Parasitic Protozoa

Give examples of Parasitic Helminths (1)

Invertebrate parasites may cause infection in humans via food/water/insect vectors. Toxoxara spp. (dogs and cats, albendazole). Fasciola spp. (sheep and cattle, triclabendazole). Taenia spp. (pigs and cattle, albendazole) - worldwide

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Give examples of Parasitic Helminths (2)

Schistosoma spp. (snails, mammals, praziquantel) - tropical regions

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Describe features of parasitic protozoa (1)

Range of protozoa can cause clinical infections. Can be found in: CNS (amoeba, malaria, Toxoplasma, trypanosomes), blood (malaria, trypanosomes), liver (Entamoeba, Leishmania), intestine (Entamoeba, Giardia, Trichomonas), skin (Leishmania)

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Describe features of parasitic protozoa (2)

Urinogenital tract (Trichomonas). Protos (first) zoon (animal). Unicellular eukaryotes of 100-150 microns in length. Important diseases of (sub)tropical regions. Highly evolved parasites, complex life cycles, different hosts, morphological forms

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Describe features of parasitic protozoa (3)

Immature forms in intermediate hosts and mature forms (sexual stages) in definitive hosts

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Describe the structural characteristics of parasitic protozoa (1)

Gross structure varies from gelatinous mass to rigid forms with cytoskeleton. Cell membrane permits ingestion (endocytosis) and excretion (exocytosis). Contractile vacuole involved in osmoregulation and excretion

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Describe the structural characteristics of parasitic protozoa (2)

Possess various means for locomotion - flagella, cilia or pseudopodia. Organelles - mitochondria, nucleus, vacuoles, RER, Golgi

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Describe features of nutrition in protozoa (1)

Heterotrophs - need external source of organic C. Holozoic nutrition - ingest/digest solid material via endocytosis and food vacuoles, waste material egested via exocytosis. Saprozoic nutrition - uptake of water/soluble nutrients from environment

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Describe features of nutrition in protozoa (2)

20% of protozoan species are parasitic (majority of these are pathogenic). Site of entry into body may not result in localised clinical infection in that entry (e.g. malaria via mosquito bite on arm can affect CNS)

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Describe features of nutrition in protozoa (3)

Some exist in environment, some live in a vector/host (e.g. malaria in the body)

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Describe the transmission of parasites (1)

Transmission relies upon survival outside the host, achieved in various ways. Shedding of larvae or resistant forms such as eggs or cysts. Passage to intermediate host (vector) for part of life cycle. New hosts actively sought by invasive parasites

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Describe the transmission of parasites (2)

Needs to live outside host in order to be passed onto another host. Life cycle of malaria - mosquito bite, affect human (malaria), mosquito bites affected human, picks up malaria to be transferred to another host (vector/environmental)

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Describe features of encystation and excystation (1)

Encystation (cyst formation) - common in GIT parasites, dormant infective forms, passed to environment via faeces e.g. Entamoeba histolytica. Excystation - occurs unable favourable conditions found in host (e.g. temp, pH, O2 etc)

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Describe features of encystation and excystation (2)

Cyst transforms into vegetative (feeding) form of parasite (trophozoite)

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What are cilitates?

Parasites which have cilia/flagella to move around when they are in the host e.g. Balantidium coli

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Describe features of Balantidiasis

Balantidiasis - pain, diarrhoea, ulceration. Mostly in tropical regions but not common. Cysts transmitted via faecal-oral route. Also have animal reservoirs

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Describe the life cycle of Balantidium coli

Cyst in the environment is taken up via transfer of faeces. Cyst enters the body, opens up to form trophozoite. Affects lumen of colon (tissue damage). Forms back into cyst to be passed out into stool to enter environment and infect another host

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What are the symptoms of Balantidiasis?

Can be asymptomatic (may get symptoms where there is tissue damage). Dysentery similar to amoebiasis (ulceration of SI), rarely fatal, significant diarrhoea/water loss (chronic/low level)

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How is Balantidiasis diagnosed?

Presence of cysts and trophozoites in stool samples

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What is the treatment for Balantidiasis?

Oxytetracycline (protein synthesis inhibitor) - kills gut bacterial flora to make environment less supportive. Antibacterial/anti-microbial

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Describe features of amoebic dysentery

50 million people affected. Kills 10-100 K pa. Not only confined to tropics. 5% prevalence in EU and US. Amoebae secretes proteases which facilitate invasion of gut lining and promote inflammation

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Describe the life cycle of Entamoeba histolytica (1)

Ingested by contaminated water/food. Cyst opens up in SI (right environment). Transform in trophozoite (can result in - asymptomatic colonisation, invasive/amoebic LI colitis or amoebic/liver abscess). Encystation in colon, excretion in faeces

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Describe the life cycle of Entamoeba histolytica (2)

Enters environment, cycle repeats. Effects in gut lining - causes loss of inflammation, reduce effectiveness of gut lining, increase permeability (allows water to pass into stools - watery diarrhoea/can be fatal if fluids are not replenished)

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What are the symptoms of amoebic dysentery?

May be symptomatic. Abdominal pain, bloody/dark stools, fever, causes ulcers, dysentery. Migration to brain, liver, lung, causes abscesses (death).

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How is amoebic dysentery diagnosed?

Cysts and trophozoites present in stools

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What is the treatment for amoebic dysentery? (1)

Diloxanide furoate (kills non-invasive luminal amoebae and cysts, MOA unknown). Metronidazole (originally developed as anti-protozoal drug) very effective against tissue infection

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What is the treatment for amoebic dysentery? (2)

Metronidazole becomes reduced in parasite cells forming a radical which damages amoeba macromolecules such as DNA. Metronidazole used to treat active infection and diloxanide furoate for dormant cysts (puromycin also used)

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What would happen if you treated amoebic dysentery with metronidazole only?

Treat active infection but not effective at killing parasites in GIT due to being absorbed into the stomach and enters circulation, doesn't cover all sites. If only invasive forms killed, dormant cysts could be activated (patient infected again)

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Describe features of Trypanosomiasis

African sleeping sickness (trypanosomiasis). Transmitted by tsetse fly bite. Effective control and treatment reducing incidence (7000 in 2012). Wild and domestic animals act as reservoir (zoonosis)

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Describe the life cycle of Trypanosoma brucei (1)

Human bitten by tsetse fly. Parasites taken into insect gut during blood meal. Migration to salivary gland, development of epimastogote. Infective metacyclic form injected into host blood during feeding. Parasites undergo division in host circulation

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Describe the life cycle of Trypanosoma brucei (2)

Altering surface antigens. Cell division/changes in surface glycoproteins occurs every 7-10 days (antigenic variation). Enters CNS in human host (signs and symptoms)

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What are the symptoms of Trypanosomiasis?

Lesion at entry site. Fever, headache, tongue, eyelid tremors, organ damage, upon CNS invasion, apathy, paralysis, lethargy permanent coma, death

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How is Trypanosomiasis diagnosed?

Parasite not excreted into the stool. Take blood sample and a blood smear, detect parasites by viewing the blood smear under a microscope

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What is the treatment for Trypanosomiasis? (1)

Depends on part of life cycle. During early haemolymphatic stage, Suramin (selective binding and inhibition of parasite proteins) or Pentamidine (binds to DNA halts replication). Nirfutimox generates free radicals used in combination with other drugs

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What is the treatment for Trypanosomiasis? (2)

For late neurological stage, melarsoprol (arsenic compound binds to protein thiols, not available in the UK) or eflornithine (inhibits protozoal DNA synthesis). Widespread condition

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What is the treatment for Trypanosomiasis? (3)

Could modify the fly/act on the vector to reduce the incidence of the disease (reduce number of cases). Unable to formulate vaccine due to antigenic variation

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Describe features of the Trypanosoma cruzi

South and North America Chagas' disease (trypanosomiasis). Transmitted by Reduvid 'kissing' bug faeces (autoinoculation). Estimated 7-8 million people affected. Forest animals act as reservoir (zoonosis)

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Describe the life cycle of Trypanosoma cruzi (1)

Reduvidae bug bits host (and deposition of faeces), causes irritation, scratching. Inoculating yourself with organism rather than getting infection from organism. Enters bloodstream, trypomastigote forms amastigote in cells, replications in cells

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Describe the life cycle of Trypanosoma cruzi (2)

Cell wall ruptures to release amastigote into circulation. Colonisation of muscle or neural tissue. Amastigote taken up by bug (blood meal)

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What are the symptoms of a Trypanosoma cruzi infection?

Lesion at entry site, fever, headaches, malaise prostration. Invasion of muscle/liver/spleen causes massive tissue damage, including myocardial damage (cardiac syndrome, arrhythmias, MI)

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What is the treatment for Trypanosoma cruzi?

No effective treatment for intracellular stage (cell penetration stage). Benznidazole - effective upon trypanosomes in blood (via free radical production). S/E increase with age of patient

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Describe features of Leishmania sp.

Endemic Central and South America, Asia, Africa, Middle East. 30 known disease causing species. 1.3 million cases per year of which 4.5% are fatal. Animal reservoirs (e.g. dogs)

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Describe the life cycle of Leishmania sp. (1)

Sand fly bites host, injects active form into host. Promastigotes phagocytosed (intracellular form). Differentiation. Amastigotes replicated until macrophage bursts. Released amastigotes infect more macrophages. Cycle in the blood

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Describe the life cycle of Leishmania sp. (2)

Sand fly ingests parasitised macrophages. Amastigotes released in sand fly gut differentiate into promastigotes, cycle repeats with another host

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What are the symptoms of a Leishmania sp. infection? (1)

Cutaneous leishmaniasis - ulceration around bite on skin, prone to secondary bacterial infection and may spread to mucous membranes of lips to form mucocutaneous leishmaniasis (disfiguring but not fatal)

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What are the symptoms of a Leishmania sp. infection? (2)

Macrophages may spread disease to liver and other organs visceral leishmaniasis (fatal unless treated). Immunity is attenuated by altering Mφ cytokine signalling pathways

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What is the treatment for a Leishmania sp. infection? (1)

Miltefosine (very effective but teratogenic). Sodium stibogluconate (antimony compound may induce oxygen radical formation which kills, requires multiple injections over a long period of time)

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What is the treatment for a Leishmania sp. infection? (2)

Amophotericin also used (anti-fungal - drug gets to site where the organism is infecting)

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Describe features of Giardiasis

Most common human intestinal parasite. Contaminated water or food. Encountered in UK. Common in children under 10 (more exposed to environment, poor hand hygiene)

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Describe the life cycle of Giardia duodinalsis

Cyst enters GIT, excystation, forms excyzoite, trophozoite invades gut lumen/epithelium, replication, inflammation, damage to villi (absorptive/excretory function affected), excreted into environment to affect another host

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What are the symptoms of Giardiasis?

Severe diarrhoea (water/electrolyte loss). Malabsorption of vitamins. Infected gall bladder can lead to relapse over many years

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How is Giardiasis diagnosed?

Large quantities of cysts and trophozoites in stools

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What is the treatment for Giardiasis?

Whole family needs to be treated (including pets). Metronidazole (TDS), tinidazole (OD) - highly effective, medicines have different PK and half lives

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Describe features of Trichomoniasis

Encountered in UK. STI (not always directly). Inhabits vagina and urethra in females, epididymis and prostate in males (linked to prostate cancer)

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Describe the life cycle of Trichomonas vaginalis

Infective trophozoite form passed between males and females. Trophozoite in vaginal/urethra. Trophozoite in vaginal/prostatic secretions and urine (longitudinal, binary fission)

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What are the symptoms of Trichomoniasis

15% of infected women complain of vaginitis syndrome, discharge, irritation and burning sensation. Symptoms less noticeable in men (urethritis and epididymitis)

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How is Trichomoniasis diagnosed?

Flagellates present in discharge and urine

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What is the treatment for Trichomoniasis?

Metronidazole (resistance is increasing). Tinidazole (similar action to metronidazole but longer duration)

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What are apicomplexans?

Large phylum of parasitic alveolates. Possess a unique form of organelle that comprises a type of plastid called an apicoplast, and an apical complex structure (penetration of a host cell)

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Describe features of Plasmodium sp. (1)

40% of world population are at risk of malaria (increasing, due to climate change). ~200 million cases worldwide (2013). Major cause of death in tropics and sub-tropical regions (especially in children/lack of immunity)

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Describe features of Plasmodium sp. (2)

Transmitted during feeding by female Anopheles mosquito (vector)

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Describe the life cycle for Plasmodium sp. (1)

Infected mosquito bites human host, injection into bloodstream. Enters liver, infects liver cells. Can form dormant phase in liver (activated to be released into bloodstream at any time). Cells bust open to release merozoites into bloodstream

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Describe the life cycle for Plasmodium sp. (2)

Infection of red blood cells (clinical symptoms appear). Blood cell ruptures when merozoites reach a certain size. Trophozoite - intermediate between clinical infection and signs and symptoms. Red cells circulating, undergoing cycle

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Describe the life cycle for Plasmodium sp. (3)

Ring form in blood - eaten by further mosquitos (blood meal). Gametocytes formed (transformed to macro-gametocyte to micro-gametocyte to zygote to ookinete to oocysts to sporozoites)

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Describe the life cycle for Plasmodium sp. (4)

Sporozoites released into circulation of mosquito which enters human again when bitten

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Describe features of malaria (1)

Delay between time bitten and getting clinical symptoms. 4 different types of species (P. falciparum/most fatal, P. vivax, P. ovale, P. malariae). Pre-patent period (spore inoculation, bite, time from sporozoite to merozoite, hepatic period)

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Describe features of malaria (2)

Incubation period - time of clinical symptoms (combination of merozoites and enough of infected red blood cells). Merozoite maturation. Merozoites produced (numbers/days of periods vary between species). High numbers/short periods of Falciparum

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Describe features of malaria (3)

Lower parasite burden with other 3 types of Plasmodium

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Describe features of fever intervals, dormant liver hypnozoite and pathology for the Plasmodium species (1)

Red blood cells bursting causes release of parasite which results in a spike in fever. Different fever intervals/patterns for different species. P.ovale/vivax have dormant liver phase (considered when deciding drug treatment)

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Describe features of fever intervals, dormant liver hypnozoite and pathology for the Plasmodium species (2)

Pathology - P.ovale (recurrent malaria). P.vivax (non-fatal, current). P.malariae (benign, chronic malaria). P.falciparum (fatal malaria)

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What are the symptoms of malaria? (1)

Periodic fever, sweating, chills (due to RBC rupture). Haemolytic anaemia (bone marrow not able to replenish red blood cells which have ruptures, breakdown of rbc, lack of rbc)

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What are the symptoms of malaria? (2)

Adhesion of erythrocytes to capillary endothelium via adhesion proteins (60 types), impaired microcirculation (P.falciparum), renal failure, cerebral malaria (poor blood flow to brain, drowsy/coma), facilitate antigenic variation

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What are the symptoms of malaria? (3)

May continue for 30 years (until immune system destroys parasite)

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What are the symptoms of malaria - cold/hot/sweating stages?

Cold stage (feeling intense cold, vigorous shivering, lasts 15-60 mins). Hot stage (intense heat, dry burning skin, throbbing headache, lasts 2-6 hours). Sweating stage (profuse sweating, declining temperature, exhausted and weak - sleep, lasts 2-4h)

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What is the treatment for malaria? (1)

Depends on type of parasite. Drugs taken as prophylactics or as therapy interfere with parasite Hb metabolism. Quinine and derivatives are selectively toxic for parasite

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What is the treatment for malaria? (2)

Prevent degradation or sequestration of haem (by haem polymerase) in parasite which leads to toxicity. Primaquine + chloroquine effect radical cure of P.ovale and P.vivax (dormant form in liver)

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What is the treatment for malaria? (3)

Artemisinin (TCM) - very effective schizonticidal drug (Ca pump blocker). Quinine for Falciparum - injection/infusion/PO. Quinidine replaced by artemisinin derivatives - injection (more effective than quinine in terms of speed of killing infection)

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Describe features of Toxoplasmosis

Very common in Europe. Problem for immunocompromised and infants (newborns, transfer during pregnancy). 30% of UK population affected. Cats affected by parasite

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Describe the life cycle of Toxoplasma gondii (1)

Cyst in stool. Cyst gets into human host, enters red blood cells. Can affect the brain/muscle/liver. Localised brain tissue infection. People might colonised but don't have clinical symptoms

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Describe the life cycle of Toxoplasma gondii (2)

Ingested cyst. Cyst released bradyzoites in stomach and intestine. Oocyte releases sporozoites that differentiate into tachyzoites and incase tissue. Bradyzoites invade epithelial cells and start division

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Describe the life cycle of Toxoplasma gondii (3)

Faecal oocytes - bradyzoites differential between tachyzoites and gametocytes. Gametocytes fuse to form zygote to mature into oocyst. Oocyst release in faeces (cycle repeats)

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Describe the life cycle of Toxoplasma gondii (4)

Tissue cysts - bradyzoites differentiate into tachyzoites. Tachyzoites invade almost every kind of cell multiplying until cell dies and releases for tachyzoites. Tachyzoites differentiate into bradyzoites, form cysts main in brain/liver/muscle tissue

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Describe the life cycle of Toxoplasma gondii (5)

(Look are serum CSF). Cycle repeats

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What are the symptoms of Toxoplasmosis? (1)

Usually asymptomatic, self limiting (needs serological test for identification). For immunocompromised patients, brain damage may occur by toxoplasmic meningitis and encephalitis

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What are the symptoms of Toxoplasmosis? (2)

Toxoplasmic choroidretinitis (inflammation of vascular tissue behind the retina) causes blindness. Transplacental infection result in abnormalities in CNS, eyes and viscera of foetus. Can cause still birth or death occurs shortly after birth

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What is the treatment for Toxoplasmosis?

Pentamidine. Or a combination of pyrimethamine (anti-protozoa drug) and sulfadiazine - inhibits folate metabolism (needed by parasite for replication)

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Parasitic Protozoa

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