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Medical Microbiology > Pathogenesis of Parasitic Infections > Flashcards

Pathogenesis of Parasitic Infections Flashcards

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USMLE® Step 1 flashcards Biology 101 flashcards
1
Q
  1. Which type of parasite causes Chagas Disease?
A

Protozoa

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2
Q
  1. What is the name of the prorozoa that causes chagus disease?
A

Trypansoma Cruzi

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3
Q
  1. Explain the life cycle of Trypansoma Cruzi - how does it infect humans?
A

Trypansoma cruzi first is a bug and the bugs feeds on you at night
It then defecates
When you scratch the bite, you spread the parasite through the faeces (or if you rub your eyes , it spreads through your mucosa- swelling)
The parasite enters the bodies and multiplies in nerves and muscle cells
Eventually these cells rupture - release thousands of Trypansoma

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4
Q
  1. What kind of vector does chagus disease have?
A

A biological vector - complex parasite life cycle

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5
Q
  1. Explain the distribution of chagus cases worldwide?
A

There are currently 10m infected in endemic areas

  • 325 000 cases in the USA
  • Due to migration of latin America’s = 100,000 cases in Europe but 87% of that is in spain
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6
Q
  1. Explain the acute phase of chagus disease?
A

There is an incubation period for 1-2 weeks after the bite
If it from blood transfusion it could last months
You can detect Trypanosomes in the blood
Its usually asymptomatic or generally mild symptoms- inflammation (last 8-10wks) such as:
• Local swelling (Romaña)
• Nodule or chagoma
• Fever
• Anorexia
• Lymphadenopathy

Only 1-2% of patients are diagnosed in the acute phase

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7
Q
  1. What are some rare symptoms of chagus disease that might occur in the acute phase?
A
  • Hepatopsplenomegaly
  • Acute myocarditis
  • Meningoencephalitis
  • Fatality <5% of symptomatic
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8
Q
  1. What is the chronic “Indeterminate” phase of chagus disease?
A

This phase may be lifelong , due to the immune system kicking in trypanosomes are usually not detectable in the blood can detect parasite DNA using PCR

  • Seropositive
  • 60-70%
  • Normal ECG and X rays shown on tests
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9
Q
  1. What is the chronic “determinate” phase of chagus disease?
A

-Seropositive
-For 30-40% of infected people this is usually 10-30 years after infection. Before the immune system was containing the parasite now to a weakened immune system (age, opportunistic infections)
Only 5-10% of patients will develop chronic chagus immediately after acute chagus

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10
Q
  1. Which two main biological systems are attacked in chagus disease?
A
  1. Cardiac System

2. Digestive system

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11
Q

11 . How is the cardiac system attacked during chagus disease?

A

More inflammation—> Damage to the conduction of the heart— Arrhythmia’s
Damage to the muscle of the heart—–> cardiomyopathy
Aneurysms and thrombus formation

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12
Q
  1. How is the digestive attacked during chagus disease?

- mention : what % of infected patients get chagus, which areas most infected

A

Develops in 10-15% of patients with chronic infections

• Esophagus, rectum, and sigmoid colon most affected

Megacolon”:
• Presentation – Constipation

• Complications
– Faecaloma
– Obstruction
– Sigmoid volvulus
 – Ulceration
– Perforation
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13
Q
  1. Explain the pathogenesis of acute phase chagus?
A

issue damage caused by inflammatory response to parasite in nests of
amastigotes in cardiac, skeletal, and smooth muscle

• Parasite killing by antibodies, activated innate immune response and Th1 pro- inflammatory cytokines.

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14
Q
  1. Explain the pathogenesis of indeterminate phase chagus?
A

Regulatory immune response characterised by IL-10 and IL-17

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15
Q
  1. Explain the pathogenesis of chronic phase chagus?
A

• Chronic inflammatory response to persistent parasites in muscle and nerve
cells
• Autoimmune mechanisms
• May vary by parasite strain and tissue tropism
• Predominance of Th1 cytokines and CD8+ T cells

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16
Q
  1. What are the two main types of leishmaniasis?- caused by prtozoa?
A

Visceral (affects internal organs) and Cutaneous leishmania’s (focus on this lecture is cutaneous)

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17
Q
  1. Explain the worldly distribution of Visceral leishmanias and the different strains in the area’s?
A
  1. Asian (India ) = strain is Leishmania donovani
  2. Middle East/Africa = strain there is L.Infantum Variants
  3. Latin America = strain is L.chagasi
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18
Q
  1. Explain the life cycle of a Leishmaniasis?
A
  1. Sandfly bites you
  2. Transmits promastigote
  3. Invades our immune cells eg macrophages
  4. Inside evaded macrophages, there are nests of amastigotes
  5. Eventually the macrophages burst and release many many amastigotes
  6. These amastigotes are taken up by another sandfly at another blood meal –>transmission
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19
Q
  1. What are the types of vectors in leishmaniasis’s ?
A

In Latin America = Lutzomyia

In Middle East/Asia = Phlebotomus

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20
Q
  1. What is the reservoir host of leishmaniasis?
A

2 types:

  • domestic animals (how you get urban transmission)
  • Sylvatic (wild animals)
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21
Q
  1. What are the clinical forms of Cutaneous Leishmaniasis?
A
  • A couple weeks after the bite a papule forms - usually on the cheek
  • This spreads
  • In the centre a volcano shaped ulceration forms
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22
Q
  1. What happens in children that are infected with leishmaniasis in endemic areas?
A
  1. Child infected
  2. Children get immunity
  3. Left with a scar
  4. They’re not vulnerable to the disease anymore but if they get exposed to a new strain they might get infected again:(
  5. Scar re-activated lesion forms
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23
Q
  1. What are some other forms of Cutaneous Leishmaniasis?
A
  1. Disseminated form -> Multiple Ulcers
  2. Goes along the lymphatic vessels –> Sporoctrichoid leishmaniasis
  3. Diffuse cutaneous leishmaniasis (very poor immune response, packed full off parasites - lots of nodules)
  4. Mucocutaneous Leishmaniasis (breakdown of nasal septum- lesions)
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24
Q
  1. What is the pathogenesis of acute lesions in leishmaniasis ?
A

• Tissue damage caused by inflammatory response to presence of parasites in
macrophages

• Parasite killing by Th1 pro-inflammatory responses and macrophage killing.

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25
Q
  1. What is the pathogenesis of the latency period of leishmaniasis ?
A

Parasites remain present long-term. Regulatory immune response characterised by
balance of Th1 and anti-inflammatory responses

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26
Q
  1. What is the pathogenesis of the relapse period - which is rare ie infected again?
A
  • Alteration in immune response (i.e change in Th1 vs. immune regulation secondary to HIV, malnutrtition) may trigger relapse
  • Mucocutaneous disease associated with strong but inadequate inflammatory response to parasites that have metastasized to mucosa
  • Diffuse cutaneous leishmaniasis associated with uncontrolled parasite replication
  • Recividans–recurrence of lesions at old ulcer site.
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27
Q
  1. Which type of parasite causes Schistosomiasis?
A

Helminths

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28
Q
  1. What are the three main species of Schistosomiasis
A
  • Schistosoma mansoni
  • S. haematobium
  • S. japonicum
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29
Q
  1. What is the life cycle of a Schistosomiasis?
A
  1. Miracdia enters snails and undergo cycle
  2. Cercarie emerge from snails
  3. Cercarie penetrate unbroken skin or mucous membranes
  4. Schistosomula migrate to heart via portal vein
  5. Shistosomula develop into males and female adult worms in mesenteric and portal veins
  6. Worms copulate and migrate to vesicle veins
  7. Eggs are deposited here in great numbers and extruded through bladder mucousa
  8. Egg passed in urine
  9. Egg hatch, releasing miracidia in water
  10. Miracidia enter snails and undergo cycle ..
30
Q
  1. What is cercarial Dermatitis ?
A

Allergic type reaction to cercariae in the water source/animals or bird schistosomes
Requires pre-sensitization

31
Q
  1. What is a key feature of the immune response to schistosomiasis?
A
  • Granuloma Formation
  • Response to the EGG mainly - TH2 delayed type hypersensitivity
  • Eggs become organised into granulomas
  • Repeated insults and tissue repair —> Fibrosis and organ damage
32
Q
  1. What causes Hepato-intestinal schistosomiasis?

What can this result in?

A

• Infections with S.mansoni and S. japonicum
• Pathology caused by immune response to eggs
- Splenomegaly + Hepatomegaly

33
Q
  1. How do you get urinary schistomiasis?
A

Adults live in vessels around bladders

Eggs pushed out of the mucosa of the bladder and then excreted in the urine

34
Q
  1. What might occur as a result of Urinary Schistosomiasis?
A

Haematuria ( Blood in urine due to damage in bladder wall)

35
Q
  1. Which type parasite causes onchocerciasis?
A

Helminths

36
Q
  1. What is onchocerciasis?
    - Which parasite?
    - How is it transmitted?
A

• Major blinding disease
• Caused by filarial parasite (Onchocerca
volvulus)
• Transmitted by blackflies

37
Q
  1. Explain the geographical distribution of onchocerciasis?
A

Equatorial region of Africa , Central and South America

38
Q
  1. Explain the life cycle of Onchocerciasis?
A
  • Black-fly bites you
  • Transmits infectious larvae
  • Larvae travels under the skin
  • Develops into adult and female , they mate
  • Female releases 1000s of micro-filarie
  • Taken up by backfly
  • Process development in blackfly
  • Transmitted
39
Q
  1. What is the vector of an Onchocerciasis?
A

Simulium vector flies (so called blackflies)

40
Q
  1. What is the pathology of a onchocerciasis?
A

• Repeated episodes of inflammation to presence of microfilariae leads to permanent damage and scarring in skin and eyes

41
Q
  1. What is the clinical presentation of a disease caused by Onchocerciasis?
A
  • Onchocercal nodules
  • Skin disease
  • Eye disease
42
Q
  1. What three types of disease can be caused by skin diseases in Onchocerciasis?
A
  • Acute papular onchodermatitis
  • Chronic onchodermatitis
  • sowda
43
Q
  1. What types of disease can be caused by eye diseases in Onchocerciasis?
A

Anterior segment:
• Punctate keratitis
• Acute iridocyclitis
• Sclerosing keratitis

Posterior segment:
• Optic neuritis/atrophy
• Chorioretinopathy

44
Q
  1. Why is it hard to treat onchocerciasis using pharmacotherapy?
A

The parasite in down regulating the immune response so that we have no immune response
We can stop this down regulation using drugs eg Diethylcarbamazine however you get a strong inflammatory response
This blocks eosinophils
We get an abscess of eosinophils –> Rash

45
Q
  1. What is acute papular onchodermatitis?
A

Acute paplar rash

If you were to look in the skin —-> Microfilaria surrounded by immune cells –> loss of eosinophils

46
Q
  1. What is chronic onchodermatitis?
A

Repeated inflammation over periods of time
Damage to elastin and collagen in the skin
Presperdemia (aged skin)

47
Q
  1. What is punctate Keratitis?
A

Microfilaria invade cornea
Little fluffy parasites in cornea
Microfilaria killed by immune response

48
Q
  1. What is sclerosing Keratitis?
A

Chronic inflammation—–> Damage to the retina —> overdying opacification of cornea—>Blindness
Effects retina , early on you see small white spots in the eye (dead microfilaria) eventually microfilariae gets into the optic nerve

49
Q
  1. What is Chorioretinopathy?
A

a condition in which fluid accumulates under the retina, causing a serous (fluid-filled) detachment and vision loss.

50
Q
  1. What is Optic atrophy?
A

Optic atrophy refers to the death of the retinal ganglion cell axons that comprise the optic nerve

51
Q
  1. What is the immunopathogenesis of onchocerciasis?
A

Acute:

  • Rapid allergic reaction to dead microfilae
  • Results in activation of Immune cells (mast cells, eosinophils)
  • Eosinophil Assesses
  • Strong TH2 response - decrease in IL4 (IgG) and iL5 (eosinophils)

Chronic:

  • -Immune response shut down
  • Modified TH2 response
  • Decreased IL10 and TGFbeta
52
Q
  1. Which type of parasite causes ticks?
A

Ectoparasites

53
Q

53, How do ticks get stuck into skin?

A
  • Stick the mouth part into the skin
  • Form a cement
  • Quite difficult to get it out - feeds off blood
54
Q
  1. What are ticks a vector of?
A

A large number of infections

55
Q
  1. What are the two types of ticks?
A

Hard ticks

Soft ticks

56
Q

56.What some forms of sucking lice?

A

Head Lice and body lice

57
Q
  1. What do head lice do?
A
  • Suck blood from scalp and lay eggs on hair

- Common and easily spread by close contact, sharing of combs etc

58
Q
  1. What do body lice do?
A
  • Suck blood from body and lay eggs on clothing
  • Uncommon and spread by bodily contact, sharing of clothing or bedding
  • Vector diseases (epidemic typhus, trench, fever,relapsing fever)
59
Q
  1. What are some factors that would increase your chances of getting sucking lice?
A
  • Lousiness related to sanitation
  • Crowded conditions
  • Long periods without bathing or changing clothes
60
Q
  1. What are the two important families of sucking lice that attack humans?
A

PTHIRIDAE

  • Crab lice
  • Pubic Lice (bites cause irritation and typical rash. Spread by close body contact.Doesnt transmit infectious disease)
61
Q
  1. What are pthiridae-crab lice?
A
  • Broad flat lice that appear crab-like
  • Mid and Hind legs are stout with very large claws
  • Abdominal Segments have distinct lateral lobes
62
Q
  1. Which type of parasite causes botfly (Dermatobia Hominis)?
A

Ectoparasites

63
Q
  1. What is the life cycle of a botfly?
A
  1. Dermatobia Hominis is a certain type of fly
  2. Doesnt directly transmit infection
  3. Lays egg on mosquito
  4. Mosquito latches on animal ,due to change in temp, the egg hatches
  5. Larvae migrate into the skin
    * Common in cattle , although humans can be infected**
64
Q
  1. What is the geographical distribution of Dermatobia Hominis (the human botfly)?
A

-Central and Latin America

65
Q
  1. What is Myiasis?
A

A version of the botfly
head outside , rest of the body in the skin
Difficult to get out as larvae has rows of spines on the skin which stick to surrounding tissue

66
Q
  1. What are 5 drug treatments we can use for Protozoa infections?
A

Tinidazole

Metronidazole

Nitazoxanide

Benznidazole

Heavy metals (meglumine antimoniate)

67
Q
  1. What are 5 drug treatments we can use for Helminths infections?
A

Albendazole/ mebendazole

Praziquantel

Ivermectin

Diethylcarbamazine

Pyrantel

68
Q
  1. What are two drug treatments we can use for ectoparasites?
A

Ivermectin

Benzyl/malathion lotions

69
Q

69, What are the three main ways to control parasitic infections? Give examples of each way?

A

Behaviours
• Education
• Hand washing and hygiene behaviours

Environmental interventions
• Spraying of residual insecticides for household vectors • Mosquito nets for malaria
• Improved housing
• Sewage disposal and potable water
• Drainage of swamps

Poverty reduction
• Micro-financing, etc

70
Q
  1. How could we use pharmcotheraphy to treat parasitic infections in endemic areas?
A

For many parasite infections in an endemic settings, treatment must be given periodically over long periods of time because re-infections are rapid or because the treatment kills larval rather than adult stages

71
Q
  1. Which drug and doses would you give to treat
    - STH infections
    - Onchocerciasis
    - Schistosomiasis?
A

• a single dose of albendazole is given to high risk groups such as schoolchildren
up to every 4 months to control STH infections.

  • a single dose of ivermectin is given to endemic communities (mass drug administration) every 6 or 12 months to control onchocerciasis
  • a single dose of praziquantel is given to endemic communities (mass drug administration) every 6 or 12 months to control schistosomiasis

Medical Microbiology (15 decks)

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