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Eukaryotic Microbio > Parasitology > Flashcards

Parasitology Flashcards

1
Q

What is a parasite?

A

An organism which lives briefly or permanently in the human body

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2
Q

Why are parasitic diseases so bad?

A
  • No licensed vaccine for any human parasitic pathogen
  • Drug discovery is lacking
  • Can affect growth retardation in children, loss of cognitive skills and development in young children
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3
Q

What is symbiosis?

A

When two different organisms live/interact together

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4
Q

What is mutualism?

A

A obiligatory relationship between two organisms. both partners benefit from the association

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5
Q

What is commensalism?

A

Where one partner benefits from the association, but the host is not helped or harmed.

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6
Q

What is parasitism?

A

One organism will harm or live at the expense of the host

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7
Q

What are the 5 modes of transmission of a parasite?

A
  • Fecal-oral transmission (intestinal protozoa and intestinal helmiths rely on this route)
  • Trophic transmission (Parasites make use of the predator-prey relationship present between the hosts)
  • Vertical transmission (Transmission from mother to offspring, through placenta or breast milk)
  • Direct penetration (Parasites bore their way in to the hosts)
  • Vector transmission (Parasites move between vector and host as the vector takes a blood meal)
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8
Q

What is vector competence?

A

The ability of a particular type to become infected with a specific pathogen, to transmit a specific pathogen, or both.

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9
Q

What is vector capacity?

A

Vector capacity is linked to the extrinsic factors contributing the ability of vector to transmit

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10
Q

How do parasites find their way around?

A

Parasites acquired mechanisms to recognise host cues to find their specific site

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11
Q

What are the strategies parasites have to maintain their position on or within the host?

A
  • Invasion of intestinal tissue
  • Use of adhesive disks
  • Tapeworms use scolex
  • Plasmodium falciprarum erythrocyte membrane protein 1, protrudes from the membrane of infected cells and forms knobs> important for the binding to capillary walls
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12
Q

What are the main sources of parasitic infection or infestation?

A
  • Water
  • Soil
  • Raw veg and fruit
  • Animals
  • Fish
  • Vector (arthropods)
  • Contact
  • Blood transfusion
  • Congenital or transplacental
  • Sexual intercourse
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13
Q

What are the methods to prevent and treat parasitic infections?

A
  • Intervention designed to reduce parasite transmission
  • Use of anti-parasitic drugs
  • Vaccines
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14
Q

What are the strategies to reduce parasite transmission?

A
  • Most effective way is to cut the contact between the parasite and host
  • Mosquito control
  • Clean food and water supplies (many parasites are spread due to consumption of contaminated undercooked or raw meat, Toxoplasma gondii prevalence has decreased by freezing meat, modern farming has also helped in reducing parasite transmission)
  • Adequate sanitation (proper removal of faecal matter is important Example, Hook worm caused by necator americanus eradicated from 1909-1914, poor could not afford shoes )
  • DDT (kills insects by opening sodium ions channels on neurons leading to unregulated neuron firing, spasms and death)
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15
Q

How do insects maintain resistance to DDT?

A
  • Insects carry mutations in the genes coding sodium ion channel proteins
  • Upregulation of P450 genes, enzymatically oxidise certain molecules including DDT in certain insects
  • Can mean that malaria levels are increased
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16
Q

What are some alternatives to DDT?

A
  • Organophosphates: malathion, inhibits acetylcholineesterase, which hydrolyze the neurotransmitter acetylcholine
  • Carbamate insecticide: bendiocarb, toxic to mammals
  • Pyrethroids: deltametrin, disrupts sodium ion channel proteins on neurons (harmless to humans but toxic to fishes)
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17
Q

What are heliminths?

A

They are multicellular, bilaterally symmetrical parasites

  • Trematodes
  • Cestodes
  • Nematode
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18
Q

What are trematodes?

A

They are parasites of vertebrates, require one or more intermediate hosts

Eggs shed by the adult worm pass outside to the environment, and larva hatches and swims away to infect the intermediate host

Infiltrate directly through the skin and develop into adults

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19
Q

What is a stage known as metacaercariae?

A

Enter a second intermediate host, and wait to be ingested

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20
Q

What are examples of termatodes?

A
  • Blood flukes
  • Hepatobilary flukes
  • Lung flukes
  • Intestinal flukes
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21
Q

What is Schistosomiasis-Bilharzia?

A
  • Affects approx 200 million people worldwide
  • Schistosoma mansoni, S. haematobium, and S. japonicum

Schistosoma are diecious and human infection takes place by direct penetration of carcariae

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22
Q

`What is the lifecycle for Schistosoma?

A
  1. Eggs pass from the host in stool and urine
  2. Eggs hatch in water and release immature larvae
  3. Miracidia penerate a snail
  4. In the snail miacida develop into sporocysts
  5. Sporocysts become cercariae, which are released in water and may penetrate a persons skin
  6. During penetration, cercariae develop into schistosomula and travel to the liver to mature
  7. Paired adult worms travel to veins in the intestine or bladder, where they lay eggs
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23
Q

What are the symptoms to Schistosomiasis-Bilharzia?

A
  • Itchy skin
  • Fever
  • Chills
  • Cough
  • Muscle aches
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24
Q

What are the symptoms of Schistosomiasis-Bilharzia caused by?

A

By the eggs produced by worms, and NOT the worms themselves

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25
Q

What are Cestodes?

A

They are tapeworms

Flat and ribbon-like body

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26
Q

Where are adult tapeworms found?

A

In the small intestine

May cause abdominal distress

Infections are usually well tolerated or asymptomatic

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27
Q

Where are larval tapeworms found?

A

In extraintestinal tissues

They produce systemic infections with clinical effects related to the size, number and location of the cysts

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28
Q

What are the characteristics of cestodes?

A
  • No mouth, digestive tract or vascular system
  • Scolex (head) attaches to intestinal wall by suckers
  • Tegument (body) of scolex absorbs nutrients
  • Proglottids (segments) forming tegument
  • Tegument contains male and female reproductive organs producing infective eggs
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29
Q

In the gut, what do the hatching eggs release?

A

Motile larva (onchosphere) that migrates through the gut wall and blood vessels to encyst in muscle forming cysticerci

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30
Q

What are some important flatworms?

A

Intestinal
- Taenia saginata (caused by contaminated, uncooked beef)
- Taenia solium
(caused by contaminated, uncooked pork)

Systemic

  • Echinococcus granulosus (dog tapeworm)
  • Echinococcus multilocularis (rodent tapeworm)
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31
Q

What is the lifecycle of Taenia soilum and T. saginata?

A
  1. Eggs passed in faeces
  2. Cattle and pigs infected from ingesting eggs
  3. Eggs hatch releasing onchospere which migrates through gut wall and blood vessels to encyst in striated muscle forming cysticerci
  4. Raw or uncooked meat
  5. Scolex attaches to intestine
  6. Adults in small intestine
32
Q

What are the symptoms of taeniasis?

A
  • Most people have no or mild symptoms
  • Digestive tract problems
  • Proglottids can be detected in the faeces
  • Infection with T. solium tapeworms can result in human cysticercosis, which can cause seizures and muscle or eye damage
33
Q

What is Ascaris lumbricoides?

A
  • Found more in tropical climates
  • Estimated to affect one billion people worldwide
  • Female worms produce approximately 200,000 eggs per day
  • Eggs are highly resistant to adverse conditions
34
Q

What is the life cycle of Ascaris lumbricoides?

A
  1. Adult worms in small intestine lay large numbers of eggs
  2. Eggs passed with faeces and contaminate vegetables
    3-4. Larvae develop inside eggs; swallowed when present in uncooked food
  3. Enter small intestine where larvae hatch
  4. Larvae penetrate gut mucosa; carried through the hepatic circulation to heart and lungs
  5. Larvae develop; escape from capillaries into the alveoli. Re-enter stomach via trachea and oesophagus, pass to small intestine and grow to adulthood
35
Q

What is the lifecyle of Toxocara canis and cati?

A

1-2. Eggs from dogs and cats passed in faeces and mature in soil

  1. Eggs ingested and hatch in small intestine
  2. Larvae penetrate intestinal mucosa, enter blood stream and are carried to a variety of tissues
36
Q

What are Protozoa?

A

Unicellular, heterotrophic, eukaryotic organisms comprising four organization types: amebae, flagellates, ciliates, and parasitic sporozoans.

Most species causing human disease are members of the phyla Sacromastigophora and Apicomplexa.

Some protozoa have structures for propulsion or other types of movement.

37
Q

What are the organelles of movement for protozoa?

A
  • Euglenoid Flagelum
  • Paramecium Cilia
  • Amoeba Psuedopodia
38
Q

What are the 3 life cycle stages?

A
  • Trophozoite (active multiplying stage. Spend time for eating)
  • Cyst (inactive stage. non growing, and engulfed within a tough wall, and infective to the human host)
  • Oocysts (results from sexual reproduction in the Apicomplexa)
39
Q

What are the 3 forms of reproduction in protozoa?

A
  • Asexual (binary fission, schizogony, endodyogeny)
  • Sexual: involves the production of gametes, fertilisation to form the zygote, encystation of the zygote to form an oocyst and the formation of infective sporozoites within the oocyst.
  • Asexual and sexual: In the Apicomplexa of medical importance
40
Q

What is the nutrition for protozoa?

A

Protozoa are holozoic: can use organic materials, particulate or in solution.

Amebas engulf particulate food or droplets through a sort of temporary mouth, perform digestion and absorption in a food vacuole, and eject the waste substances.

Many protozoa have a permanent mouth, the cytosome or micropore, through which ingested food passes to become enclosed in food vacuoles.

Pinocytosis is a method of ingesting nutrient materials whereby fluid is drawn through small, temporary openings in the body wall

41
Q

What are the causative agents for Malaria?

A

Plasmodium falciparum, P. vivax
P. ovale
P. malariae

42
Q

What are the health impacts of malaria?

A
  • 40% of world population at risk
  • 300 to 500 million cases annually
  • In 2013, approximately 584,00 people died from malaria
  • 3000 children under the age of 5 fall victim to malaria every day
43
Q

What are the general features of apicomplexa?

A
  • Monophyletic group of almost exclusively parasitic protozoa with specialised invasive stages.
  • The invasive stage display a polarity and has unique organelles & subcellular structures at the apical end (i.e’ apical complex).
  • Most apicomplexans invade and replicate within the host cells.
  • Membrane bound apical organelles, micronemes and rhoptries, play an important role for invasion and attachment.
  • A protein-motor complex provides the force needed for motility, which is required for invasion.
44
Q

What are Anopheles vector?

A

Only Anopheles can transmit human malaria

They can also transmit filariasis and some arboviruses

NOT found in altidues above 2500m

They can fly 2-3 km from their breeding sites

Larvae can survive in small ponds and puddles

Larvae avoid organically polluted waters, such as those contaminated with human or animal faeces

45
Q

How does plasmodium manipulate vectors for efficient transmission?

A
  • Alters the behaviour of mosquito vectors to increase the likelyhood of transmission
  • Decreases the mosquito blood-feeding and other risky behaviours during the pro-infectious phase
  • Parasites then increase vector feeding rate once they have become infectious
  • Infectious females are more attracted to hosts
46
Q

What are the determinants of transmission?

A
  • Frequency of transmission depends on density and infectivity of anopheline vectors
  • Temperature (between 25-30C)
  • Rainfall & Humidity
  • Man made environmental changes and agricultural patterns
  • Population displacement, urbanisation and mobility
  • Socio-economic and housing factors
  • Personal protection
  • Effect of vector control and drugs
47
Q

What are the determinants of risks of disease and health?

A
  • Host genetics
  • Susceptibility
  • Nutrition
  • Socio-economic factors
  • Drug resistance
48
Q

What is the plasmodium life cycle?

A
  1. Mosquito blood meal
  2. Pre-erythrocytic human infection
  3. Asexual erythrocytic stage
  4. Intra-erythrocytic gametocyte development
  5. Mosquito midgut
  6. Oocyst
49
Q

How long is the exoerythrocytic phase?

A

5 and 21 days

50
Q

How long is the erythrocytic phase?

A

48 hours

51
Q

What are the stages of malaria?

A
  1. Sporogonic cycle
  2. Infective period
  3. Prepatent period
  4. Incubation period
  5. Clinical illness
52
Q

What are the 4 species of human plasmodia?

A
  1. Plasmodium falciparum
  2. Plasmodium vivax
  3. Plasmodium ovale
  4. Plasmodium malariae
53
Q

What are the early symptoms of malaria?

A
  • Headache
  • Malaise: a general feeling of discomfort
  • Fatigue
  • Nausea
  • Muscular pains
  • Slight diarrhea
  • Slight fever, usually not intermittent
54
Q

What is malarial paroxysm?

A

The malaria paroxysm comprises three successive stages:

  • Cold stage
  • Hot stage (temp can reach 40-41C)
  • Sweating stage (profuse sweating so temp goes down)
55
Q

What are factors effecting clinical presentation?

A
  • Parasite factors
  • Host factors
  • Mode of transmission
56
Q

What are some malaria complications?

A
  • Cerebral malaria
  • Congenital malaria
  • Anaemia
  • Renal disorders
  • Blackwater fever
  • Dysenteric malaria
  • Algid malaria
  • Pulmonary oedema
  • Splenomegaly
57
Q

How does malaria develop?

A
  • Pathogenesis is due to parasite and its way of altering the immune system and red blood cells
  • Rupture of infected red blood cells cause anemia. Also a decrease of RBC production
  • Massive intravascular haemolysis results in excretion of increased amount of haemoglobin in the urine (dark urine). This is known as blackwater fever, which has been linked to quinine use, and the development of antibodies to the infected erythrocytes.
  • Parasitized erythrocytes adhere to capillary walls and each other (rosetting), which leads to the blockage of small blood vessels. If this blockage happens, the consequences are very severe.
  • Increased activity of the reticuloendothelial system leads to enlarged liver and spleen. Splenomegaly is related to overproduction of, IgM, and the reduction of T lympocytes.
  • Acute renal failure may occur due to tubular necrosis resulting from red blood cells sludging and renal anoxia.
  • Due to focal ischemic changes in intestinal wall capillaries, abdominal pain, nausea, vomiting and upper gastrointestinal bleeding may occur.
  • Rapid development of hypotension and impairment of vascular perfusion can happen (known as algid malaria). Vascular collapse and shock can develop quickly due to gram-negative septicemia, pulmonary edema, gastrointestinal hemorrhage, splenic rupture or untreated dehydration.
  • Pulmonary edema may manifest in an oliguric or anuric patients as a complication of overzealous parenteral fluid administration. Pulmonary edema also leads to metabolic acidosis (low blood pH).
  • Hypoglycaemia can be seen especially in children and pregnant women due to increase consumption of glucose by parasites, and host after quinine therapy which stimulates B cells of the pancreas. This then decrease production of glucose by the liver due to cytokine mediated suppression of gluconeogenesis.
58
Q

What are the 3 RBC changes?

A
  • Cytoadherance and sequestration
  • Rosetting
  • Deformability
59
Q

What are the 3 types of acquired immunity against plasmodia?

A
  1. antidisease immunity, conferring protection against clinical disease, which affects the risk and extent of morbidity associated with a given parasite density;
  2. antiparasite immunity, conferring protection against parasitemia, which affects the density of parasites;
  3. premunition, providing protection against new infections by maintaining a low-grade and generally asymptomatic parasitemia.
60
Q

What methods are used for malaria diagnosis?

A
  • Clinical Diagnosis
  • Malaria Blood Smear
  • Fluorescent microscopy
  • Antigen Detection
  • Serology
  • Polymerase Chain Reaction
61
Q

What is the clinical diagnosis for malaria?

A
  • Hyperendemic and holoendemic areas
  • Laboratory resources not needed
  • Fever or history of fever
  • Sensitivity ranges from poor to high
  • Often has poor specificity and predictive values
  • Overlap with other syndromes
62
Q

How is malaria diagnosed in labs?

A
  • On thick or thin blood films after staining with Romanowsky stains
63
Q

What are thick blood stains for?

A

The detection of parasites

64
Q

What are thin blood stains used for?

A

The identification of species

65
Q

What is the objective of a blood examination?

A
  • To see if the patient is infected
  • The level of infection
  • The identity of infecting species
66
Q

In optimal conditions, what can microscopy detect?

A

Parasetaemia

67
Q

What are the limitations of microscopy?

A
  • Mixed infections can be difficult to diagnose
  • Low parasitemia can be difficult to diagnose
  • Hands on time is very high
68
Q

What are serology techniques?

A

Indirect fluorescent antibody test and indirect haemagglutination assays: they have limited value because they detect antimalarial antibody and cannot reveal whether it is past or current infection.

69
Q

What are some molecular methods used for detection of malaria?

A

PCR for detection of Plasmodium. They are used for epidemiologic studies rather than for routine diagnosis

70
Q

Name an example of a antigen detection test?

A

BinaxNOW Malaria Test

71
Q

What does the BinaxNOW Malaria Test do?

A

It detects circulating malaria antigens in whole blood

15 minute test

Test has monoclonal antibodies directed against these proteins, which detects them in a modified lateral flow format

72
Q

What are 4 ways in which malaria can be prevented?

A
  • Avoidance of infected mosquito bites through screening windows, spraying residential places, the use of mosquito nets and prophylactic drugs (proguanil hydrochloride or chloroquine).
  • If Plasmodium species are resistance to these drugs combinations of pyrimethamine and sulfadoxine can be used.
  • Reduce vector density. Reduce mosquito breeding grounds through environmental modifications, targeting the larva stages with chemical and biological agents, and massive insecticide spraying for the adult mosquitoes.

– Biological control: Introduction of fish that eat the mosquito larvae or bacteria such as Bacillus thruingiensis, which excrete larval toxins.

  • Reduce parasite reservoir: Identify and treat infected persons, especially asymptomatic individuals
  • Critical points for bed-net programs: Bed net program has been effective in Africa but some questions whether bed net programme is viable in the long term:
    • Needs repair, respraying
    • They may reduce the exposure but do not eliminate
    • Reduction in exposure may delay the acquisition of immunity and postpone morbidity and mortality to older age groups.`
73
Q

What is the treatment for malaria?

A
  • Cholororquine: For treatment of acute infection, prevent hemozoin formation, it acts upon food vacuole, cheap, non-toxic
  • Artemisinin: A natural product antimalarial drug inspired by traditional chinese medicine
74
Q

What is the ‘radical cure’ for malaria?

A

Choloroquine + primaquine

75
Q

What are issues with drug resistance?

A
  • Chloroquine resistance is a major problem
  • Occurs due to genetic mutations
  • The use of subtherapeutic doses of drugs or not completing the treatment regimen result in resistance.
  • Mass administration: The wide spread use of a drug in an area of intense transmission increases drug pressure by exposing a larger parasite population to the drug.
  • Long-drug half life: Drugs that are slowly eliminated will lead to a longer exposure of the parasite to subtherapeutic levels of drug.
  • Transmission intensity: High levels of transmission may allow reinfection while drugs are at subtherapeutic levels.

Eukaryotic Microbio (4 decks)

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