Parasitology Flashcards

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1
Q

What is a parasite?

A

A parasite is an organism that lives on or in a host organism and gets its food from or at the expense of its host.

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2
Q

What are the 3 main classes of parasite?

A
  • Protozoa
  • Helminths
  • Ectoparasites
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3
Q

What are protozoa?

How are they transmitted?

A

Protozoa are microscopic, single-celled organisms that can be free- living or parasitic in nature.
They are able to multiply in humans allowing serious infections to develop from a single organism.

Transmission:
• Protozoa living in the human intestine can be transmitted by the fecal-oral route
• Protozoa living in blood or tissues are transmitted by an arthropod vector

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4
Q

What are the types of protozoa?

A

Types of protozoa – protozoa are classified by mode of movement

  • Amoeba, e.g. Entamoeba
  • Flagellates, e.g. Giardia, Leishmania
  • Ciliates e.g. Balantidium
  • Sporozoa – organisms whose adult stage is not motile e.g. Plasmodium, Cryptosporidium
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5
Q

What are helminths?

What are the 3 main groups of helminths?

A

Helminths are large, multicellular organisms (worms) generally visible to the naked eye in their adult stages. In their adult form, helminths cannot multiply in humans.

There are three main groups of helminths that are human parasites:
• Nematodes (roundworms)
• Trematodes (flukes)

Schistosoma mansoni/haematobium/japonicum- schistosomiases. Adults live in mesentery vessels.
Clonorchis sinensis- lives in bile duct. Chronic infection leads to clonangial carcinoma. From poorly cooked fish. Fluke.
Fasciola hepatica- liver fluke. Used to be common in Europe.
Paragonimus spp.- lung worm infection. TB-like symptomsm

• Cestodes (tapeworms)

Taenia saginata- beef tape worm. Chronic infection. Not too serious.
Taenia solium- pig tape worm is an intestinal infection with adult tapeworms that follows ingestion of contaminated pork. Infected by wrong stage of life cycle, can causes cysticercosis. Forms nodules on brain if exposed to larvae, associated with epilepsy.
Echinococcus granulosus- infection affects dogs. Eggs from dog causes hydatid disease, causing cysts in organs, such as liver. Rupture leads to rapid death from anaphylaxis- related to release from allergens from parasite into circulation.

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6
Q

Give some examples of medically important soil transmitted helminths

A

Medically important helminths - nematodes
• Soil-transmitted helminths • Ascaris lumbricoides
o Trichuris trichiura
o Hookworm spp.
o Enterobius vermicularis

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7
Q

What are ectoparasites?

A

Blood-sucking arthropods such as ticks, fleas, lice, and mites that attach or burrow into the skin and remain there for relatively long periods of time (e.g., weeks to months).

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8
Q

Give some examples ectoparasites

A
•	Mites
o	Scabies 
o	Trombiculid
•	Ticks 
o	Hard
o	Soft 
•	Lice
o	Pediculus humanus capitis 
o	Pediculus humanus humanus 
o	Pthirus pubis 
•	Flies
o	Botflies
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9
Q

What are the determinants of parasitic infections?

A

• Depends on mode of transmission and opportunities for transmission
• Faeco-oral
o House hold sanitation
o Access to clean water
o Personal hygiene behaviours
• Food
o Animal husbandry
o Surveillance
o Regulations and government controls
• Complex life cycles
o Distributions of vectors and intermediate/definitive hosts
• Others
o Government resources and level of human development/per capita income
o Education
o Country-level and regional control programmes
o Availability of cheap and efficacious treatments
o Construction and building regulations (e.g.Chagas)
o Urban vs. rural residence
o Environmental sanitation

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10
Q

Describe the life cycle of Trypansoma cruzi

A

On image

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11
Q

What are the phases of disease?

A
•	Acute 
o	Incubation 1-2 wks after bite 
o	Up to months after transfusion 
o	Trypanosomes in blood 
•	Chronic ‘indeterminate’ 
o	Lifelong infection 
o	Generally trypanosomes not detectable but often positive for parasite DNA 
o	Seropositive 
o	60-70% 
o	Normal ECG and X rays 
•	‘Determinate’ Chronic disease
•	Seropositive 
•	30-40% of infected 10-30 years after infection 
•	5-10% develop chronic Chagas immediately after acute disease
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12
Q

What is acute chagas?

A

Reduvidae (kissing) bug that live in cracks.
Big colonies when in proximity with chickens or dogs.

Caues by trypansoma- feeds on you at night and then defecates. Scratching allows entry of faeces into skin (or rubbed into eyes).

Multiplies in nerve and muscle cells. Rupture.
Biological vector.

Migration from spain (where 87% of cases are) to US, so
seen there too.

Acute- 1-2 weeks incubation and transplanted in blood.
Chronic indeterminate- picked up in DNA not blood as not detectable. Seropositive and appear normal- ECG and x-ray.

High proportion develop chronic Chagas disease (30-40%). Cardiac and intestinal disease 10-30 years after. Some straight after acute illness.

May swell locally (Romana) or on hand (chagoma). Few people are diagnosed as symptoms 2 weeks. Also, anorexia, fever and lymphadenopathy.

Rarely, but in young, can get hepatosplenomegaly, acute mayocarditis, meningoencephalitis and less that 5% will die.

Chronic Chagas- damage to conduction of heart (arrhythmia) and to muscle wall (cardiomyopathy), causing apical aneurysum or thrombus formation.
Sudden death.

Digestive disease- unable to move contents on so wells. 1-15%- affects oesophagus, rectum and colon, giving constipation, impaction, etc.

Pathogenesis- tissue damage caused by inflammatory response to parasite in nests of amastigotes in cardiac, skeletal and smooth muscle.

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

Indeterminate- regulatory immune response with IL-10 and IL-17.

Chronic inflammatory response to persistent parasites in muscle and nerve bells.

Autoimmune mechanisms- loss of tolerance and causing autoimmunity.

Varies by strain and tissue tropism.

Predominance of Th1 cytokines and CD8+ cytotoxic T-cells.

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13
Q

Where can Acute Chagas occur?

A

Chronic Chagas: Cardiac
Chronic Chagas: Digestive
• Develops in 10-15% of patients with chronic infections
• Esophagus, rectum, and sigmoid colon most affected

Chronic Chagas; Megacolon
•	Presentation 
o	Constipation 
•	Complications 
o	Faecaloma
o	Obstruction
o	Sigmoid volvulus 
o	Ulceration
o	Perforation
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14
Q

Describe the pathogenesis of chagas

A

• Acute
o Tissue damage caused by inflammatory response to parasite in nests of amastigotes in cardiac, skeletal, and smooth muscle
o Parasite killing by antibodies, activated innate immune response and Th1 pro- inflammatory cytokines.
• Indeterminate
o Regulatory immune response characterized by IL-10 and IL-17
• Chronic
o Chronic inflammatory response to persistent parasites in muscle and nerve
o cells
o Autoimmune mechanisms
o May vary by parasite strain and tissue tropism
o Predominance of Th1 cytokines and CD8+ T cells

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15
Q

Describe the life cycle of Protozoa - leishmania

A

On image

  • Lifecycle- Caused by sandfly bite and transmits promastigote which invades immune cells- macrophage. Amastigote formed and released when cell bursts.
  • Infects other cells.
  • Bite form sand-fly takes up parasite and transmitted to others.
  • Vector- Lutzomyia/phlebotomus (sand fly). Common in tropical regions in cracks. Also in proximity to chicken. Can see bites.
  • Zoonotic infections- domestic (dogs) and slyvatic (sloths).
  • Papules spread from bite and necrosis into ulcer. Infection as a child will have immunity as adults, if stay in area with same strain. Many adults in latin America have scars. Will never go away and scar can be reactivated.
  • Can have reactivation or dissemination.
  • Sporotrichoid leishmaniasis - follows along lymphatics.
  • Some cannot mount proper defense- diffuse cutaneous leishmaniasis. Packed with amastigotes.
  • Mucocutaneous- stuffy nose and lesions in mucosal area. Break down of nasal septum.
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16
Q

Describe the Pathogenesis of cutaneous leishmaniasis

A

• Acute lesions
o Tissue damage caused by inflammatory response to presence of parasites in macrophages
o Parasite killing by Th1 pro-inflammatory responses and macrophage killing.
• Latency
o Parasites remain present long-term. Regulatory immune response characterized by balance of Th1 and anti-inflammatory responses
• Relapse (rare)
o Alteration in immune response (i.e. change in Th1 vs. immune regulation secondary to HIV, malnutrition) may trigger relapse
o Mucocutaneous disease associated with strong but inadequate inflammatory response to parasites that have metastasized to mucosa
o Diffuse cutaneous leishmaniasis associated with uncontrolled parasite replication
o Recividans–recurrence of lesions at old ulcer site.