Babesia and Toxoplasma Flashcards
outline some basic characteristics of the parasite Babesia
Apicomplexan, intracellular parasite which utilises an arachnid vector
three stage lifecycle like malaria
definitive hosts= ticks (which are also the vector)
intermediate host= a wide group and growing range of mammals
main vectors are the Boophilus annulatus and B.microplus
where is the parasite Babesia usually found
predominates in costal areas, wetlands, marshes and lake shores but not limited to these areas
the distribution of the disease is correlated with tick distribution as without the tick there is no parasite
outline the history of Babesia prevalence
1880s:outbreaks of Texas Cattle fever devastated cattle agriculture
1888: Romania, Victor Babes first documented the parasite
1893: Newyork state, Theobald Smith and Fred Kilbourne identified Babesia as the cause of Texas cattle fever and the ticks as vectors
1957: first case in humans discorvered through a splenectomised patient
1969: first case in non splenectomised patient, possible mutation allowing it to infect humans?
1970-present:disease in horses, humans and cattles called prioplasmosis
outline the pathology overview of Babesia
- infects erythrocytes and causes haemolytic (red blood cell bursting) disease which is known as babesiosis or prioplasmosis
- common name of the disease is red water fever due to the presence of lysed haemoglobin in urine
zoonotic species which infect humans
= B.microti (USA) and B.divergens (Europe)
symptoms similar to those of malaria so is often misdiagnosed
what are the two main species of Babesia which infect cattle
Babesia bigemina and B.bovis
- over 100 species identified but few pathogenic to humans
when is the parasite Babesia most severe
in splenectomised, immunosuppressed, elderly, young or pregnant people
outline the vector of Babesia
Ticks act as both the definitive host (where sexual reproduction occurs) and the vectors
- they are relatively host specific with most transmission caused by nymphal stages but all stages can be infected
- only feed on one host before dying
how does the type of tick affect distribution of the parasite
Hard ticks are long term feeders, remaining on the host for a few days compared to soft ticks which only feed for a few hours.
Therefore hard ticks have a greater distance over which they can be dispersed as the host travels
what is meant when the Babesia parasite is described as allowing transovarial transmission
the parasite is transmitted from the adult tick to the eggs then to the larvae (vertical transmission)
the parasite survives each moult stage; the nymph will attach to a host to feed also transmitting the parasite so it becomes very well established in tick populations
outline similarities between the apicomplexan parasites Babesia and Plasmodium (malaria)
- transmitted by an arthropod vector
- have asexual multiplication in vertebrate erythrocytes
- sexual reproduction within a vector
- produce sporozoites in vector salivary glands
- similar symptoms and mechanisms for infection
- both have equal importance to human health, and agriculture
what are the distinct processes in the lifecycle of Apicomplexans also including Babesia
three distinct stages
1) Sporogony
2) Merogony
3) Gametogony
what is the difference between monoxenous species and heteroxenous species
mono= all three of these process seen in apicomplexan life cycles occurs in a single host, often in a single cell/tissue type
hetero= processes carried out in different hosts and generally involve different tissues = Toxoplasma and Babesia
how do the merozoites formed from the trophozoites differ in plasmodium and Babesia parasites
in Babesia four merozoites form a tetrad called the Maltese cross which is diagnostic of the parasite
up to 12 parasites may infect a single erythrocyte compared to 3 in plasmodium
outline some adaptations of ticks for parasite transmission
Ticks are able to survive some time without a blood meal therefore Babesia form dormant sporoblasts near the salivary gland
as soon as the tick prepares to take blood meal the sporoblasts rupture releasing 10,000 sporozoites into saliva (takes about 24 hours)
outline a case study using the B.canis species which use dogs as a host and how numbers increased
2011= government policy changed to spend less money on public services so got rid of biocontrol at UK ports so dogs no longer had to be inspected for ticks
2016= first case of tick borne disease in canines that had never left the UK showing local transmission established in Harlow and Essex with 25% dog mortality
outline symptoms of the B.microti in humnas
malaria like
- fever
- sweating
- chills
- anaemia
- jaundice
- malaise
symptoms appear within 1-8 weeks and can last 1-4 weeks however 25% of adult cases and 50% of child cases are asymptomatic
outline symptoms of B.divergens in humans
more severe than B.microti with 42% fatality rate, similar symptoms as before but also haemoglobinuria (red water), jaundice, high fever, shock- like symptoms, kidney failure
- symptoms appear within 1-3 weeks
how is Babesia diagnosed and how is it controlled
diagnosed by serological antibody testing, or blood smeas and giemsa staining
- trophozoite, the terapad formation is the key diagnostic stage
- drugs and vaccines are available; blood transfusions can lower parasite load
- removal of ticks in good time (24 hours needed for transmission to occur)
outline characteristics of the parasite toxoplasma gondii
definitive hosts are felids
intermediate hosts are virtually all warm blooded mammals and birds
- opportunistic zoonotic parasite of vertebrates
- asexual and sexual reproduction in intracellular
- facultative heteroxenous life cycle
- high prevelance in definitive and intermediate hosts
why does the prevelance of Toxoplasma gondii vary in different countries
different countries have different eating habits which effect prevelance in humans
- pathology more serve in pregnant woman
outline the history of Toxoplasma gondii
1908- first discovered by Nicolle and Manceaux and Alfonso Splendor
1938- first discovered in humans in the eyes and brains of an infant showing congenital transmission
1965- transmission by under cooked meat discovered
1970- oocysts discovered in cat faeces
how is Toxoplasma gondii transmitted
several potential routes of transmissions with three infectious stages
1) oocyst in shed felid faeces
2) a motile disease causing phase known as tachyzoite
3) a non motile phase in tissues called a bradyzoite
outline the oocyte phase of toxoplasma gondii
1) develops after cats ingest bradyzoites in intermediate host tissues
2) bradyzoites mature into gametocytes which develop in small intestines
3) gametocytes undergo their sexual cycle which produce oocyts which appear in faeces 3-5 days after infection
4) oocyst require oxygen allowing sporulation making it infectious containing 2 sporocysts which are highly resistant containing 4 sporozoites
outline Tachyozite phase of Toxoplasma gondii
follows ingestion of oocytes or vertical transmission
Tachyzoites are crescent shaped with a pointed apical complex allowing entrance into cells
- move by gliding, flexing and rotating
- adheres to target cell using apical complex using conoid and rhoptires to bind
- secretes protolytic enzymes
- creates a vacuole inside the cell and asexually reproduces
outline the bradyzoite phase in Taxoplasma gondii
- slow growing stage within tissue cysts, chronic stage
- cysts reactivate in immunocompromised patients
- become infective when consumed
- resistant to low PH and digestive enzymes where wall is dissolved releasing bradyzoites which transform into tachyzoites
outline asexual and sexual reproduction in toxoplasma gondii
sexual cycle= vital for generating diversity to adapt to variation e.g. host immunity and evolutionary arms race
comes at a cost e.g. reliance on single definitive host, breaking up advantage combination alleles which enabled them to get to sexual cycle to begin with
how is toxoplasma gondii transmitted
- both horizontal and vertically
Main routes - food or water contaminated with faecal oocysts
- undercooked meat
- mother to foetus through placenta
how does Toxoplasma gondii alter behaviour of rodents hosts for transmission
infection shown to alter behaviour of infected rodents increasing risk of predation from cats (berdoy et al 2000)
increased attraction to predator urine
higher activity rates and lower cat avoidance
impaired motor functions and reduced learning
= all increase parasite transmission
how does Toxoplasma gondii alter behaviour of human hosts for transmission
Johnson et al 2018 found students testing positive for T.gondii are more likley to study business subjects at university
- correlation not causation
outline Toxoplasmosis pathogenisis
generally asymptomatic but can have flu like symptoms
10-20% of immunocompromised people will develop symptomatic diseases such as cervical, retroperitoneal and mesenteric lymphadenopathy; fever; malsie and night sweats
50% will have CBS toxoplasmosis e.g. seizure or altered mental status
outline cogentical (transplacental) toxoplasmosis
most severe when maternal infection occurs in early pregnancy with 67% patients having no symptoms
- Anaemia, thrombocytopenia and jaundice at birth
- mental retardation, seizures, visual defects and hearing loss (28%)
how is Toxoplasma gondii diagnosed
range of tests for toxoplasmosis in blood, spinal fluid, amniotic fluid, lymph nodes, CT and MRI scans
most common= serology or measuring IgM and IgG antibodies
how is Toxoplasma gondii prevented
avoid eating raw or undercooked meat
dont drink untreated water
wash all fruit and veg
keep a cover on child’s outdoor sandbox
wear gloves when gardening or changing litter box
avoid all cat and cat related items if pregnant
