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Parasitology and entomology > Gut protozoa and opportunistic parasites > Flashcards

Gut protozoa and opportunistic parasites Flashcards

1
Q

What usually occurs within the cyst once shed and it is waiting to be eaten?

A

Usually divide within the cyst.

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2
Q

How can one explain the disparity in the number of cases shedding entamoeba cysts and the number of those actually being ill/showing symptoms?

A

THought to be because of two histologically identical cysts of dispar and histolytica. Dispar is actually not pathogenic and whatsmore, only a small number of people positive for histolytica actually get ill.

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3
Q

How many species of entamoeba are there?

A

11

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4
Q

Why is it odd that histolytica is so common?

A

Because only a small percentage of those infected actually get ill.

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5
Q

Describe the invasive amebiasis of histolytica.

A

It can leave the lumen and invade tissues in the trophozoite form.

  • Can invade the large bowel and form large blood ulcers.
  • Can migrate to the liver and form fatal cysts (ALA- amoebic liver abscess).
  • Can ulcerate through the liver to the heart and lung tissue.
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6
Q

Which form of entamoeba histolytica infection confers a high mortality rate? What are the symptoms of this form of infection?

A

The fulminant form which is a complication of infection that leads to high morbidity and mortality.
Causes abdominal pain and bloody diarrhoea.

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7
Q

Why is infection with E. histolytica called amoebic colitis?

A

Because it can infect and cause necrosis of the colon.

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8
Q

What do trophoziotes do in tissues?

A

They avidly eat red blood cells.

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9
Q

What happens to the liver when E. histolytica spread there?!

A
  • General destruction of tissues
  • Exudate
  • Dead hepatocytes
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10
Q

Describe the gender epidemiology of E. histolytica causing amoebic dysentery. What might be the reasons for this distribution?

A

equally as common in males and females but particular affects post puberty males.
May be hormonal or due to males drinking more alcohol or that they are more likely to brew alcohol in iron containers which are perfect conditions for amoebas as they LOVE iron. Could also be that females have better immune systems.

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11
Q

How long generally does E. histolytica amoebic infection in the gut last? Why may we not detect infection?

A

Usually around 6-12 months. May not detect and diagnose infection as trophoziotes may spread and invade the liver and disappear from the gut before cysts are found.

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12
Q

Which is more common, dispar or histolytica?

A

Dispar, but is non pathogenic.

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13
Q

What is the infective dose of cysts for E. histolytica?

A

Usually greater than 1000 cysts.

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14
Q

What is the percentage of infected individuals (histolytica) that show symptoms?

A

10-20%

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15
Q

What is the usual cause of histolytica in high income counties?

A

Almost always from travelling.

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16
Q

What can cause low level seropositivity for dispar in cases where the individual is infected but is not showing pathology (i.e. because dispar is non-pathogenic)?

A

The amoeba can “nibble” at the gut but not enough to cause pathology.

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17
Q

What are the arguments for and against defensive mechanisms of hustolytica “spilling over” being the cause of human pathology?

A
  • We think this might be true and arise from defensive mechanisms against the bacteria that the amoebas ingest- may be spilling over and killing/damaging human host cells.
  • We think this may not be the case as apoptosis is often induced which would not be defensive against bacteria.
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18
Q

Children secreting which antibodies are more likely to be infected and conversely secreting which antibodies are likely to be protective?

A

IgA appears to be protective.

IgG may increase likelihood of infection.

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19
Q

How would one diagnose entamoeba histolytica/dispar? What are the drawbacks of some of these methods?

A

Wet film microscopy, PCR (remnants of bile acids are very inhibitory of the PCR reaction), serology/ antigen detection (however these tests didnt work well or sell well), tissue biopsy.

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20
Q

What are the names of two other entamoeba that have cysts almost identical to dispar and histolytica?

A

Bangladeshi and moshkovskii

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21
Q

What is a hallmark for E hisyolytica (e.g. what can we look for in trophoziotes that would tell us it is histo not dispar?)

A

Ingestion of RBC is a hallmark of histo, with 99% confidence.

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22
Q

What kind of titre is significant in endemic regions and what titre is significant in non endemic regions (histo).?

A

High titres are significant in endemic regions because a large proportion are seropositive but asymptomatic (e.g. 30% of Mexico is seropositive for histo) whereas low titres are significant in non-endemic regions (histo serology).

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23
Q

What drug is used for the treatment of histolytica. Is it effective? How does it work?

A

5 nitroimidazole. Yes it is very effective, shows rapid improvement (within 24 hours).

It works by inhibiting thioredoxin reductase enzymes to deplete intracellular thiol pools as well as inhibiting translation elongation factor EF1gamma. This kills parasites in the tissues. We need an additional lumenal amoebicide to kill parasites in the gut, such as furamide.

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24
Q

Which drug is used to treat trophozoites of e histolytica to prevent them forming cysts in the gut (i.e. is a lumenal amoebicide)?

A

Furamide.

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25
Q

How and why does giardia stick to the small bowel?

A

Sticks via a notched disc. Does this so peristaltic movement does not remove it.

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26
Q

Describe the structure of giardia trophoziotes.

A
  • Bilateral symmetry
  • 8 flagella
  • 4 vasobodies and 2 nuclei
  • Axonemes
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27
Q

What occurs to the nuclei when the trohoziote encysts?

A

The 2 nuclei replicate to become 4.

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28
Q

What are other potential symptoms of giardia that are not intestine related? What are these thought to be caused by?

A

-Conjunctivitis
-Aching joints
These have no relation to the gut infection but are thought to be immune mediated.

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29
Q

What are the symptoms of giardia infection?

A
  • Malabsorption (only really causes serious problems in those already malnourished).
  • Reduced digestion of food.
  • Buildup/overgrowth of bacteria which produce gasses leading to unpleasant gaseous stools. (this overgrowth is due to bacteria fermenting undigested food)
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30
Q

Coinfection of giardia and which other pathogen are responsible for growth deficits and malnutrition?

A

Shigella

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31
Q

How is giardia identified? (Which technique is used, and describe the identification process used to eliminate giardia infection).

A

Light microscopy (especially important as research in this area is underfunded due to death seldom occurring unless the individual is already malnourished).

Minimum of 3 stool samples two days apart are needed to exclude giardiasis as cyst shedding is intermittent.

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32
Q

Describe the epidemiology of the cysts of giardia. Why could this be?

A

Lots shed by children but less so from adults.

Thought to be due to differing immune responses.

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33
Q

Describe the environmental resistance of giardia cysts.

A

Require 3ppm of chlorine to kill them, this water would be undrinkable.
Can also be destroyed by 3ppm of iodine but this needs to be exposed for a long time and then the iodine must be removed.
Boiling is best.

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34
Q

How is giardia transmitted?

A

Lots of outbreaks are waterborne, also spread in pre-packed salads, in food, from person to person.
As few as 10 cysts needed for transmission.

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35
Q

Which assemblage (of the two we are concerned with) has the broader reach?

A

Half of the A assemblage has range in humans, livestock and pets whereas the other half of the A assemblage and also B are human restricted.

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36
Q

Which drug is used to treat giardia?

A

Nitazoxinide.

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37
Q

How many trichomonads infect humans?

A

3

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38
Q

How many trichomonads infect humans? Which is the most siognificant?

A
  1. Trichomonas vaginalis.
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39
Q

What are the symptoms of T vaginalis?

A
  • Malodorous discharge

- Fragile cervical mucosa which bleeds to the touch.

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40
Q

How is T vaginalis diagnosed?

A
  • Wet film microscopy
  • PCR
  • Liquid based pap smears
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41
Q

How is T vaginalis transmitted?

A

Almost exclusively sexual transmission. (Neonatal infections are exceedingly rare).

42
Q

Which demographic is most affected by T vaginais?

A

Black women more so than hispanic or white women.

43
Q

What are the potential outcomes of T vaginalis in pregnant women? Why may treatment of this demographic NOT make the defects go down?

A
  • Low birth weight
  • Foetus abortion
  • Premature delivery

May not decrease these outcomes as half of the parasites are infected with a ds virus. Killing the trichomonas may release this viral DNA causing an immune response and immunopathology.

44
Q

How is trichomonas treated?

A

Tinidazole, however this is expensive and should be avoided in pregnancy.

45
Q

What is an unusual feature of the structure of dientamoeba fragilis.

A
46
Q

How is D fragelis thought to be spread?

A

Evidence for transmission in pinworm eggs.

47
Q

Is D fragelis pathogenic?

A

Controversial! Not sure.

Is thought NOT to produce resistant cysts.

48
Q

How is D fragelis treated.

A

Chemotherapy but is hard to get rid fo with drugs and they don’t always work,

49
Q

What is the general coccidia lifecycle?

A

Three major stages: sporogony, schizogony, gametogony.
Sporogony: thick-shelled oocysts pass unsporulated inthe faeces, once conditions are right, the single nucleus divides (number of divisions depends on the species).Conical bodies form around each nucleus. Nucleus and conical body come together to form a sporoblast. Sporoblast creates a wall around itself. Simultaneously, the protoplasm forms two sporozoites.

Schizogony: sporulated oocyst is now infective and is ingested. Sporozoites are released from the oocyst and ar activated by bile and trypsin to invade intestinal epithelium where they become trophozoites. Trophozoite divides into merozoites (collectively meront). Meront grows and matures and ruptures epithelial cell to infect another epithelial cell. Can repeat or progress to sexual stage.

Gametogony: merozoites infect new cells and differentiate into gametocytes. Divide into a large number of small cells with flagella (male) or a large single cell (female). Fuse and from a new oocyst which develops a wall. Remains in this stage until excreted by the host.

50
Q

What is unusual about cystoisospora belli?

A

Forms liver cysts. Common in AIDS patients.

51
Q

Why is cystoisospora belli easy to diagnose?

A
  • Can easily identify in faecal samples as spores are very big: 20-30 micrometers.
  • Are acid fast so can be stained.
52
Q

What is the clinical presentation of cystoisospora belli and how is it treated?

A

Self limiting watery diarrhoea (worse in immunocompromised people).
Treated with trimethaprim sulfamethoxazole.

53
Q

How can we identify cryptosporidium?

A

Rectal biopsies show little spheres that look like they are extracellular but are not. They look like this because the crypto merozoite embeds in the microvilli. Some of these rupture inside host and cause autoinfection.

54
Q

How big are cryptosporidium cysts?

A

5 to 5.5 micrometers. VERY tight size range for identification.

55
Q

How can cryptosporidium be transmitted?

A

Coughing (airborne) and faecal-oral route.

56
Q

Describe the pathogenesis of cryptosporidium.

A

Not well understood but disrupts barriers and inserts RNA transcripts into cells (not sure what this does). It makes the gut leaky and bacterial antigens can drift across into the bloodstream and cause persistent inflammation throughout the body.

57
Q

How do we diagnose cryptosporidium?

A

Ziehl Nielsen strain stains the spherical spores cherry red (other spores that are not of interest but are also acid fast are seen as purple).
Dipstick tests may be useful.

58
Q

Which are the two species of cryptosporidium that infect humans?

A

Parvum and hominis.

59
Q

Which gene is used to genotype cryptosporidium?

A

GP60, a glycoprotein gene.

60
Q

Treatment for cryptosporidium?

A

No standard treatments as nothing is really helpful in immunocompetent people, only really repurposing of statins may be helpful.

61
Q

Why is cryptosporidium hard to treat?

A

May be because of the apicoplast being absent from parvum and hominis- lacking a huge drug target.

62
Q

In whom are cases of cyclospora cayetanensis usually found?

A

Prevalent in returning travellers.

63
Q

Describe symptoms of cyclospora cayetanensis .

A

Prolonged diarrhoea in both immunocompetent and incompetent individuals, however a lot of cases are aymptomatic.

64
Q

How is cyclospora cayetanensis transmitted?

A

Waterborne and foodborne from fruit and salad.

65
Q

Which species does toxoplasma gondi affect?

A

Has a wide range and affects most mammals and birds, whereas most coccidia are host specific. It affects any nucleated cell.

66
Q

Describe infection by toxoplasma gondi.

A

Oocysts taken up from contaminated food, water, soil etc. Tachyzoites penetrate cells and multiply (in the enteric cells). Can rapidly spread through the body inside WBC (however don’t NEED these cells). In immunocompetent individuals, this rapid multiplication is prevented, causing the parasite to form bradyzoites in cysts in brain and muscle. Reactivation can occur when this infected tissue is eaten undercooked.

67
Q

Can toxo exist without cats?

A

Theoretically yes but in practice no.

68
Q

How is immunity to toxo conferred?

A

Persisting cysts in tissues confer immunity.

69
Q

Describe how congenital toxiplasmosis can occur? How does severity of infection change with when during the pregnancy infection is acquired?

A

Tachyzoites can cross the placenta.
If infection is acquired early on in pregnancy, infection is very unlikely but if it does occur will be severe.

If infection is acquired later in pregnancy, it is very likely the baby will be infected however it will not be severe.

70
Q

What is retinochondritis/ eye infections with respect to infections of foetus/baby with toxo?

A

If infection is acquired later in pregnancy, it is very likely the baby will be infected however it will not be severe: most likely an inapparent eye infection or retinal lesions (which may cause blindless if in the wrong place).

Retinochondritis is persistent eye infections that can be acquired after birth

71
Q

How does toxo infection present in AIDS patients?

A

Very rapid infection with tachyzoites in every organ/tissue, Can also cause toxoplasmic encephalitis

72
Q

Describe the link between toxi and schizophrenia. Why might this be? Is there evidence for this?

A

Thought that potentially it is more likely that people with schizophrenia had/have toxo. Children that have toxo are more likely to become schizophrenic/ are at greater risk.

May be because parasite changes host cells/ changes properties of the host to propagate itself.

Evidence may be in animal studies on mice which usually have an innate fear response to avoid cats but when infected with toxo, lose this fear response- helps propagate the toxo when the mouse is eaten.

73
Q

What are the clonal lineages of toxo? How does this vary in south america?

A

Clonal linages 1, 2 and 3. In S america there are around 20, with these atypical genotypes being much more virulent and causing much more severe infection and death even in immunocompetent individuals.

74
Q

How is toxo treated?!

A

Spiromycin (targets apicoplast) or pyrimethamine sulfonamide.

75
Q

Which parasite (fungus) is responsible for human pneumocystosis? (Pneumocystis pneumonia=PCP).

A

Pneumocystis jirovecii

76
Q

Which parasite became an AIDS-defining illness in the 60s?

A

PCP from pneumocystis jirovecii.

77
Q

Why is PCP described as opportunistic? (i.e. who does it mainly affect?)

A

Only really affects those who are immunosuppressed or malnourished.

78
Q

Pneumocystis jirovecii infection occurs through which tissue and how does pathology present?

A

Adheres to type I pneumocytes and usually presents as insidious breathlessness.

79
Q

How does HIV positivity affect the load and mortality rates in pneumocystis jirovecii infection?

A

HIV+: increased fungal load but decreased mortality

HIV-: less fungal load but increased mortality.

80
Q

What are the two forms of interest of pneumocystis jirovecii?

A
  • Small asexual form that divides in the lungs

- Conjugation forms (precysts) which get released during excystment

81
Q

What are the two ways we stain Pneumocystis jirovecii and what do they show?

A

Geimsa shows exudate containing trophic forms which clog up lungs
Grocott silver stain selectively stains cyst walls in lung biopsy samples (diagnostic).

82
Q

How is Pneumocystis jirovecii transmitted?

A

Exclusively airborne.

83
Q

How can we diagnose Pneumocystis jirovecii ?

A

Use saline aerosol to induce sputum, or wash out alveolar contents and inspect it. Can stain these specimens or use PCR.

Some leakage into blood may allow detection of 1,3- beta D glucan which is a cell wall component which is a less invasive method.

84
Q

Describe the unique cell invasion/ adherence method of mocrosporidia.

A

Microtubules that are wound around its bilobed nucleus shoot out (polar filament shoots out) and impale surrounding/ target cell when the spore comes into contact with water.

85
Q

What is the size of microsporidia spores?

A

1.5 micrometres

86
Q

How does microsporidia replicate inside a host?

A

Replicates inside host cell vacuoles and causes cells to rupture to release spores.

87
Q

What are the two big enteric species of microsporidia?

A

Enterocytozoan bieneusi and encephalitozoan intestinalis.

88
Q

What does encephalitozoan hellem cause and how is infection acquired?

A

Causes eye infections (lots of reports in immunocompetent people). From soil contact.

89
Q

How is microsporidia transmitted?

A

Faecal oral route, recreational water, foodborne, eye infective forms from local contact.

90
Q

How is microsporidia diagnosed?

A

Calcofleur white staining and UV or normal staining and light microscopy. Can also amplify nucleic acids.

91
Q

How does the chemotherapy for microsporidia work?

A

Inhibits polymerisation of fungal tubulins specifically (doesnt affect human counterpart).

92
Q

Describe where in cells bieneusi and intestinalis are? (Microsporidia)

A

Bieneusi is in vacuoles whereas intestinalis is free in the cytoplasm.

93
Q

What causes myositis? And what is it?

A

It is muscle problems/ lesions caused by microsporidia.

94
Q

Primary amoebic meningoencephalitis can be caused by niglaria fowelri. What is the route of infection?

A

Infected water up nose, through olfactory nerve and into brain.

95
Q

How is niglaria fowelri diagnosed?

A

Look in cerebrospinal fluid.

96
Q

How is niglaria fowelri treated?

A

Death is sudden but if time for treatemtn, amphotericin B and miltefosine are often used.

97
Q

Which amoeba causes granulomatous amoebic encephalitis (GAE)? HOw can this be lethal?

A

Acanthamoeba. Cysts in tissues- can slowly migrate to the brain.

98
Q

How is acanthamoeba diagnosed?

A

PCR, biopsy, imaging, looking for antibodies.

99
Q

Describe how amoebic keratitis can occur?

A

Acanthamoeba can infect the immunoprivilaged site of the cornea- occurs lots in contact lens wearers.

100
Q

HOw is amoebic keratitis diagnosed?

A

Scraping of cornea, stained and cultured to look for trophozoites.

101
Q

How is acanthamoeba treated?

A

PHMB every hour for 4-8 weeks.

102
Q

What does balamuthia mandrillaris cause?

A

ALso causes GAE. Has a high mortality rate.

Parasitology and entomology (26 decks)

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