Parasitology and Pathogenesis of Parasite Infections 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 three main classes of parasites that cause disease in humans

A
  • Protozoa
  • Helminths
  • Ectoparasites
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3
Q

What are protazoa

A
  • Protozoa are microscopic, single-celled, free-living or parasitic organisms.
  • They are able to multiply in humans allowing serious infections to develop from a single organism.
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4
Q

How are protozoa trasmitted

A
  • 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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5
Q

How are protozoa classified

A

They are classified by they mode of movement

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6
Q

What are the different groups of protozoa

A
  • 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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7
Q

Name some medically important protozoa infections

A
  • Entamoeba histolytica
  • Giardia lamblia
  • Trichomonas vaginalis
  • Malaria (Plasmodium spp.)
  • Toxoplasma gondii
  • Cryptosporidium
  • Leishmania spp.
  • Trypansoma cruzi
  • Trypansoma brucei (gambiense/rhodesiense)
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8
Q

What are 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.

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9
Q

What are the main groups of helminths

A
  • Nematodes (roundworms)
  • Trematodes (flukes)
  • Cestodes (tapeworms)
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10
Q

List some medically important helminths - nematodes

A

Soil-transmitted helminths:

  • Ascaris lumbricoides
  • Trichuris trichiura
  • Hookworm spp.
  • Enterobius vermicularis

Filarial parasites:

  • Wuchereria bancrofti
  • Loa loa
  • Onchocerca volvulus
  • Dracunculus medinensis

Others:

  • Toxocara canis/cati
  • Trichinella spiralis
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11
Q

List some medically important helminths - Trematodes

A
  • Schistosoma mansoni/haematobium/jap nicum
  • Clonorchis sinensis
  • Fasciola hepatica
  • Paragonimus spp.
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12
Q

List some medically important helminths - cestodes

A
  • Taenia saginata
  • Taenia solium
  • Echinococcus granulosus
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13
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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14
Q

List some medically important ectoparasites

A

Mites:

  • Scabies
  • Trombiculid

Ticks:

  • Hard
  • Soft

Lice:

  • Pediculus humanus capitis
  • Pediculus humanus humanus
  • Pthirus pubis

Flies:

  • Botflies
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15
Q

Where are causes of high incidence rates of parasite infections

A
  • Tropic and subtropic climates
  • Temperate climates
  • In rural areas of low-income countries
  • High migration
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16
Q

What types of hosts can parasites have in their life cycle

A
  • Intermediate – host in which larval or asexual stages develop
  • Definitive – host in which adult or sexual stage occurs
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17
Q

What are the type of vector parasites can have

A
  • Mechanical when no development of parasite in vector
  • Biological when some stages of life cycle occur
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18
Q

What are the determinants of parasite infections

A
  • Depends on mode of transmission and opportunities for transmission
  • Faeco-oral
  • Food
  • Complex life cycles
  • Others
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19
Q

What are the Faeco-oral determinants of parasite infections

A
  • Household sanitation
  • Access to clean water
  • Personal hygiene behaviours
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20
Q

What are the food related determinants of parasite infections

A
  • Animal husbandry
  • Surveillance
  • Regulations and government controls
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21
Q

How can complex life cycles be a determinant of parasite infections

A

There are distributions of vectors and intermediate/definitive hosts

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22
Q

What are the other determinants of parasite infections

A
  • Government resources and level of human development/per capita income
  • Education
  • Country-level and regional control programmes
  • Availability of cheap and efficacious treatments
  • Construction and building regulations (eg Chagas)
  • Urban vs. rural residence
  • Environmental sanitation
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23
Q

Describe the life cycle of Trypansoma cruzi

A
  • Triatomine bug takes a blood meal
  • Metacyclic trypomastigotes penetrate various cells at the bite wound site. Transform not amastigotes inside cells
  • Multiply by binary fission in infected tissue cells
  • Transform into trypomastigotes then burst out into the bloodstream
  • Triatomine bug takes a blood meal and trypomastigotes ingested
  • Epimastogtes in midgut multiply and become metacyclic trypomastigotes in hind gut
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24
Q

What are the three phases of the Chagas disease

A
  • Acute
  • Chronic ‘indeterminate’
  • ‘Determinate’ Chronic disease
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25
Q

Describe the onset of the acute phase of Chagas

A
  • Incubation 1-2 weeks after bite
    – Up to months after transfusion
    – Trypanosomes in blood
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26
Q

Describe the symptoms in acute chagas

A

Occurs within 3 weeks
Generally mild or asymptomatic:

  • Local swelling (Romaña)
  • Nodule or chagoma
  • Fever
  • Anorexia
  • Lymphadenopathy

1-2% diagnosed

Symptoms last 8-10 wks

Rarely (young and IS):

  • Hepatopsplenomegaly
  • Acute myocarditis
  • Meningoencephalitis
  • Fatality <5% of
    symptomatic
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27
Q

Describe the Chronic ‘intermediate’ phase of chagas

A
  • Lifelong infection
  • Generally trypanosomes not detectable but often positive for parasite DNA
  • Seropositive
  • 60-70%
  • Normal ECG and X-rays
  • Cardiomyopathy/Heart failure
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28
Q

Describe the ‘Determinate’ Chronic disease phase of Chagas

A
  • Seropositive
  • 30-40% of infected 10-30 years after infection
  • 5-10% develop chronic Chagas immediately after acute disease
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29
Q

What is the digestive effect of chronic chagas

A
  • Develops in 10-15% of patients with chronic infections
  • Esophagus, rectum, and sigmoid colon are most affected
  • Patients present with constipation
  • Complications seen as: Faecaloma, Obstruction, Sigmoid volvulus, Ulceration, Perforation
30
Q

Describe the pathogenesis in acute chagas

A
  • Tissue damage caused by inflammatory response to parasites in nests of
    amastigotes in cardiac, skeletal, and smooth muscle
  • Parasite killing by antibodies, activated innate immune response and Th1 pro- inflammatory cytokines.
31
Q

Describe the pathogenesis in intermediate chagas

A

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

32
Q

Describe The pathogenesis in chronic chagas

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
33
Q

Describe the existence of the Leishmaniasis disease across the world

A

Visceral leishmaniasis:

  • Asia - Leishmania donovani
  • Middle East/Africa/Asia - L. infantum variants
  • Latin America - L. chagasi

Cutaneous leishmaniasis:

  • Mediterranean/Middle East - L. Infantum/L. major/L. tropica
  • Central and South America - L. braziliensis/amazonensis/mexicana
34
Q

Describe the life cycle of Leishmaniasis

A
  • Sand fly bites skin
  • Promastogote enters and is engulfed by histiocyte
  • Multiply by binary fission in cell
  • Amastigotes released from histiocytes and can infect other cells
  • When sand-fly bites again it takes up amastigotes
35
Q

What is the vector for leishmaniasis

A

Lutzomyia/Phlebotomus
Sand-fly

Bites at night and is small enough to fit though mosquito nets

36
Q

what can act as reservoirs for leishmaniasis

A
  • Domestic animals
  • Sylvatic animals
37
Q

What forms can cutaneous leishmaniasis show up as

A
  • Small papule
  • Plaques
  • Ulcers

Diagnosed by scarping ulcer and analysing with microscope

38
Q

Describe the effect of diffuse cutaneous leishmaniasis

A

Occurs when individuals cannot mount an immune response against the parasite

Highly pappilated

39
Q

Describe the symptoms faced in mucocutaneous leishmaniasis

A
  • Destruction of soft tissue in nose and facial regions.
40
Q

What is the pathogenesis in acute lesions of cutaneous leishmaniasis

A
  • Tissue damage caused by inflammatory response to presence of parasites in
    macrophages
  • Parasite killing by Th1 pro-inflammatory responses and macrophage killing.
41
Q

What is the pathogenesis in latent cutaneous leishmaniasis

A

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

42
Q

What is the pathogenesis in relapse of cutaneous leishmaniasis?

A

Alteration in immune response (i.e change in Th1 vs. immune regulation secondary to HIV, malnutrition) 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.
43
Q

What are the three main species involved in schistosmiasis

A
  • Schistosoma mansoni
  • S. haematobium
  • S. japonicum
44
Q

Describe the life cycle of schistosomiasis

A
  • Miracidia enters snails and undergo cycle
  • Cercaria emerges from snails
  • Enter host by penetrating skin or mucous membranes
  • Migrate via the heart to the portal vein
  • Schistosmula develops into male and female adult worms in portal and mesenteric veins
  • Worms copulate and move to vesicle veins, eggs are deposited and extruded through bladder mucosa
  • Eggs are passed in urine
  • Eggs hatch and release mircidia in water
45
Q

Describe the presentation of cercarial dermatitis due to schistosomiasis

A
  • Exposure to cercariae from
    animal or bird schistosomes
  • Requires pre-sensitization
  • Allergic-type reaction
46
Q

What are the key features of immune response in granuloma formation

A
  • Eggs become organized in granulomas
  • Repeated insults and tissue repair leads to fibrosis and
    organ damage
  • Cirrhosis - Damage of the liver by the eggs
47
Q

Describe Hepato-intestinal schistosomiasis

A

Infections with
S.mansoni and S.
japonicum

Pathology caused by
immune response to
eggs

Causes hepatospenomagaly

48
Q

Describe Urinary schistosomiasis

A

Damage to bladder by granulomas and damage to epithelial layer when eggs are pushed through

Blood present in the kidney - Haematuria

Higher risk of carcinoma of baldder

49
Q

What is Onchocerciasis

A
  • Major blinding disease
  • Caused by filarial parasite ( Onchocerca
    volvulus)
  • Transmitted by blackflies
  • Causes river blindness
50
Q

Describe the lifecycle of onchocera volvulus

A
  • Black fly takes a blood meal, L3 larvae enter at bite wound
  • Grows into adults in subcutaneous tissue
  • Adults produce unsheathed microfilarie that is found in skin but also in urine and sputum
  • Black fly takes a blow mean and ingests microfilarie
  • They penetrate blackly’s midgut and migrate to thoracic muscles
  • Become L1 Larvae
  • Become L3 larvae
  • Migrate to head and blackly’s proboscis
51
Q

what is the vector for onchocerca

A

The simulium, a species of fly

52
Q

Describe the pathology of onchocerciasis

A

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

53
Q

How does microfilariae present in patient

A
  • Presents as little bumps on the skin
  • An inflammatory response to microfilariae in the skin
54
Q

How is onchocerciasis a clinical disease

A

Onchocercal nodules

Skin disease:

  • Acute papular onchodermatitis
  • Chronic onchodermatitis
  • sowda

Eye disease:

Anterior segment:

  • Punctate keratitis
  • Acute iridocyclitis
  • Sclerosing keratitis

Posterior segment:

  • Optic neuritis/atrophy
  • Chorioretinopathy
55
Q

What is acute papular onchodermatitis

A

Bumps on the skin as an immune response to nodules

56
Q

How does chronic onchodermatitis present

A
  • Present as elephants skin symptoms
  • Chronic inflammatory response
57
Q

How does punctate keratitis present

A

damage to the eye

58
Q

How does sclerosis keratitis present

A

Occlusion of the cornea

59
Q

how does chorioretinopathy present

A

retina damage

60
Q

How does optic atrophy present

A

Damage to optic nerve

61
Q

What diseases are transmitted via hard ticks

A
  • Tick typhus
  • Viral Encephalitis
  • Viral fevers
  • viral hemorrhagic fevers
  • Tularemia
  • Tick paralysis
  • Human babesiosis
62
Q

What diseases are transmitted by soft ticks

A
  • Q fever
  • Relapsing fever
63
Q

why are ticks medically important

A
  • Mechanical injury by the bite
  • Tick paralysis
  • Tick’s toxins produce a block in motor nerve fibres
  • Ticks are carriers of many diseases
64
Q

What are head lice

A
  • Suck blood from the scalp and lay eggs in the hair
  • easily spread with contact and sharing of combs
65
Q

What are body lice

A
  • Sucks blood from the body and lays eggs on clothing
  • Spread by bodily contact, sharing of clothing and bedding
  • Vectors for diseases such as epidemic typhus, trench fever and relapsing fever
66
Q

What are 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
  • Pthirus pubs confined to human pubic region
67
Q

What drugs are used to control Protozoa

A
  • Tinidazole
  • Metronidazole
  • Nitazoxanide
  • Benznidazole
  • Heavy Metals
68
Q

What drugs are used to control Helminths

A
  • Albendazole/mebendazole
  • Praziquantel
  • Ivermectin
  • Diethylcarbamazine
  • Pyrantel
69
Q

What drugs are used to control Ectoparasites

A
  • Ivermectin
  • Benzyl/malathion Lotions
70
Q

What behavioural changes can control parasite infection

A
  • Education
  • Hand washing and hygiene behaviour
71
Q

What environmental interventions can control parasite infections

A
  • Spraying of residual insecticides for household vectors
  • Mosquito nets for malaria
  • Improved housing
  • Sewage disposal and potable water
  • Drainage of swamps
72
Q

How else can parasite infections be controlled

A

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