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MICR332 - Health Microbiology > PARASITOLOGY > Flashcards

PARASITOLOGY Flashcards

FUCKING PARASITES

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1
Q

what is the correlation between parasitological health burden and wealth/development?

A

as wealth and development increases, parasitological health burden decreases

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2
Q

outline the issue of the rise and spread of drug resistant malaria?

A

only anti-malarial drugs still working are those based on artemisinin plant which has end-peroxide bond causing oxidative bomb inside malaria

however resistance to artemisinin now emerging; evidence of delayed clearance time using drug (important for severe forms of malaria - hours matter)

only drug with no resistance showing is pyronaridine which is best used as combination drug

WHO never declared this an emergency despite their being 241 million malaria cases in 2021

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3
Q

outline the importance of parasites still common in developed countries?

A

trichomonas vaginalis most common pathogenic protozoan infection in developed countries, ST, burden not understood

toxoplasma gondii causes toxoplasmosis (a leading cause of death from food borne illness) and asymptomatic infection in heaps of cunts, thought to have significant effects on host psychology

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4
Q

outline the potential for parasites as immunological therapies?

A

parasitological health burden has decreased with the increase of wealth and development, but autoimmune diseases has also increased

hypothesis that we co-evolved w parasites which wind down our immune system so when they go our immune system naturally higher functioning and less regulated

helminths covered in anti-inflam molecules, have been shown to increase lifespan in mouse models

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5
Q

what are nematodes?

A

nematodes are fucking parasites - roundworms

two examples are enterobius vermicularis and hookworm

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6
Q

what are enterobius vermicularis?

A

common in temperate developed areas like NZ

eggs (ova) very sticky to fomites objects and can remain viable for weeks

male and female ones attach to ascending colon and mate after which female goes to perianal region and lays lots of eggs - person scratches these spreading infection back to you or others

enterobiasis (disease caused) can cause secondary bacterial infection, vulvovaginitis and also there may be possible fertility implications

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7
Q

outline the chain of infection for enterobius vermicularis?

A

causative agent: enterobius vermicularis

reservoir/source: human/fomite/food

means of exit: excretions

mode of transmission: contact/food

portal of entry: GI tract

person of risk: especially infectious for young institutionalised people but generally unpick and no association with gender, social class, race or culture

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8
Q

how do you break the chain of infection for enterobius vermicularis?

A

treat causative agent with 2 doses mebendazole pyrantel pamoate

portal of entry: break this link by hygienic practices e.g. short fingernails, wash hands, wash bed linen

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9
Q

what is the association of enterobius vermicularis and dientamoeba fragilis?

A

D. fragilis commonly found in acute gastro cases and has been associated with E. vermicularis

D. fragilis cysts may attach to surface of nematode eggs and hitch a ride causing co-infection

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10
Q

what are hookworms?

A

hookworm filariform larvae can live for 2 weeks in soil and sense the warmth of your feet so go in your follicle

often accidental infection by dog/cat hookworm causing cutaneous larva migrans

human specific hookworms way worse; filariform live 4 weeks in soil, get into your blood>heart>pulmonary vessels>lungs

larvae stops at alveoli, breaks into airways causing coughing/shortness of breath, coughed up and swallowed in mucus to finally infect intestine

attach to intestinal epithelia and can let their for up to a decade drinking blood - can cause severe anaemia and protein deficiency > can retard growth and mental development in children

leading cause of anaemia in developing world

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11
Q

what are the two most common human specific species of hookworm?

A

ancylostoma duodenale

necator americanus

these are also the two biggest human pathogens we find in soil

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12
Q

why can diagnosis of hookworm be difficult?

A

worms take six weeks to reach maturity and symptoms of infection can therefor appear before eggs found in faeces

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13
Q

outline the chain of infection for hook worm?

A

causative agent: ancylostoma duodenal or nectar americanus

reservoir: soil

means of exit/way out of body: excretions

mode of transmission: contact

portal of entry/way into body: skin

person of risk: anyone in endemic areas

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14
Q

how do we break the chain of infection for hookworm?

A

treatment of causative agent with albendazole and mebendazole

sanitation critical way: breaks reservoir (soil) and means of exit (excretion) cause you stop people shitting everywhere

portal of entry - wear shoes

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15
Q

what is hookworm therapy?

A

hookworms excrete proteins which down regulate parts of your immune response

potential as a medication-free treatment for inflammatory bowel disease

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16
Q

what is wucheria bancrofti?

A

worm causes lymphatic filiaris (LF)

people with LF more at risk of malarial or hookworm infection causing co-morbidities e.g. anaemia

most infections somewhat asymptomatic

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17
Q

what are the three causative agents of lymphatic filiaris?

A

Wucherin bancrofti (most cases), brugia malayi, brugia timori

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18
Q

outline the chain of infection for wucheria bancrofti?

A

causative agent: wucheria bancrofti

reservoir: human (only really found in humans)

means of exit: blood

mode of transmission: vector (mosquito picks up microfilaria which are transmissible form)

portal of entry: skin

persons at risk: people getting bit by mosquito good tasting people, indiscriminate who it infects

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19
Q

outline the chain of infection for wucheria bancrofti?

A
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20
Q

how does wucheria bancrofti and other LF causing parasites actually cause LF?

A

adult larvae cause blockage to lymph nodes causing hydrocele and elephantiasis

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21
Q

outline the life cycle of wucheria bancrofti, brugia malayi and brugia timori?

A

mosquito takes a blood meal - larvae enter skin

adults in lymphatics (causes LF) and produce sheathed microfiliriae that migrate to lymph and blood channels (all over the body)

mosquito takes blood meal - ingests microfiliriae

microfiliriae shed sheaths and infect mosquito and go through some growth stages, eventually migrating to mosquito head/proboscis

cycle repeats!

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22
Q

how do you break the chain of infection for wucheria bancrofti?

A

treatment of causative agent with DEC and ivermectin together - this also deals with reservoir

repellents/nets to break portal of entry

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23
Q

what is schistosomiasis?

A

disease caused by trematodes e.g. S. mansion, S. haematobium, S. japonica

infects hundreds of millions of people world wide, between 4000 and 200,000 deaths annually

emerge from aquatic snails, go through hair follicle>blood stream>liver> mature and start drinking your blood out your vein and fuck and lay eggs

eggs excreted back to environment but are spiky so get caught in different tissues causing problems like granuloma

schistosomiasis is primarily a immunological disease

symptom is pissing blood cause spiky eggs stuck in your kidneys

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24
Q

how do trematodes infect snails?

A

the eggs in environment hatch and shit like miracidia then go seek out the snails

25
Q

outline the chain of infection for Schistosoma haematobium/japonicum/mansoni?

A

causative agent: S. haematobium, S. japonicum, S. mansoni

reservoir/source: aquatic snails

means of exit: excretions

mode of transmission: contact

portal of entry: skin

person at risk: anyone in endemic areas

26
Q

how do you break the schistosoma chain of infection?

A

treatment of causative agent with praziquantel (only kills mature parasite so must give 4-6 weeks after presumed infection)

sanitation (e.g. weed removal, stop shitting in water) deals with reservoir and means of exit

stop swimming in infected waters (deals with portal of entry)

27
Q

what happened when we switched from microscopy to PCR for examining protists (clue - fragilis)?

A

showed that some parasites e.g. D fragilis stand out a lot more

shows that these parasites are common among New Zealanders

28
Q

what is blastocystis?

A

most common eukaryotic microbe in human intestinal tract (1 billion infected ww)

luminal protist comprising numerous genetically-distinct subtypes (ST)

ambiguous clinical significance (present in symptomatic and asymptomatic, possibly ST related

different forms e.g. vacuolar, granular, amoeboid

blastocystosis - symptoms include abdominal pain, diarrhoea, bloating, nausea

29
Q

outline what we know about the lifecycle of blastocystis spp.?

A

people eat fecal cysts which are resistant to stomach acid

cysts end up in large intestine and here they just absorb nutrients from existing food

30
Q

what is a key thing that needs to be done to better understand blastocystosis?

A

genetically typing the different serotypes

there is evidence that one serotype (ST7) is more associated with pathogenesis well others may be commensal

but at the end of the day no-one knows atm as funding limited

31
Q

what is dientamoeba fragilis?

A

fragile parasite so PCR better than microscopy which can destroy it

current surveillance mostly uses microscopy hence inconsistent statistics between countries

higher rates in children and 40 year olds (especially in parents and siblings suggesting transmission)

high rates in pig farmers

32
Q

what commonalities do dientomoeba fragilis and blastocystis spp. share (in terms of research)?

A

we don’t understand pathogenesis (a big step to fixing this is genotyping them)

better diagnosed using PCR than microscopy

more research needed on lifecycle

both associated with large intestine and free living (not attached)

co-infection frequent

33
Q

what is the current evidence for intestinal protozoa significantly affecting human microbiome diversity?

A

evidence that D. fragilis affects microbiome by increases alpha diversity/species richness

some intestinal parasites seem to reduce variation in microbiome between patients (uniform between patients)

therefor it is important that we look at full ecology of microbiome not just focus on bacteria

34
Q

what is giardia intestinalis?

A

intestinal protozoa caught by cyst contaminated food or water

low MID (10) so highly virulent

outer wall of giardia cyst acid resistant but broken down by proteases in small intestine allowing trophozoites to emerge which attach to small intestine wall via ventral adhesive disc and start divide

inhibit absorbance of fats and fat soluble vitamins

35
Q

outline the clinical progression of giardiasis?

A

diarrhoea

gas

greasy stools that float(key diagnostic cause inhibited fat absorbance)

stomach/abdominal cramps

upset stomach or nausea/vomiting

dehydration/fluid loss

36
Q

outline the giardia lifecycle?

A

eat cysts

cysts hatch trophozoites which attach to small intestine

encystation (cyst forming) occurs under conditions of bile salt conc. changes and alkaline pH, this occurs in large intestine

shit out cysts which survive in focal matter well trophozoites die

37
Q

outline the chain of infection for giardia?

A

causative agent: giardia lamblia/intestinalis

reservoir: animals/humans/water

means of exit: excretion (100m cysts in one shit)

mode of transmission: food/water

portal of entry: ingestion (MID 10 cysts)

person of risk: anyone can get infected but people in places where giardia common, cunts with aids, people drinking directly from waterways

38
Q

how do you break the chain of infection for giardia?

A

stop causative agent with treatment with metronidazole, tinidazole or nitazoxanide (combination, resistance emerging)

portal of entry: boil drinking water, wash hands, use clean water to wash food

encourage breast feeding cause people mix with water and fuck up their babies

39
Q

what is cryptosporidium paarvum?

A

intestinal protozoa

peaks around calving season as common in young animals

oocysts target small intestine

key difference to giardia is that rather than adhere, it burrows into cell so is intracellular parasite, in cell they multiple and release oocysts

40
Q

outline the clinical progression of cryptosporidium?

A

watery diarrhoea (unlike giardia)

stomach cramps

dehydration

nausea

vomiting

fever (unlike giardia)

weight loss

41
Q

outline the cryptosporidium chain of infection?

A

portal of entry - 30 oocysts MID

person of risk - anyone but AIDs people, immunosuppressed most at risk

break it by treating with nitrazoxanide (can’t be used with AIDS cause requires high CD8 cell count), encourage breast feeding, boil drinking water

42
Q

what is Trichomonas vaginalis (Tv)?

A

most common pathogenic protozoan in developed countries and a highly neglected STD

sexually transmitted and full burden not understood

causes trichomoniasis - 70% of people no symptoms, men may notice burning after urination or discharge/itching sensation in dick, woman may notice itching, burning of vagina, discomfort w urination, change in colour in vaginal discharge with fishy smell, unpleasant sensation during sex

treat trichomonas w metronidazole

NZ assessing cost associated with surveillance, best option check people with other STD cause they most likely to have Tv

43
Q

what is toxoplasma gondii?

A

causative agent of toxoplasmosis, thought to have significant effects on host psychology

can only reproduce in cats, mouse is intermediate host

cat shits out oocysts, mice eat, oocysts hatch and move from intestine to tissues in mouse, cat eats mouse, cysts burst open in cat and cycle repeats

pregnant woman vulnerable to infection cause down regulated immune system, toxoplasma can cross placental barrier (and all barriers) and infect fetus, likes infecting the retina leading to blind/deaf children

asymptomatic in a shit load of people, considered to be leading cause of death attributed to food borne illness, chances are you won’t know you infected till immunosuppressed

use IgG or IgM serology to test for infection, symptoms varied as cysts can be anywhere

treat with pyrimethamine and sulfadiazine plus folinic acid, most healthy people recover

44
Q

outline the effects of toxoplasma gondii on host psychology?

A

makes mice less afraid of/sexually attracted to cats - run towards cat urine/faeces smell

we know it effects psychoactive modulators

probably somehow regulates hypomethylated arginine vasopressin promoters in medial amygdala (emotion) leading to higher expression of mRNA for AVP

potentially linked to depression and schizophrenia in humans

45
Q

what is Naegleria fowleri?

A

parasite found in still, warm water - its amoeba feed on pond scum

causes primary amoebic meningoencephalitis (PAM) which is almost always fatal

infection occurs from water going up nasal cavity from water-related activities (e.g. diving) allowing amoeba to penetrate nasal mucosa migrate to brain via olfactory nerves to cause PAM

diagnosis from Naegleria fowleri in CSF or tissue specimens

potential for miltefosine as treatment (breast cancer and anti leishmania drug)

46
Q

outline the journey from mosquito to the liver for malaria?

A

mosquito injects saliva during bite along with about 10 sporozoites

sporozoites travel to host liver via blood stream and are covered in circumsporozoite proteins (CSP) which they shed to evade immune cells - this makes them very virulent

sporozoites reach liver sinusoids, move across endothelium and interact with heparin sulphate proteoglycans (HSPGs), and then cross sinusoidal layer through kupffer cells

sporozoite then targets parenchymal liver cells in which they develop into an exoerythrocytic parasite

47
Q

outline malaria development in the liver, how is this different between P. vivax and P. falciparum ?

A

7-10 days post successful sporozoite infection, they develop into schizonts and then released as merozoites which enter blood stream (one sporozoite can produce as many as 30,000 merozoites)

no symptoms prior to RBC infection stage (10-12 days post-bite)

Difference in this process between P. falciparum and P. vivax is some P. vivax (about 3 in 10) enter a dormant phase (metabolically dormant hypnozoite - could be 28d to 1 year) before developing into schizont; this can result in relapses of malaria

only two drugs which can target it in metabolically dormant phase (primaquine and tafenoquine) which are both 8-aminoquinolines which can cause serious adverse affects (haemolysis) in those with G6PD mutations

48
Q

what are the two kinds of parasites causing malaria?

A

Plasmodium falciparum (killer)

Plasmodium vivax (relapser)

49
Q

what are the differences in RBC tropism between P. falciparum and P. vivax?

A

falciparum merozoites can invade all RBC types (e.g. normocytes, reticulocytes) (invasion ligand-receptor pair is PfEBA-175/glycophorin A)

vivax merozoites can only invade nascent reticulocytes which are early stage RBCs (<2% circulating circulating RBCs) (invasion ligand-receptor pair is (PvDBP/DARC)

this means patients infected with vivax show 2% parasitemia at worst

50
Q

how do malarial parasites invade RBCs when they move through blood like cars on a fucking highway?

A

cause RBCs accumulate in spleen so I think they like slow down here

I DONT KNOW IF THIS IS ACTUALLY RIGHT

51
Q

why do people with malaria get a really bad reoccurring fever every 48 hours?

A

because merizoites develop in RBCs and once this has reached a certain point they burst out to infect other RBCs

bursting releases a bunch of contents, particularly hemazoin which is a product of parasite metabolism

the release of RBC contents causes the really bad fever

52
Q

what stages do antimalarials treating symptomatic malaria (artesunate, chloroquine, malarone, mefloquine) target?

A

target the blood stages where parasite replicating in RBC

these stages are merozoites invading RBC, develop to trophozoite, then schizont which burst the cell

53
Q

why is malaria caused by P. falciparum more fatal than that caused by P. vivax?

A

P. falciparum can significantly alter biomechanical properties of host RBC by 18 hours post invasion (trophozoite phase)

this occurs as parasite proteins crosslink RBC spectrin causing knob formation on RBC surface (making it stiff). These knobs covered with multi-domain PfEMP-1 proteins capable of sticking to a wide range of endothelial receptors

this causes a more severe form of malaria as stiff, sticky RBCs bind capillaries and each other causing blockages which can be fatal if in organs like kidney or brain (cerebral malaria biggest cause of malarial death)

54
Q

why is how soon treatment with artemisinin (key antimalarial) occurs so important with P. falciparum?

A

stiff/sticky RBC pathology starts occurring 18 hours post invasion so chances get worse

artemisin cures by clearing parasite quickly but resistance beginning to emerge which is associated with slower parasite clearance time

55
Q

what is causing artemisinin resistance to emerge?

A

K13 propellor protein mutations are associated with AS resistance - mutation causes artemisinin to not work somehow

this is spreading throughout SE Asia, India, China, Middle East

56
Q

how does artemisinin usually kill parasite?

A

finds its way into digestive vacuole of parasite where it reacts with Fe2+ break some bonds and form an explosion of ROS within the parasite

57
Q

what is different about P. vivax pathogenesis which means it doesn’t form stiff/sticky reticulocytes?

A

P. vivax remodels reticulocytes and instead of making them sticky makes them deformable somehow

that’s literally it so its not more deadly or anything just like squishy

58
Q

why do P. falciparum and P. vivax have different pathologies?

A

falciparum proteins crosslink RBC spectrin making stiff/sticky RBCs which can cause blockages and fatality

vivax just makes reticulocytes deformable so less deadly

ultimately different pathologies is due to the differing receptor tropism and the changes it makes in those RBCs

MICR332 - Health Microbiology (5 decks)

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