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Flashcards in Parasitology Deck (56)
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1
Q

Define a parasite

A

An organism that lives on or in a host organism and gets food from or at the expense of its host

2
Q

What are the three classes of parasites?

A
  1. Protozoa - unicellular organisms
  2. Helminths - Worms
  3. Ectoparasites - fleas of scabes
3
Q

Describe protozoa

A
  • Microscopic, single celled organisms that can be free living (like amoeba) or parasitic in nature
  • They are able to multiply in humans allowing serious infections to develop from a single organism
4
Q

How can protozoa be transmitted?

A
  • Protozoa living in human intestine can be transmitted by the faecal-oral route
  • Protozoa living in blood can be transmitted by an arthropod vector
5
Q

Provide examples of the different types of protozoa (FACS)

A

Protozoa are mainly classified by their mode of movement

  • Flagellates, e.g. Giardia, Leishmania
    • propelled by flagella
  • Amoeba, e.g. Entamoeba
    • Moves by pushing out of pseudopodia
  • Ciliates e.g.Balantidium
    • use cilia around them
  • Sporozoa– e.g. Plasmodium, Cryptosporidium
    • organisms whose adult stage is not motile
6
Q
  • Entamoeba histolytica → Causes amebic dysentery
  • Giardia lamblia → Causes diarrhoea, contains flagella which propel through intestinal contents causes blunting of villi in small intestine
  • Trichomonas vaginalis → Motile protozoa which causes vaginal discharge
  • Malaria (Plasmodium spp.)
  • Toxoplasma gondii → Common parasite worldwide, transmitted from cat faeces to children
  • Cryptosporidium → Cause of epidemic diarrhoea, can cause growth stunting in children, can also cause chronic diarrhoea in patients with HIV (opportunistic diarrhoea)
  • Leishmania spp. → Causes systemic illness and cutaneous ulcers
  • Trypanosoma cruzi → Causes Chagas disease, endemic parts of Latin America
  • Trypansoma brucei (gambiense/rhodesiense)→ Acute inflammatory illness
A
7
Q

Describe Helminths and their main groups

A
  • Large, multicellular organisms (worms) visible to naken eye at later stages
  • In their adult form, helminths cannot multiply in humans

Three main groups of helminths

  1. Nematodes (roundworms)
  2. Trematodes (flukes)
  3. Cestodes (tapeworms)
8
Q

List some medically important helminths (nematodes)

A
  • *SOIL-TRANSMITTED HELMINTHS:**
  • Ascaris lumbricoides - the most common helminth parasite (can go up to 20-30 cm)
  • Trichuris trichiura – 3-4 cm, lives inside the large intestinal mucosa
  • Hookworm spp. – causes anaemia, they feed off of the blood supply of the small intestinal mucosa
  • Enterobius vermicularis – ‘itchy bum worm’, common
  • *FILARIAL PARASITES:**
  • Wuchereria bancrofti – lives in the blood, enters lymphatics and causes inflammation, causing elephantitis
  • Loa loa – eye worm
  • Onchocerca volvulus - can cause blindness
  • Dracunculus medinensis – guinea worm infection, lives in superficial tissues, female causes itching which causes a blister; victim goes to water to relive itching, which is when female releases her larvae
  • *OTHERS**
  • Toxocara canis/cati - get from cats/ dogs
  • Trichinella spiralis – comes through contaminated meat, causing trichonosis
9
Q

List some medically important helminths (trematodes and cestodes)

A
  • *TREMATODES:**
  • Schistosoma mansoni/haematobium/japonicum – live in the mesenteric vessels
  • Clonorchis sinensis – (fluke) lives in the bile duct, can cause cholangiocarcinoma, common in parts of asia, comes from eating poorly cooked fish
  • Fasciola hepatica – (liver fluke) used to be common
  • Paragonimus spp. – lung worm infection, can cause a TB-like illness
  • *CESTODES:**
  • Taenia saginata – beef tapeworm, causes a chronic infection
  • Taenia solium – pig tapeworm infection, if get infected at a certain lifecycle stage, can cause cycsticercosis, it has a world-wide distribution and is associated with epilepsy
  • Echinococcus granulosus – causes Hytadid disease which causes very large cysts in the organs such as liver, infection of dogs
10
Q

Define Ectoparasites

A
  • Bloos sucking athropods (e.g fleas, ticks, lice and mites)
  • These attach or burrow into the skin and remain there for relatively long periods of time (e.g weeks to months)
11
Q

Define some medically important ectoparasites

A
  • Mites
    • Scabies
    • Trombiculid
  • Ticks
    • Hard
    • Soft
  • Lice (head, body and pubic)
    • Pediculus humanus capitis
    • Pediculus humanus humanus
    • Pthirus pubis
  • Flies
    • Botflies – Cause myiasis (maggot lives under the skin)
12
Q

What are the two types of hosts that parasites can infect?

A

Two types of hosts are:

  • Intermediate → Host in which larval or asexual stages develop
  • Definitive → Host in which adult or sexual stage occurs
13
Q

What are the two types of vectors ?

A
  • Mechanical when there is no development of the parasite in the vector
  • Biological when some stages of life cycle occur in the vector
14
Q

What is the geographical distribution of parasitic infections?

A
  • The poorer the country = the more parasites present
  • You wont get NTDs (neglected tropical diseases) in wealthier and colder parts of the world
15
Q

Describe some determinants of parasitic infections

A

⇒ Depends on mode of transmission and opportunities for transmission

  • Faeco-oral
    • Household sanitation
    • Access to clean water
    • Personal hygiene behaviours
  • Food
    • Animal husbandry
    • Surveillance
    • Regulations and government controls
  • Complex life cycles
    • Distributions of vectors and intermediate/definitive hosts
  • Others
    • 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 (egChagas)
    • Urban vs. rural residence
    • Environmental sanitation
16
Q

What is chagas disease?

A
  • Tropical parasitic infection caused by the protist
    • Trypanosoma cruzi (protozoa)
  • It is transmitted through the faeces via the Reduviid kissing bug
  • Endemic in Latin America but also present in USA and Europe (mainly spain) due to migration
17
Q

Describe the life cycle of trypanosoma cruzi (Chagas Disease)

A
  1. Parasite will first develop in the midgut of the reduviid kissing bug
  2. Epimastigote→ Trypomastigote
  3. The kissing bug will feed on the face and defecate, if defecation contains trypomastigotes it can infect the skin through scratching the infected area
  4. The parasite will enter and multiply in nerve and muscle cells
  5. This will cause the release of thousands of blood trypomastigotes
  6. The life cycle is continued if another reduviid bug bites the individual taking up the infected blood
18
Q

How long is the incubation period in chagas?

A

1) ACUTE

  • Incubation 1-2 weeks after bite
    • (incubation means the time between when pathogen is first exposed and when symptoms show)
  • Up to months after transfusion
  • There will be presence of trypanosomes in blood
19
Q

What is the difference between chronic determinate and chronic indeterminate in chagas disease?

A

CHRONIC ‘INDETERMINATE’ - will have posotive serology but will be asymptomatic (no clinical manifestations)

  • Lifelong infection
  • Generally trypanosomes not detectable but often posotive for parasite DNA (through PCR)
  • Seroposotive (+ in blood)
  • 60-70% reach this stage
  • Normal ECG + X-rays

‘DETERMINATE’ CHRONIC DISEASE

  • Seroposotive
  • 30-40% of infected 10-30 years after acute infection
  • 5-10% develop chronic chagas immediately after acute disease
  • Involves heart and GI tract
20
Q

Describe acute chagas

A
  • This occurs within 3 weeks of exposure
  • Mild and non-specific symptoms
  • Fever, lymphadenopathy, anorexia
  • Swelling at bite site (nodule/chagoma) or eyelid swelling (romana)
  • 1-2 diagnosed, symptoms last 8-20 weeks

RARELY (when young and immunosuppressed)

  • Hepatosplenomegaly
  • Acute myocarditis
  • Meningoencaphalitis
21
Q

Describe how can acute chagas develop into chronic chagas?

A
  • Acute chagas can develop into chronic chagas 10-30 years later
  • This is where the host immune response will recognise the amastigotes and try to kill them causing more inflammation
  • The T.cruzi antibodies will still be high
  • Chronic chagas can be indeterminate (asymptomatic) or determinate (develop progressive symptoms)
22
Q

Describe what the cardiac effects that happen in chronic chagas

A
  • Inflammation can cause damage to the heart such as
    • Conduction system = cardiac arrhythmias
    • Heart mucle and wall = cardiomyopathy
    • Apical anuerysms = thrombus formaiton (can cause stroke)
      • Cardiac damage can lead to sudden death
23
Q

What digestive changes can occur due to chagas?

A
  • Develops in 10-15% of patients with chronic infections
  • Rectum, sigmoid colon and oesophagus are most affected
  • Can also cause damage to NS of gut = gut is unable to move contents and starts to swell. Thus, you get mega organs
  • A megacolon presents with constipation and can lead to faecaloma, obstruction, sigmoid volvulus, ulceration and perforation
24
Q

Describe the pathogenesis of Chagas

A

ACUTE

  • Tissue damage caused by inflammatory response to parasite in nests of amastigotes in cardiac, skeletal and smooth muscle
  • Parasite killing by antibodies, activated immune response and Th1 pro-inflammatory cytokines

INDETERMINATE

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

CHRONIC

  • 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
25
Q

What is Leishmaniasis?

A
  • Caused by a protozoan parasite called leishmania
    • Different forms of leishmaniasis
      • Visceral and Cutaneous (also different forms of cutaneous)
        • Visceral affects the visceral organs
  • Transmitted to humans via a sandfly
26
Q

Describe the leishmania life cycle

A
  1. Leishmaniasis is caused by sand fly which bites you
  2. This will transmit a promastigote
  3. This will infect immune cells succh as macrophages
  4. Here it will form nests of amastigotes
  5. The cells then burst releasing the pathogen to infect other cells
  6. Or a sand fly will bite you again taking up the infected blood causing continuation of the life cycle
27
Q

What is the vector in Leishmaniasis?

A

The vector is a sand fly known as Lutzomyia/Phlebotomus

28
Q

How does leishmaniasis result in formation of ulcers on the skin?

A
  • An individual will get bitten by a sand fly = formation of a papule that will spread
  • The centre will become necrotic and result in ulcer formation
  • Once an individual is infected they will usually develop immunity and not be infected again

Diffuse cutaneous leishmaniasis is when there is not an adequate immune response, the skin will become packed with parasites

29
Q

Describe the pathogenesis of cutaneous leishmaniasis

(acute lesions and latency)

A

ACUTE LESIONS

  • Tissue damage caused by inflammatory response to presence of parasites in macrophages
  • Parasite killing by Th1 pro-inflammatory responses and macrophage killing
    • Th1 will release beta and gamma interferon which will activate macrophages to kill parasites inside the cells

LATENCY

  • Parasites will remain present long-term
  • Regulatory immune response characterized by balance of Th1 and anti-inflammatory responses
30
Q

Describe the pathogenesis of cutaneous leishmaniasis

(relapse)

A
  • RELAPSE
  • Alteration in immune response (i.e change in Th1 vs immune regulation secondary to HIV, malnutrition) may trigger relapse
  • Mucocutaneous disease is associated with strong but inadequate inflammatory response to parasites which have metastasized to mucosa
  • Diffuse cutaneous leishmaniasis is associated with uncontrolled parasite replication
  • Recividans = recurrence of lesions at old ulcer site
31
Q

Describe the life cycle of Schistosomiasis

A
  1. Some water is contaminated with human faeces and the eggs of the schistosomiasis are in the water
  2. It develops into an intermediate stage called the miracidium which infects the snail (intermediate host)
  3. They asexually reproduce and release lots of cercariae which infects humans when they walk in contaminated water
  4. They develop into adults in the human mesenteric system and undergo sexual reproduction to produce many eggs
  5. These are released back into the environment = continum of life cycle
32
Q

What are the three main species of schistosomiasis?

A
  • Schistosoma mansoni (affects hepatic and intestinal system)
  • S. haematobium (affects urinary tract)
  • S. japonicum (affects hepatic and intestinal system)
33
Q

What is a common symptom following schistosoma infection

A
  • You can get cercarial dermatitis
  • Allergic type reaction when people who have become sensitised are exposed to cercarie in the water source
34
Q

What is the key feature in the immune response to schistosomamiasis

A
  • Eggs will become trapped in tissues leading to granuloma formation
  • In schistosomiasis you get repeated episodes of inflammation, and then damage to the tissues = damage related to the disease
    • Example of Th2 delayed hypersenstivity
35
Q

How can you get hepato-intestinal schistosomiasis?

A
  • Infection with S.mansoni and S.japonicum
  • Adults will be in mesenteric vessels, females will release eggs these go into intestines through capillaries and are pushed by immune response through mucosa and are excreted
  • Pathology is due to immune response of the egg
36
Q

Describe urinary schistosomiasis

A
  • Adults live in vessels around baldder, they will be pusged through mucosa in bladder and pushed into urine
  • Symptoms is HAEMATURIA
  • Inflammation of the bladder wall can also lead to cancer development
37
Q

What is onchocerciasis? (river blindness)

A
  • Major blinding disease
  • Caused by Helminth filarial parasite (Onchocerca volvulus) and transmitted by blackflies
  • Mainly in South America and Africa
38
Q

Life cycle of onchocerca volvulus

A
  • Black fly wil bite you and transmit larvae
  • Larvae will migrate under the skin and develop into adult worms
  • Adults will mate and produce unsheathed microfilariae which are found in the skin and lymphatics
39
Q

What is the pathology of onchocerciasis?

A
  • Repeated episodes of inflammation triggered by the presence of microfilariae leads to permanent damage and scarring of the eyes and skin
  • Skin → Parasite will actively down-regulate host immune response (drug will be used to try and trigger immune response and kill microfilariae
  • Can cause blindness in the eye
40
Q

What are the clinical features of the skin in onchocerciasis

A
  • Will appear as onchocercal nodules
    • Acute paular onchodermatitis
    • Chronic onchodermatitis
      • Due to loss and damage to the elastin of the skin
41
Q

What clinical features of the eye can present in oncocerciasis ?

A
  • Invasion of microfilariae will cause damage to the anterior segment (iris) of the eye first and then the back of the eye (damage to retina and optic nerve)
    • Anterior Segment
      • Punctate keratitis
      • Acute iridocyclitis
      • Sclerosing keratitis
    • Posterior Segment
      • Optic neuritis
      • Chorioretinopathy (damage to the RPE, able to see choroid underneath retina)
42
Q

What is the main reason why you go blind in onchocerciasis?

A

Due to chorioretinopathy

  • Chronic inflammation, damage to retina
  • RPE dies and overlying neural cells will also die
  • Choroid becomes visible underneath the retina
    • Once a person loses their macula they will become blind
43
Q

Immunopathogenesis of onchocerciasis

A
  • There are acute and chronic responses to the disease
    • Acute
      • Strong Th2 allergic response
      • IL4 (make IgE) and IL5 (recruits and activates eosinophils to site of inflammation) will be made
    • Chronic
      • Chronic episodes of inflammation causing the immune response to be shut down
        • Modified Th2 response = release of IL-10 and IgG4 so no apparent response to microfilariae in the skin
        • Complex interaction between host and parasite
44
Q

How does a tick attach itself to an organism?

A
  • The tick stick its mouth part into the skin and release a cement keeps it lodged
  • It will sit there and suck the blood of the organism
45
Q

Describe the two types of ticks and the diseases transmitted by them

A
  • Soft ticks = Q fever, Relapsing fever
  • Hard ticks = Ticky typhus, viral encephalitis, viral fevers, viral haemorrhagic fevers, tick paralysis

Lyme disease is a disease that can also be transmitted by ticks

46
Q

How can ticks cause paralysis ‘tick paralysis’?

A
  • Result of progressive flaccidity due to failure of Ach production in the neuromuscular junction
  • The ticks toxins will produce a block in the motor nerve fibres
47
Q

What are the different types of lice?

A

Head lice

  • Suck blood from the scalp and lay eggs on the hair
  • Common and easily spread by close contact, sharing combs, brushes and hats

Body lice

  • Suck blood and lay eggs on clothing
  • These are uncommon and spread by bodily contact, sharing of clothing or bedding
  • Transmit vector diseases like (epidemic typhus, trench fever, relapsing fever)
48
Q

What are the classification of suckling lice?

A
  • Pediculus humanus capitis
  • Pediculus humanus humanus
  • Pthirus pubis
49
Q

Describe pthiridae

A
  • Crab lice or pubic lice
  • Broad, flat lice that appear crab-like
  • Mid and hind legs are stout with very large claws
  • Abdominal segments have distinct lateral lobes
  • Single species (Pthirus pubus) confined to human pubic region
    • Bites cause irritation and typical rash
    • Spread by close body contract (usually sex)
    • No disease
50
Q

Describe how a botfly (Dermatobia hominis) infects organisms

A
  • Midflight it grabs the mosquito and lays its eggs on it
  • The mosquito will then go and bite an animal
  • Larvae will enter the host after the vector takes a blood meal
51
Q

Describe myaisis

A
  • Myaisis is an infection with fly larvae occuring in subtropical and tropical areas
  • There is a row of spines in the surrounding tissue making it difficult to remove
  • If larvae multiply too much it will be left untreated and result in death
52
Q

Describe some medications which are used to treat protozoa

A
  • Tinidazole
    • Shorter dose regiments
  • Metronidazole
    • More adverse reactions
    • 1 week or 2-week course
  • Nitazoxanide = used to treat protozoal infections
  • Benznidazole - Chagas disease used but causes very adverse reactions
  • Heavy metals (meglumine antimoniate) - used to be used in the past
53
Q

Describe some medications which are used to treat helminths

A
  • Albendazole/Mebendazole
  • Single dose, very effective
  • Praziquantel
  • Effective treatment for trematodes, flutes
  • Ivermectin
  • Diethylcarbamazine
  • Pyrantel
54
Q

Describe some medications used to treat ectoparasites

A
  • Ivermectin
    • Effective for most ectoparasites
      • Kill lice, botfly etc
      • Single dose
  • Benzyl/malathion lotions
    • Put on shampoos to treat head lice for example
    • However, not as effective
55
Q

How can we control parasitic infecitons?

A
  • Behaviours
    • Education
    • Hand washing and hygiene behaviours
  • Environmental intervations
    • Spraying of residual insectidices for household vectors
    • Mosquito nets for malaria
    • Improved housing
    • Sewage disposal and potable water
    • Drainage of swamps
  • Poverty reduction
    • Micro-financing, etc
56
Q

In terms of control of parasitic infections, what are implications of the treatment regime?

A
  • For many parasitic infections in an endemic setting, 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
    • E.g a single dose of ivermectin is given to endemic communities (mass drug administration) every 6 to 12 months to control onchocerciasis (kills larvae, not adults)

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