages

45
Q

What happened in the US Mississippi River valley?

A

Malaria from African slaves spread into the boggy swamp areas between the Appalachian and Rockies making a great mosquito habitat; 80% settlers in Pike County IL die and many Norwegian settlers; destroyed effort to build a canal between the great lakes & Mississippi river.

46
Q

What happened during the Coosa river dam project?

A

○ In Alabama; damned the Coosa river increasing the 25 cases from the year before to 600 hundred; schools close down & county officials beg for funding to enact Gorgas’ methods; many damns in the south were created for hydropower industry but the local power company denied any connection between the dam and malaria; residents file 700 lawsuits
○ Gorgas was a witness for the power company and said many people agreed they cant fly more than 200 meters from birthplace; says the mosquitoes came from the locals’ land even though the quadrimaculotus species specializes in clear water not dirty puddles
Lawsuits were thrown out and they had the greatest outbreak in the history of Alabama

47
Q

Why did malaria vanish from the US?

A

○ Railroads were built = people can move away from rivers
○ Farmers reclaim wetlands by burying tiles & pumping water out
○ Agriculture adjustment act mechanizes southern farms
○ Black sharecroppers relocate to cities = less reservoirs for mosquitoes
○ Government antimalarial regulations for future dams
Better housing and roads = DEC mosquito habitat and INC protection

48
Q

Why did malaria vanish from Britain?

A

4 crop rotation system from Holland

More plentiful cow & hog flesh diverted anopheles; local maculopennis preferred calves

49
Q

What’s the story on quinine?

A

Comes from the cinchona tree & is used to treat malaria. It is the earliest medication for malaria but it does have side effects: cinchonism - tinnitus/deafness, headache, nausea, bleeding, renal failure. Is known as Blackwater fever because it caused diarrhea, vomiting, black urine and death

50
Q

What’s the story on quinicrine

A

persists in blood for a week; not as effective as quinine against vivax; causes jaundice and psychotic reactions; soldiers hated it
○ Soldiers started to get sick and it was thought that they weren’t taking it correctly; many infected with malaria
Resistance spreads thanks to heavy use

51
Q

What’s the story on chloroquine?

A

lasts longer in blood, lower side effects, more effective, easy to make; widely available and encouraged to take as soon as fever comes = INC drug pressure on malaria
○ Quinine prices drop when chloroquine hit the market and interest in quinine decreases
Resistance developed as well in SEA; resistant falciparum developed the ability to live better than non resistant malaria in 2 mosquitoes = becomes the dominant strain

52
Q

What’s the story on artemisinin compounds?

A

○ Created after everything above; artemisia is one of the first plants tested; boiled in tea (incorrectly) then learned to prepare with lukewarm tea and chinese kept it a secret. Caseload drops from 2 million to 90k
○ Novartis launched an artemisinin derivative (artemether + lumefantrine called Riamet)
Still took years to get support for this drug and by the time it was supported, resistance had already developed due to unethical and criminal sales & recommending insufficient doses

53
Q

How could bacteria be used against malaria?

A

B. thuringiensis israelensis designed to only infect mosquito larvae; more environmentally friendly than fish

54
Q

How can a fungus be used against malaria?

A

entomopathogenic fungi that will invade and multiply inside the mosquito and kill it like beauveria bassiana and metarhizium anisopliae on gambiae

55
Q

Red flag indicators:

A

Rain, sunshine, humidity levels can all predict times when malaria is going to peak or drop
Can keep track of the rise or drop of malaria cases if we monitor these factors

56
Q

Examples of diffuse solutions

A 
Improving economy + poverty
Roads
Electricity
Safe water
Strengthen healthcare systems
Education/awareness
Avoid mosquito habitats
57
Q

Examples of focused solutions

A

Vaccines
New Meds
Spraying/vector control
Genetic modification

58
Q

Anti-parasitic immunity:

A

antibody response & cell mediated response.

Targets parasite to try to prevent the infection

59
Q

Anti-toxic immunity

A

suppresses toxic response and reduces symptoms.

Doesn’t reduce parasite load, just makes you feel less sick

60
Q

What type of targets could a vaccine have?

A
  1. Parasite stage: direct anti sporozoite
    1. Hepatozoite: direct anti hepatozoite
    2. Asexual erythrocytic: anti host erythrocyte, antibodies blocking invasion, anti receptor ligand
    3. Gametocytes: anti gametocyte, anti host erythrocyte, antibodies blocking fertilization, antibodies blocking egress (leaving) from mosquito gut
      Must target the sporozoite if you want to prevent infection
61
Q

What are some challenges to vaccines?

A 
Malaria can easily mutate
Protozoa are more complicated than bacteria = complex vaccine 
High cost to develop
Multiple doses needed
Different vaccine for different strain
Partial immunity for short duration
Side effects
62
Q

DDT :

A

use started in WWII; it was long lasting, odorless, did not dissolve, did not seem to affect people, easy to make, easy to spray; DDT war on insects propaganda. Rockefeller Foundation
Resistance accumulated & several side effects from over-using

63
Q

Insect treated nets ITN

A

extremely effective when used correctly; long lasting ITN or LLITNs; SSA population still doesn’t have complete access and 20% of anyone with ITNs don’t use them correctly; complaints of itching and headaches from the insecticide; unable to afford them; used for fishing (bad for fish ecology); used to create privacy; embarrassed to show poverty and bringing a torn net in for a new one; difficulty hanging the net; too hot to sleep under; some people believe other things cause malaria too; no protection for daytime feeding; resistance to insecticide

64
Q

Indoor residual spraying IRS

A

works well but has to be maintained and continuously sprayed; health considerations and potential for resistance

65
Q

Chemoprevention

A

intermittent preventive treatment in pregnancy IPTp has increased; half of eligible pregnant women are taking 1 dose, less are taking 2 and much less are taking 3 or more. IN children, it has been limited due to concerns about what age is ok; some countries do seasonal malaria chemoprevention SMC like Niger, Mali, Guinea

66
Q

Better treatment

A

some increase in Children Under 5 with falciparum treated with an ACT

67
Q

Diffuse solutions:

A

improving poverty & economy, leveling roads, providing electricity, safe water, strengthen healthcare systems, increase awareness and education, minimize and avoid mosquito habitats

68
Q

Mosquito life cycle

A

Eggs hatch in water and transition into larvae
4 aquatic larval stages
Aquatic pupae stage
Adult (imago) emerges

69
Q

Mosquito mating cycle

A
  1. Mated adult females hibernate in sheltered sites
    1. Females become active in late spring/early summer and take a blood meal
    2. Females lay eggs in standing water; eggs hatch within 2-3 days
    3. Adults appear 7-10 days later; adults mate; female takes blood meal
    4. Females lay eggs on standing water; eggs hatch within 2-3 days
      a. Last generation of adults appear in fall; adults mate; males die and females enter hibernation
      b. Steps 4 and 5 can be repeated = amplification stage
70
Q

What do mosquitoes feed on?

A

nectar and other sugar sources; females need protein from blood to develop their eggs

71
Q

What do mosquitoes use to home in on prey

A

Olfactory cues: sensors on antennae to search for CO2 (which rises in plumes because it is warm); sensed from hundreds of feet away

Visual cues: two types of eyes
Large compound eyes for motion detecting
2 photosensitive simple eyes (ocelli) to home in on light and bright colors (which can be used to trap mosquitoes with colorful contrasts)

Thermal cues: sensors on antennae and mouth helps fish for veins; detect heat from warm blooded bodies

72
Q

What is the first thing mosquitoes do when they take a blood meal?

A

Injects saliva that numbs area and keeps blood from clotting, then sucks blood

73
Q

2 mosquito eye types

A

Large compound eyes for motion detecting

2 photosensitive simple eyes (ocelli) to home in on light and bright colors (which can be used to trap mosquitoes with colorful contrasts)

74
Q

What does mosquito saliva do

A

Negatively affects:

  • Vascular constriction: makes vessels dilate
  • Blood clotting: blood flows more easily
  • Platelet aggregation: no clotting
  • Angiogenesis and immunity: reduces local immunity
  • Stimulates inflammation
  • contains enzyme to breakdown sugar and antimicrobial to reduce infection in their sugar meals
75
Q

Open marsh water managment

A

connect the marsh to a pond or canal and give predators like fish access to larvae; reduces other control methods

76
Q

Rotational impoundment management

A

pump water into marsh in late spring and summer to prevent laying eggs on damp soil; marsh is allowed to drain in the fall, winter and early spring; gates in the culverts permit fish, crustaceans and other marsh organisms to enter and exit, and feed on whatever is left

77
Q

Removal of breeding habitats

A

Dredging (wash the larvae away), larvivorous fish

78
Q

Insecticidal use types

A

larvacide and adulticide

79
Q

larvacide

A
  • contact posion means bug has to come into contact in high enough concentrations to kill; ex: organophosphates like Raid; some resistance
  • insect growth regulators like methoprene which is more targeted and persists longer
  • Surface films: larvae will get in more contact with it
  • Stomach poisons: bacterial agents
  • Biological agents: fungi, nematodes, fish
  • Treat mud several meters from puddles
80
Q

adulticid

A
  • Paris Green (copper acetoarsenite) and petroleum byproducts; discontinued because of high toxicity and pollution
  • Treated bed nets
  • Indoor residual spraying IRS
81
Q

predators for mosquito control

A

gambusia affinis but they have negative impact on fauna; dragonfly adults eat mosquitoes and larvae; some lizards and geckos; predator mosquito toxorhynchites; predator crustaceans

82
Q

releasing insects with lethal genes

A

GM to express a repressible lethal gene; offspring with that gene do not survive to adult stage because they are missing the dietary additive in the wild

83
Q

Sterile insect technique

A

sterile males compete with native population and unable to produce viable offspring; eradicate native population
○ Challenges: loss of male fitness after sterilization = less attractive to males

84
Q

Transgenesis

A

make them refractory to plasmodium infection; self limiting

Need effective germline transformation system
Need suitable promoters
Need effector genes that impair parasite development or act as parasiticidal agents

85
Q

Paratransgenesis

A

introduce modified symbiotic bacteria to deliver anti pathogenic gene products and reduce vector competence; not self limiting

Need to choose symbiont related to vector and malaria
Needs to be easily cultivable and amendable
Needs uncompromised fitness of symbiont
Needs suitable method for reintroduction like feeding in nectar
Needs spread of symbiont in vector population

86
Q

behavioral modification

A

eliminate part of their sense of smell; develop new repellants; photosensory

87
Q

monitor mosquito population

A

track adult mosquito (landing rates, mechanical traps) or larvae (traps or in situ counting)

88
Q

human factors

A

herd immunity; migration; parasite reservoir

89
Q

drug factors

A

half life; dosing; pharmacokinetics; cross resistance; drug pressure

90
Q

Parasite factors

A

fitness, GM; transmission level; cross mating; recombination; migration

91
Q

vector/environment factors

A

clonal multiplicity; vector affinity of parasites

92
Q

Challenges on data collection

A
  • 36.5% of statistics are made up
  • Politicization of results: highlighting successes and not failures
  • Lack of staff, hardware & software
  • Indonesia: 2 encounters are counted as 2 or more cases
  • Cases not presenting to clinic are not counted
  • Most of malaria reporting is done on clinical diagnosis not lab
    ○ 80% false + in Angola and 90% false + in Sudan

PMI & WHO use diagnoses from deaths from fevers as they can “retroactively diagnoses malaria with household questionnaires”

93
Q

challenges/limitations overall

A

○ Seasonal variations =red flag indicators could help overcome complexity of environment
○ Politicization of results = Oliver Sabot using map of countries that ever had malaria shaded and showing its regression through time (no regional distinctions and historically inaccurate)
○ Lack of software and hardware =expensive and can’t train/retain personnel
○ Paper records and poor collection records
○ Decision makers misunderstand data application-> they distort data to fit their needs and agenda
○ Measurement bias

94
Q

What is drug resistance

A

ability of parasite strain to survive/multiply despite administration and absorption of a drug in doses equal to or higher than what’s recommended

95
Q

What are the factors in generating drug resistance?

A

Drug must gain access to the parasite or infected RBC for the duration of time necessary for its normal action (bowel movement before it’s able to work does not mean resistance)

Must demonstrate parasitemia in patient who has received an observed dose or antimalarial drug

Must demonstrate that adequate blood concentrations occurred (analyze that blood has therapeutic levels of the medicine)

Can cause treatment failure but not all treatment failure is from resistance

Incorrect dosing, non compliance, drug interactions, poor absorption, misdiagnosis

96
Q

What is the most important factor in drug resistance

A

overall drug pressure

97
Q

Detecting resistance in vivo

A

treatment of group of symptomatic and parasitemic individuals with known drug doses & monitoring or parasitological/clinical response
○ Sequester patients 7-14 days after treatment to avoid reinfections

Advantage: gives best info on efficacy (does this treatment work); clinical response emphasis; can detect hematological recover after illness

Disadvantage: not standardized techniques = hard to compare studies; diminished drug therapeutic efficacy can be masked by high acquired immunity; other external factors

98
Q

Detecting resistance in lab

A

fingerprick blood exposed to known quantities of drug and observe under microscopy for inhibition of maturation into schizonts

Advantage: more control on external variables like acquired immunity; multiple tests can be done

Disadvantage: correlation of clinical response is not clear; prodrugs like proguanil that require host conversion to active metabolite cannot be tested; non-falciparum strains cannot be evaluated in vitro; more expensive

99
Q

Detecting resistance in animal models

A

in vivo in a non human

Advantage: similar to in vivo; no host immunity

Disadvantage: similar to in vivo; parasites that can survive non humans can only be tested

100
Q

Detecting resistance in molecular techniques

A

PCR to indicate presence of mutations encoding resistance to antimalarial drugs

Advantage: frequency of mutation occurrence from patients could indicate frequency of resistance in population; only need small amounts of genetic material, not live parasites; independent from host and environmental factors

Disadvantage: expensive; expertise needed; known gene mutations for resistance are limited; confirmation of association between mutation & resistance is difficult (may involve multiple genes)

101
Q

Detecting resistance in case reports & passive detection

A

use reports of treatment failure

Advantage: low investment time and money; ongoing basis; good red flag source

Disadvantage: rates of resistance cannot be calculated

Passive detection: treated patients are told to come back if symptoms return or persist and only those who return are considered treatment failures = biased results

102
Q

Preventing resistance

A

Reduce overall drug pressure, improve how we use drugs, combination therapy

103
Q

Reducing overall drug pressure

A

Most important factor in drug resistance; reduce how many bugs are exposed to the drug

Better diagnoses, encourage restrictive drug use, promote better prescribing practices, prophylaxis programs only where compliance is high, the drug is effective & in high risk regions

Founder effect: characteristics of a small founding population can greatly determine the rest

104
Q

Improving how we use drugs

A

DOT directly observed therapy

Single dose regimens (SP, mefloquine)
- Weight benefits and risks of single dose DOT against the costs (have long half lives = take longer for body to clear an adverse reaction)

Close follow up and prompt retreatment PRN

Reliable microscopy in detecting low levels

105
Q

Combination therapy

A

Combine malaria drug with artemisinin derivative

Artemesinin compounds reduce parasite levels & likelihood that gametocytes with resistant genes will pass on

Could possibly be combined with vaccines designed to inhibit transmission in the future

Promotes mismatched half lives between these combination of drugs = can be re-infected while sub therapeutic drug levels are still present

  • Take combo pill on day 1 = equal amounts of drug 1 and drug 2
  • Day 2 = 2 high drug 1 amounts and lower drug 2 amounts
  • Day 3 = 3 high drug 1 and very low drug 2
106
Q

Resistance 0 1 2 3

A

1st graph: successful treatment

RI: delayed recrudescence; same initial response as the first but there were a few bugs left that were more resistant and immune system was not able to mop them up

Level 2 resistance AKA early recrudescence: parasite levels (two types of graphs)

Level 3: virtually no response with drug

107
Q

EC: artemisinin compound discovery

A

Project 523= China found it from one of the 10 plants but kept it a secret

Was initially incorrectly extracted
WHO only approved it for use when US started producing it (Novartis)

108
Q

EC: quinine escaped africa

A

Peru banned export of cinchona seeds (the only way to get it was Andes cinchona bark until late 19th century)

Manuel Incra spent 5 yrs gathering seeds, British trader Charles Ledger smuggled them out of the country “ledgeria”

Cinchona was very difficult to cultivate and the Dutch spent 30 yrs w/Kina bureau trying to make it widely available

510 Final (1 decks)

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