Week 6 - Parasites Flashcards

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1
Q

What is a parasite?

A
  1. An organism that lives on or in a host organism and gets its food from or at the expense of its host
    a) Most successful parasites maintain life without killing their hosts
  2. Parasites have a complex life cycle
    a) May involve an insect vector in transmission
    b) Infect humans and animals which act as reservoirs of infection, there may be 2 or more hosts (e.g. in many helminth infections)
  3. Types of hosts:
    a) Definitive host - has the adult stage of the parasite
    b) Intermediate host - has immature or larval forms of parasite
    c) Accidental host - humans are not the host’s intended target but accidentally ingest parasite states (e.g. eating infected meat that contains parasite cysts)
  4. Three main classes:
    a) Protozoa
    b) Helminths
    c) Ectoparasites
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2
Q

What are protozoa?

A
  1. Microscopic, one-celled organisms that can be free-living or parasitic in nature
  2. Are able to multiply in humans which contributes to their survival but also permits serious infections to develop from just a single organism
  3. Transmission of protozoa that live in human’s intestine occurs through faecal-oral route
  4. Transmission of protozoa that live in blood or tissue occur by an arthropod vector (e.g. mosquitoes)
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3
Q

How are protozoa classified?

A
  1. Based off their 18SrDNA sequences
    a) Used to be classified by mode of movement
  2. Classifications are:
    a) Excavata (Flagellates)
    b) Rhizaria
    c) Amoebozoa
    d) Alveolata
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4
Q

What are helminths?

A
  1. Large, multicellular invertebrates that are generally visible to the naked eye in their adult stages
  2. They can be either free-living or parasitic in nature
  3. Helminths cannot multiply in humans
  4. Have organ systems; reproductive, digestive, excretory, nervous (no circulatory)
  5. Can be hermaphrodite or bisexual
  6. Features:
    a) External surface covered by a cuticle
    b) Many have hooks, suckers, teeth, plates
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5
Q

What are the types of helminths?

A
  1. Flatworms - include the trematodes (flukes) and cestodes (tapeworms)
  2. Thorny-headed worms (acanthocephalins) - the adult forms of these worms reside in the gastrointestinal tract
  3. Roundworms (nematodes) - the adult forms of these worms can reside in the gastrointestinal tract, blood, lymphatic system, or subcutaneous tissues
    a) Alternatively, the immature (larval) states can cause disease through their infection of various body tissues
    b) Long cylindrical worm with outer cuticle as body wall
    c) Contain complex and complete digestive system (mouth, intestine, anus)
    d) Sex organs on different worms - separate male (smaller) and female (ovary continuous with oviduct, uterus, and vagina): copulation requited for egg formation
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6
Q

What are ectoparasites?

A
  1. Broadly include blood-sucking arthropods such as mosquitoes, ticks, fleas, lice, and mites that attack or burrow into the skin and remain there for long periods of time
  2. Arthropods are important in causing diseases in their own right, but are also important vectors of many different pathogens
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7
Q

What are the characteristics and features of protozoa?

A
  1. 3 characteristics:
    a) Eukaryotic
    b) Unicellular
    c) Lack a cell wall
  2. Found or acquired from:
    a) In moist environments (waterways, soil)
    b) Amongst decaying organic materials
    c) Within bird and animal faeces
    d) Contaminated water
    e) Food washed in contaminated water
    f) Insect bites
  3. Features:
    a) Mostly motile (except for Apicomplexa) achieved by cilia, flagella, and pseudopodia
    b) Mitochondria vary in number (absent/multiple) and type (-discoid or tubular cristae, not platelike as for animals)
    c) Some have vacuoles to pump out water
    d) Many have feeding/reproducing forms = trophozoite
    e) Some form cysts = a hardy resting form with a capsule that can survive adverse conditions
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8
Q

How do protozoa reproduce?

A
  1. Mostly asexual via binary fission - schizogony (multiple fission)
  2. Some sexual - gametes fuse to form zygote
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9
Q

Describe the types of excavata (flagellates):

A
  1. Parabasalids:
    a) Lack mitochondria
    b) Have golgi-like structure
    c) Anaerobes
  2. Diplomonads:
    a) 2 nuclei
    b) Lack mitochondria but have mitochondrial genes in nuclear chromosome (mitosome)
  3. Euglenids:
    a) Nonpathogenic
    b) Chloroplasts
  4. Kinetoplastids:
    a) Single large mitochondria that contains kinetoplast
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10
Q

Describe the types of Rhizaria:

A
  1. Radiolaria:
    a) Planktons
    b) Covered by a porous crystallised external skeleton
    c) Silica with outer ectoplasm and inner endoplasm
  2. Forminifera:
    a) External skeleton of calcium carbonate
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11
Q

Describe the Amoebozoa:

A
  1. Move and feed with lobe-shaped (blunt) pseudopods and no shell
  2. Types:
    a) Entamoeba
    b) Gymnamoeba - free living
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12
Q

Describe the types of Alveolata:

A
  1. Ciliates:
    a) Covering or tufts of cilia
  2. Apicomplexa:
    a) Have intracellular organelles for penetrating cells
  3. Dinoflagellates:
    a) Have photosynthetic pigments, bioluminescence
    b) Have flagella that cause spinning
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13
Q

What does a Helminth infection involve?

A
  1. Comprise nutritional status
  2. Affect cognitive processes, impaired memory, and cognition leads to education deficits
  3. Diminished physical fitness
  4. Cause intestinal obstruction or rectal prolapse
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14
Q

What are cestodes (tapeworm)?

A
  1. Adult stages are intestinal parasites in definite host
    a) Adults have a head (scolex with hooks and suckers) for attachment
    b) Long chain of body segments (proglottids) - each proglottid has male and female sex organs for egg production (hermaphrodite)
    c) Immature near head, mature near end
  2. Larval forms are cystic or solid
  3. Transmission cycle:
    a) Mature proglottids detach from adult worm and are shed in the faeces to contaminate water and vegetation - each tapeworm has about 1000 proglottids which have 50,000 eggs each
    b) Eggs are ingested by the intermediate host (pig, cow, dog)
    c) Larvae burrow into intestinal wall and form a cyst in the animal tissue
    d) Humans are infected by eating infected animal tissue
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15
Q

What are trematodes (flukes)?

A
  1. Flat leaf-shaped body - 3mm-8cm
  2. Features:
    a) Muscular suckers - oral and ventral for anchoring
    b) Mouth, pharynx, intestine but no anus
    c) Complex internal reproductive system - hermaphrodite (except for blood flukes)
  3. Life cycle:
    a) Eggs passed from urine, faeces, sputum into water
    b) Eggs hatch to cilated larvae (miracidium) which are then eaten by snails
    c) Sporocyst sac develops asexually in snail
    d) Larva released from snail as mobile cerceriae into water to encyst
  4. 2 groups of flukes:
    a) Tissue flukes (attach to tissue)
    b) Blood flukes (schistosomes) (in blood vessels)
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16
Q

What is Giardia?

A
  1. Type of pathogen:
    a) Microscopic parasite (protozoa)
    b) Strict Anaerobic flagellate (with a mitosome) in gut
    c) Can exist in 2 forms; cyst (infective stage-external) and trophozoite (mostly in vivo)
  2. Symptoms:
    a) Diarrheal illness (Giardiasis) - symptoms can last for 1-2 weeks or longer
    b) Can be asymptomatic
    c) Diarrhoea
    d) Gas
    e) Greasy stools that tend to float
    f) Stomach or abdominal cramps
    g) Upset stomach or nausea/vomiting
    h) Dehydration (loss of fluids)
  3. Transmission:
    a) Found on surfaces or in soil, food, or water that has been contaminated with faeces from infected humans or animals
    b) Water is the most common mode of transmission
  4. Features:
    a) Protected by an outer shell that allows it to survive outside the body for long periods of time and makes it tolerant to chlorine disinfection
  5. Life cycle:
    a) Contamination of water or food with cysts
    b) Cysts are ingested via oral route
    c) Cysts develop into trophozoite in intestinal tract
    d) Trophozoite replicates via binary fission and these will form cysts
    e) Cysts are excreted and contaminate further food and water
  6. Diagnosis:
    a) Multiple stool collections over multiple days necessary to increase test sensitivity (this is because Giardia cysts can be excreted intermittently)
    b) Faecal immunoassays are the most sensitive and specific diagnostic test
  7. Treatment:
    a) Several drugs can be used to treat Giardia infection which include metronidazole, tinidazole, and nitazoxanide
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17
Q

What is Entamoeba histolytica?

A
  1. Type of pathogen:
    a) Amoebiasis
    b) Pathogenic ameba associated with intestinal and extraintestinal infections
  2. Life cycle:
    a) Mature cyst is ingested and moves into GIT
    b) Parasite becomes invasive and moves outside GIT into other organs such as liver, lungs, and brain
    c) Excystation into trophozoites which multiply into either more trophozoites or cysts
    d) Cysts are excreted
  3. Symptoms:
    a) Loose faeces
    b) Stomach pain
    c) Stomach cramping
    d) Amebic dysentry is a severe form of amebiasis associated with stomach, bloody stools, and fever
  4. Prevention:
    a) Good hygiene
    b) Avoid handling food if infected
  5. Diagnosis - via stools
    a) Faecal microscopy repeated over days
    b) Wet mount and staining (Trichrome)
    c) Antigen test
    d) Serology
  6. Treatment:
    a) Oral rehydration Metronidazole
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18
Q

What is toxoplasmosis?

A
  1. An infection caused by a single-celled parasite called Toxoplasma gondii
  2. Type of pathogen:
    a) Apicomplexa - non motile parasite
  3. Life cycle:
    a) Unsporulated oocysts shed in cat faeces is ingested by rats or birds
    b) Development of tissue cysts occurs in these birds or rats
    c) Cats ingest infected birds and rats and so cycle continues
    d) The cat faeces can also infect pigs and sheep through same mechanism
    e) Humans ingest contaminated meat from pigs and sheep
    f) Cat faeces can also be contaminated directly to humans by cat litter being infected with cysts
    g) When cat litter is changed, if individual does not wash hands and then eats or drinks then they get infected
    h) This microorganism can also cross placental barrier in infected pregnant women and kill foetus
  4. Modes of transmission:
    a) Eating infected meat
    b) Consuming food or water contaminated with cat faeces
    c) Blood transfusion or organ transplantation
    d) Transplacentally from mother to foetus
  5. Diagnosis:
    a) Serology
    b) Overserved in stained biopsy specimens
    c) Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR
  6. Symptoms:
    a) 4-21 days after infection
    b) Healthy individuals - 80% have no symptoms or permanent damage: mild, flu like illness with low grade fever, muscular pain, swollen lymph nodes, lethargy, headache
    c) Immunocompromised - fever, malaise, invasion into tissue (inflammation in lungs, liver, heart; blindness, encephalitis; death)
    d) Foetus - parasite can pass from mother to foetus and can lead to hydrocephaly, microcephaly, convulsions, mental retardation, defective vision and hearing
  7. Treatment:
    a) Pyrimethamine + sulfonamides 3-4 weeks
    b) Toxic in pregnancy (Spiromycin if maternal infection only - doesn’t cross placenta)
    c) AIDS patients - include steroids to reduce tissue inflammation
  8. Prevention:
    a) No vaccine
    b) Avoid contact with contaminated soil, cat faeces
    c) Eat well-cooked meat during pregnancy
    d) Test serology before pregnancy - amniocentesis
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19
Q

Describe malaria:

A
  1. Type of pathogen:
    a) Protozoa - Plasmodium spp.
    b) Apicomplexa - non motile
    c) Obligate parasites of vertebrates and insects
  2. Features:
    a) 14 chromosomes, single mitochondria, ER, Golgi
    b) Specialised rhoptries for host cell entry
  3. Infection site:
    a) Lives inside red blood cells (and hepatocytes)
  4. Forms:
    a) Sexual forms: Gametocytes
    b) Asexual forms: Sporozoite, Merozoite, Schizont
  5. Transmission:
    a) Spread via bite of female mosquito Anopheles spp.
  6. Diagnosis:
    a) Microscopy: Giemsa stain of thick (low parasitaemia) and thin blood smears to detect infected RBCs
    b) No of parasites/No of WBCs counted x 8000 = No. of parasites
    c) Serology: not feasible for route use as delay in Ab response (more useful for previous exposure)
    d) PCR: Use for confirmation of microscopy, low parasitaemias and mixed infections
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20
Q

Describe the life cycle of malaria:

A
  1. Mosquito takes blood meal and injects parasite in sporozoite form into human
  2. Parasite travels to liver cell
    a) Infected liver cell will replicate sporozoite and form Schizont
  3. Schizont causes hepatocyte to rupture and moves into blood stage
  4. Released Schizont infects red blood cells and develop into immature trophozoite (ring stage)
    5a. Immature trophozoite develops into mature trophozoite which then develops into schizont
    5b. Schizont ruptures red blood cells and released into blood and cycle continues
    6a. Immature trophozoite can also cause gametocytes
    6b. Gametocytes circulate in blood stream and when mosquito has a meal it ingests the gametocytes
    6c. Macrogametocytes form in mosquito which form oocyst
    6d. Oocyst ruptures which releases sporozoites into mosquito
    6e. Mosquito bites human and cycle begins again
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21
Q

What are the species of Malaria that infect humans?

A
  1. Plasmodium vivax - most widespread but least lethal
  2. Plasmodium falciparum - most deadly
  3. Plasmodium malariae
  4. Plasmodium ovale
  5. Plasmodium knowlesi
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22
Q

What are the symptoms of Malaria?

A
  1. Acute febrile illness
    a) Cycle of fever (40C) and chills, vomiting, headache, dizziness
  2. Fever cycles equate to in vivo growth cycles
    a) RBCs are main site of infection - parasite consumes and degrades intracellular RBC proteins (mainly haemoglobin)
  3. Severity progresses quickly (particularly in children) leading to:
    a) Severe anaemia
    b) Respiratory distress (metabolic acidosis)
    c) Increase ESR
    d) Decrease BP
    e) Increase cardiac dilation
  4. Severe symptoms can lead to:
    a) Multi-organ involvement; Fe sequestration in BM
    b) Liver damage and hepatomegaly
    c) Cerebral malaria
    d) Splenomegaly
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23
Q

What is treatment and prevention of Malaria?

A
  1. Treatment:
    a) Prophylaxis drugs kill parasite
  2. Prevention:
    a) Avoid mosquito bites (insect repellent, bed-nets, bed-nets impregnated with insecticide, protective clothing, education
    b) Kill mosquitoes
    c) Limit breeding - inhibit reproduction (destroy mosquito habitat)
24
Q

Describe malaria vaccine:

A
  1. Difficult to create vaccine due to complex life cycle - too much variability
  2. Current vaccines show:
    a) Lack of sterile immunity
    b) Partial immunity that is not long lasting
    c) Efficacy may be low and very expensive to produce
25
Q

Describe Trypanosomiasis:

A
  1. Two forms:
    a) American trypanosomiasis (Chagas disease) caused by Trypanosoma cruzi transmitted by insect bite of the kissing bug (Triatoma sp.)
    b) African trypanosomiasis (African sleeping sickness) transmitted by bite of the tsetse fly (Glossina spp.)
26
Q

Describe African Sleeping sickness:

A
  1. Type of pathogen:
    a) Protozoa
    b) Hemoflagellates of the genus Trypanosoma in subgenus Trypanozoon
    c) T.b. gambiense causes West African Sleeping sickness; T.b. rhodesiense causes East African sleeping sickness
  2. Life cycle:
    a) Tsetse fly takes a blood meal and injects metacyclic trypomastigotes into blood stream
    b) Injected parasite transforms into bloodstream trypomastigotes which is carried to other sites
    c) Trypomastigotes undergo binary fission in various body fluids
    d) Circulating trypomastigotes is undetectable in latent phase
    e) Tsetse fly takes another blood meal and ingests trypomastigotes
    f) Bloodstream trypomastigotes transform into procyclic trypomastigotes which multiply by binary fission in midgut of fly
    g) Procylic trypomastigotes leave the midgut and transform into epimastigotes
27
Q

Describe African Sleeping sickness:

A
  1. Type of pathogen:
    a) Protozoa
    b) Hemoflagellates of the genus Trypanosoma in subgenus Trypanozoon
    c) T.b. gambiense causes West African Sleeping sickness; T.b. rhodesiense causes East African sleeping sickness
  2. Life cycle:
    a) Tsetse fly takes a blood meal and injects metacyclic trypomastigotes into blood stream
    b) Injected parasite transforms into bloodstream trypomastigotes which is carried to other sites
    c) Trypomastigotes undergo binary fission in various body fluids
    d) Circulating trypomastigotes is undetectable in latent phase
    e) Tsetse fly takes another blood meal and ingests trypomastigotes
    f) Bloodstream trypomastigotes transform into procyclic trypomastigotes which multiply by binary fission in midgut of fly
    g) Procylic trypomastigotes leave the midgut and transform into epimastigotes
    h) Epimastogotes multiply in salivary gland and are transformed into trypomastigotes
    i) Tsetse fly takes blood meal and injects trypomastigotes and cycle continues
28
Q

What are the symptoms of African Sleeping Sickness?

A
  1. Can appear weeks/months after bite and are initially mild
  2. Early 1-3 weeks: sore from bite
  3. Weeks later: Parasites in blood and lymph
    a) Fever
    b) Headache
    c) Malaise
    d) Joint pain
  4. Final stages (after a month):
    a) Parasites cross blood brain barrier and enter brain, CNS, and CSF
    b) Neurological symptoms - inflammation of CNS, disruption of sleeping patterns, ataxia, mood changes, blackout, coma, multiple organ failure, and death
    c) Parasite produces the alcohol tryptophol which triggers sleep
    d) Fatal if not treated
29
Q

What is the diagnosis of African Sleeping Sickness?

A
  1. Clinical examination where travel history is attained
  2. Microscopic examination before and after centrifugation of blood
    a) Cervical lymph node aspirate can be checked
    b) CSF can be checked
  3. CBC:
    a) Increased ESR
    b) Low haematocrit (anaemia)
    c) Decreased Albumin
  4. PCR - detection of parasite DNA
  5. Serology - both IgM and IgG antibody titrates in infected individuals (this is because symptoms take so long to show that antibodies have usually begun to be made)
30
Q

What is the treatment and prevention of African Sleeping Sickness?

A
  1. Prevention:
    a) No available vaccine
    b) Insect repellent and insecticide spraying
    c) Bed nets
    d) Cover body including arms with light or dull clothing as fly is attracted to dark and bright colours
    e) Avoid bushy areas of fly habitat
    f) No prophylaxis, no vaccine
  2. Treatment (depends on stage of infection)
    a) Pentamidine (West) or Suramin (East) - Potent inhibitors of parasitic enzymes and enhance Th1 cytokines
    b) Later stage: Nifurtimox + Elfornithine via IV perfusion
31
Q

Describe Leishmaniasis:

A
  1. Type of pathogen:
    a) Protozoa
    b) Obligate intracellular of the genus Leishmania
    c) Transmitted by bite of female sandfly
  2. 3 main forms of the disease:
    a) Visceral - most serious (fatal if untreated); slow progression which includes fever, weight loss, enlarged liver and spleen, BM
    b) Cutaneous - most common; causes skin lesions and ulcers, scarring and disability, some immunity
    c) Mucosal - destruction of mucosa of nose, mouth, throat
32
Q

Describe life cycle of leishmania:

A
  1. Sandfly takes blood meal and injects promastigoes stage of parasite into the skin
  2. Promastigotes get phagocytosed by macrophages or other types of mononuclear phagocytic cells
  3. Promastigotes transform into amastigotes
  4. Amastigotes multiply in cells and causes these cells to burst, thereby releasing parasite to infect other cells
  5. Sandfly takes a blood meal and ingest macrophages infected with amastigotes
  6. Amastigotes transform into promastigote stage in gut of sandfly
  7. Parasite divide in the gut and migrate to proboscis
  8. Sandfly takes blood meal and injects parasite and cycle continues
33
Q

What is the diagnosis of Leishmania?

A
  1. Microscopy:
    a) CL (cutaneous) - tissue samples - staining of infected macrophages
    b) VL (visceral) - bone marrow samples or splenic aspirates
  2. Serology:
    a) Anti-leishmania Ab in agglutination assay for VL Ig levels
  3. Genomic:
    a) PCR to detect and distinguish species
34
Q

What is the treatment and prevention of Leishmania?

A
  1. Treatment:
    a) CL - local or IV injection of skin lesions with antimonial
    b) VL - IV antifungal (amphotericin B) which binds to parasite ergosterol precursors such as lanosterol and cause disruption of the parasite membrane
  2. Prevention:
    a) No prophylaxis and no vaccine
    b) Avoid biting times (early morning/dusk) and locations
    c) Use insecticides, screens, and bednets
    d) Cover skin - long sleeves and long pants/dresses
    e) Insecticide-impregnated dog collars and culling of infected animals
35
Q

What is Ascaris spp. (Pinworm/threadworm)?

A
  1. Type of pathogen:
    a) Nematode - roundworm
  2. Transmission:
    a) Female worm deposits eggs in perianal folds
    b) Auto-infection can occur by scratching perianal area and transferring eggs to mouth with contaminated hands
    c) Human is only definitive host and person to person transmission occurs via faecal-oral route
    d) Commonly affect young children and their contacts
  3. Symptoms:
    a) Most infections are asymptomatic with some itchiness around perianal area
    b) If worm burden is high - abdominal pain, nausea, and vomiting may occur
36
Q

What is the life cycle of pinworm?

A
  1. Eggs ingested
  2. Larvae hatch in small intestine and migrate to colon
  3. Adults mature in colon and copulate
  4. Female adults migrate to anus at night and lay eggs on perineum
  5. Eggs/worms contaminate fingers from scratching
  6. Re-infect host via oral route or infect others through contaminating surfaces
37
Q

What is the diagnosis of pinworm?

A
  1. Based on clinical symptoms
  2. Pinworm paddle or tape test to confirm
    a) Tape is applied to perianal area and removed
    b) Tape is then examined microscopically for eggs and worms
    c) Test should be performed immediately after waking up
    d) Since scratching of the anal area is common, sample can also be taken from under fingernail
38
Q

What is the treatment of pinworm?

A
  1. Mebendazole (100 mg) given to entire family of infected individual
    a) This medication is contraindicated in pregnancy and breast feeding
  2. Scrub under nails and avoid scratching
  3. Boil clothing and bed linen of affected individuals (females lay eggs at night)
  4. Prevention: appropriate hand and personal hygiene
39
Q

Describe the common roundworm (Ascaris spp.):

A
  1. Type of pathogen:
    a) Helminth - Ascaris spp.
  2. Transmission:
    a) Parasite passed in stools and contaminate food and water
  3. Infectious sites:
    a) Pancreatitis
    b) Appendicitis
    c) Liver abscess
    d) Occasionally coughed up in sputum
    e) Can cause bolus intestinal blockage
40
Q

What is the life cycle

A
  1. Adults in small intestine are released in faeces with fertilised and unfertilised eggs
  2. Fertilised eggs become an embryonated egg and is ingested by human
  3. Larvae hatch inside human and enter circulation migrating to lungs
  4. Larvae are coughed up and swallowed re-entering GIT
  5. Larvae mature in GIT and cycle continues
41
Q

What are the common clinical presentation of individuals infected with Ascaris spp.?

A
  1. Usually infection resolves spontaneously 10 days after larvae migration
  2. If persists however:
    a) Some may be asymptomatic
    b) Malnutrition; poor weight gain, malabsorption
    c) Fever and cough
    d) Abdominal swelling, pain, diarrhoea
    e) May have dyspnoea (breathlessness) and urticara (rash) where larvae have migrated to the lungs
    f) If migration to the lungs has occurs, can cause pneumonitis infection (inflammation)
    g) Peritonitis, inflammation of spleen and liver
    h) Migration to pancreatic and bile duct can cause blockages to gall bladder and pancreas
    i) Accompanied by eosinophilia (increased eosinophils) indicative of worm infection
42
Q

What is the diagnosis of Ascaris spp.?

A
  1. Presence of larvae and eosinophils in sputum
  2. Chest X-ray to confirm presence of larvae
  3. X-ray may show GI worms
  4. Stool microscopy - presence of eggs
43
Q

What are the treatment and prevention of Ascaris spp.?

A
  1. Treatment
    a) Adults (Albendazole 400 mg) or Mebendazole 500 mg
    b) Children (Mebendazole 100 mg twice daily for 3 days)
    c) Intestinal obstruction - surgery may be required
  2. Prevention:
    a) Improved sanitation
    b) Toilets and proper disposal of faeces
    c) Handwashing
    d) Regular treatment is useful in reducing cases
44
Q

What are the types of infections caused be cestodes (tapeworms)?

A
  1. Taeniasis:
    a) Taenia solium
    b) Taenia saginata
  2. Cysticercosis:
    a) Taenia solium
45
Q

Describe taeniasis:

A
  1. Type of pathogen:
    a) Tapeworm
    b) Either Taenia solium (pork) or Taenia saginata (beef)
  2. Transmission:
    a) Consumption of poorly cooked pork or beef
  3. Symptoms:
    a) Often asymptomatic infection
    b) Often only aware after passing proglottid segment in stools
    c) Gastrointestinal symptoms may include loss of appetite, nausea, abdominal pain
    d) In rare infections, segments of proglottids can migrate to appendix, bile duct, or pancreatic duct - likely to induce vomiting
    e) Several metres of tapeworm may be passed in vomiting
  4. Features:
    a) Scolex (head) contains hooks and suckers to attach
    b) Proglottids (body segments) follow and are hermaphroditic which can release multiple eggs each
46
Q

What is the lifecycle of Taenia spp.?

A
  1. Tapeworm infects pig or cow after host ingests contaminated food
  2. Tapeworm hatches inside host and penetrates intestinal wall and circulates to musculature
  3. In muscles they develop into cysticerci
  4. Humans ingest poorly cooked meat and ingest these cysticerci
  5. These develop and enter human intestine and scolex attaches to intestine
  6. Tapeworm begins to grow its proglottids
  7. Proglottids become sexually mature and develop eggs
  8. Proglottids are shed in faeces and contaminate food and cycle continues
47
Q

What is the diagnosis of Taeniasis?

A
  1. Investigation performed via stool microscopy
48
Q

What is the treatment of Taeniasis?

A
  1. Niclosamide 2mg or Praziquantel

2. Treatment is different for Pork Tapeworm due to complication of cysticercosis

49
Q

What is cysticercosis?

A
  1. If humans ingest the eggs of T. solium, an oncosphere can form and penetrate human intestinal wall
  2. This then travels to tissues to form cysticercus (similar to pig lesions) over months and occurs in:
    a) Skeletal muscle
    b) Lungs
    c) Eyes
    d) Brain - can lead to neurocysticercosis (NCC)
  3. Symptoms:
    a) Skin nodules may be present
    b) Infected persons will present with muscle pain and swelling from initial invasion because of cyst formation
    c) Calcified cysts in skeletal muscle fibres can be seen on X-ray
    d) Neurocysticercosis causes lesions in brain which results in onset of epilepsy, seizures, mental disturbances, and death
50
Q

What is the diagnosis of Cysticercosis?

A
  1. T. solium in faeces is not enough - must demonstrate cysts are present in tissue
  2. Full blood count (CBC) to check for eosinophilia
  3. Stool microscopy to check for eggs and proglottids
  4. Serology (ELISA):
    a) Production of IgE antibody against antigens on the worms (IgE is responsible for removal of Helminths)
    b) Blood or CSF reacts via immunoblot with cyst glycoprotein Ags
  5. If patient is experiencing neurological symptoms - brain CT and/or MRI is indicated
  6. Tissue biopsy
51
Q

What is the treatment and prevention of Cysticercosis?

A
  1. Treatment:
    a) Endoscopic removal of cysts
    b) Anticonvulsant therapy - if cysts in brain then also use of antiepileptic medications (e.g. Carbamazepine)
    c) Currently some vaccinations being trialled but none are available yet
  2. Prevention:
    a) Early diagnosis of both human and pig infection
    b) Education - improved sanitation and pig husbandry
    c) Meat inspection when cooking (proper cooking)
    d) Development of vaccines both in humans and pigs
52
Q

Describe trematodes (flukes) infections:

A
  1. Schistosomiasis
  2. Caused by flatworms - flukes (Schistosoma spp.)
    a) S. mansoni - South America, Caribbean, Africa, Middle East
    b) S. haematobium - Africa, Middle East
    c) S. intercalatum - Central West Africa
    d) S. japonicum - Far East
    e) S. mekongi - South East Asia
  3. Schistosoma spp.:
    a) Hermaphrodites - both female and male within same worm
    b) Female nestles in male and contain oral and ventral suckers
53
Q

Describe the lifecycle of Schistosoma spp.:

A
  1. Schistosoma begin as eggs in faeces and urine
  2. Eggs hatch, releasing miracidia
  3. Miracidia penetrate snail tissue
  4. Sporocysts develop in snail and form successive generations
  5. Sporocysts develop into cercariae and are released by snail into water (they are free swimming)
  6. Cercariae penetrate skin of humans and lost tails during penetration to become schistosomulae
  7. Schistosomulae enter into circulation and migrate to portal blood in liver where they mature into adults
  8. Paired adult worms migrate to;
    a) Mesenteric venules of bowel/rectum and venous plexus of bladder
  9. Eggs are laid in bowel/rectum and circulate to liver to be shed in stools which begins cycle again
54
Q

What are symptoms of Schistosoma spp.?

A
  1. Many are asymptomatic
  2. Disease seen after weeks of infection
  3. Fever, cough, rash, fatigue, abdominal pain, diarrhoea (bloody), hepatosplenomegaly, eosinophilia
  4. Portal hypertension
  5. Lesions in liver, bladder, and lungs (inflammation)
  6. Occasional CNS lesions (brain and SC) leading to paralysis and seizures
  7. In S. haematobium: cystitis, haematuria - bladder cancer
55
Q

What is the diagnosis of Schistosoma spp.?

A
  1. Stool and/or urine examined microscopically for eggs
    a) Eggs passed intermittently and in small numbers (may not be detected so multiple samples over multiple days necessary)
  2. Follow up blood test for serology may be needed:
    a) ELISA for Abs to S. mansoni microsomal Ag and other excretory Ags
    b) Immunoblots (westerns) for Abs to species-specific Ags
    c) Urine screen
  3. Tissue biopsy (bladder or rectum) after months with negative stools and serology
56
Q

What is the treatment and prevention of Schistosoma spp.?

A
  1. Treatment:
    a) For both urinary and/or intestinal infection: Praziquantel taken 1-2 days
    b) Treatment does not prevent re-infection
  2. Prevention:
    a) No vaccine available
    b) Avoid swimming in fresh water (salt water ok)
    c) Boil bathing water - 1 minute rolling boil (can penetrate skin)
    d) Drink bottled water - transmission not via this route but contact with lips can permit invasion
    e) Boil water if drinking fresh water from stream or tap water (Iodine treatment is not sufficient)
    f) Vigorous towel drying
    g) Reduce contamination of fresh water (prevent runoff)
    h) Eliminate snails - very difficult
57
Q

Why is vaccine development of Schistosoma spp. difficult?

A
  1. Complex lifecycle with many stages and intermediate hosts
  2. Antigenic variation in isolates
  3. Allergic responses
  4. Potential cross reactivity of response to other normal gut commensal bacteria