|MicrobiologyBytes: Microbiology Notes: Protozoa||Updated: August 23, 2007||Search|
|Sarcomastigophora||Mastigophora (mastigo = whip = flagellates)||Trypanosoma, Leishmania, Giardia, Trichomonas|
|Sarcodina (amoebae)||Entamoeba, Naegleria, Acanthamoeba|
|Apicomplexa||Plasmodium, Toxoplasma, Cryptosporidium, Isospora|
Ecological Niches in the Human Body:
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Ingestion of cysts in sewage contaminated water or on contaminated fruit, vegetables etc.; excystation in distal small intestine and colon; trophozoites feed and multiply and may invade liver via colonic mucosa; cysts pass out with faeces.
Oocysts are ingested which hatch in the intestine into sporozoites. These
invade cells; 2 asexual generations, then gamete formation and production of
oocyst containing 4 sporozoites; oocysts pass out with faeces. Danger from sewage
contaminated water supplies - have been recent outbreaks in UK.
Human infection seen in 1-4 % of patients with diarrhoea in developed countries and up to 16% in less developed countries.
Most common in children; immunocompetent adults seem to be immune, but in those who are immunodeficiency in any way, intense infections may develop. Among AIDS patients 3- 4% prevalence reported in USA and over 50% in Africa and Haiti.
Mosquito (female) inoculates sporozoites during feeding; invade first hepatocytes in liver and then red blood cells; cycles of schizogony inside rbc's, rupture and reinvasion, cause characteristic periodic fever and chills; sexual stages are taken up by mosquito; formation of oocyst in gut wall; sporogony and release of sporozoites which invade salivary glands, ready to infect at next feed.
Fly takes up trypanosomes with bloodmeal; trypanosomes multiply and undergo developmental cycle first in gut and then salivary glands of fly; infective forms (metacyclics) develop here and pass out in saliva during feeding. In host, first stage is multiplication of trypanosomes at site of bite - chancre; followed by invasion of bloodstream; waves of parasitaemia with accompanying fever and malaise; late stage is invasion of CNS - classical sleeping sickness syndrome.
Chagas' disease - initial acute phase of several weeks, subsides into chronic phase, which may continue for decades.
Mega syndromes: Megaoesophagus, megacolon. Heart damage: arrhythmias, dilatation, sudden death. South America; largely disease of poverty - poor housing. 100 million estimated at risk; 16-18 million infected. Zoonosis - oppossums and other forest animals in northern part of South America. The vectors are triatomine bugs:
Trypanosomes in bloodstream of human, taken up by bug; multiplication in gut, infective forms passed out with faeces; infect next host by contamination of bite or mucosal surface (Romana's sign); circulate in blood and then invade cells, preferably muscle or glia cells; multiplication of trypanosomes as amastigote forms and formation of pseudocyst; cycle of rupture and release of trypanosomes to invade bloodstream and other cells.
Promastigotes inoculated when sandfly bites; parasites ingested by dermal macrophages; multiply as amastigotes, which are released and ingested by further macrophages; taken up with blood by sandfly; parasites multiply first in gut and then migrate forward, to be reinoculated at next bite.
Infection is via cysts either through contamination with cat faeces or ingestion of flesh containing cysts. Cysts rupture in intestine, releasing sporozoites which penetrate gut epithelial cells; after cycles of multiplication, tachyzoites enter circulation and infect various nucleated cell types; finally tissue cysts are formed in brain and muscle, which contain many slowly dividing bradyzoites and last for years, unless new cycles of tachyzoite proliferation are initiated, e.g. in AIDS.
This rather remarkable species was known as a potential parasite of man for many years, but its true nature as a coccidian was only discovered within the past 20 years. It was known to occur in all warm-blooded animals - but its nature and means of transmission were a mystery. It was known that there was a trophozoite and it was also known that cysts formed. It was only when it was discovered that T. gondii developed a sexual stage in the intestine of a cat, that its true coccidian nature was revealed. It was also thought initially that the parasite was transmitted via the eggs of the nematode worm Toxocara cati , but it was later found that Toxoplasma could be transmitted via the faeces of worm free cats - the faeces containing what appeared to be oocysts - again indicating the coccidian nature of the parasite. Cats were infected by ingesting oocysts or cysts in tissues of paratenic hosts, such as mice, or transplacentally.
Parateny: transmission of a parasite from one host to another without the occurrence of maturation or development of the parasite - i.e. parasite in transit.
After ingestion of infective stages (oocysts or cysts) the intestinal epithelium is invaded and there follow several series of asexual generations during which the parasites divide by an unusual process known as endodyogeny.
Endodyogeny is a budding process in which two daughter cells are formed inside the original 'mother', which is then consumed by the developing daughters. Starts off with appearance of two new areas of internal membrane which will be the external membranes of the daughters. Each membrane grows within the mother, taking in a piece of the nucleus plus other organelles.
As in the 'typical' coccidian cycle asexual reproduction is followed by macro- and microgametogenesis, fertilization takes place , the zygote developing into a thick walled oocyst that is passed out with the faeces. This is not infective when laid and requires 2-3 days under appropriate conditions to sporulate, resulting in an infective oocyst containing two sporocysts each with four sporozoites.
Extra-intestinal development in cats. some of the organisms formed during intestinal asexual development pass into other tissues and organs. First mesenteric lymph nodes are infected, followed by the liver, lungs and other tissues. By the 6th day the trophozoites, now known as zoites, may be found in many tissues and persist for about two weeks after infection. By the 14th day, toxoplasma lesions begin to subside, but after acute infections cysts commonly persist in the brain and muscles of cats, as in other animals.
Intermediate (paratenic) hosts: Over 300 species of mammal and 20 species of bird have been identified as paratenic hosts. Toxoplasma can only complete its sexual cycle in the cat. In the 'wrong' host, when oocysts are ingested the sporozoites hatch, cross the gut wall and invade macrophages and almost any other cell type (except erythrocytes) and - before any immunity develops - divide rapidly by endodyogeny until the cell is full of them. The accumulation of organisms, bounded only by the plasmalemma of the host cell is known as a PSEUDOCYST to distinguish it from a cyst, a term which is only used in parasitology for a protective membrane surrounding an organism which has, at least in part, been produced by the parasite.
Within a pseudocyst, zoites divide rapidly and are known as tachyzoites (Greek tachos = speed). The host cell eventually bursts and releases tachyzoites which invade other cells. When this proliferative phase is slowed down by the influence of developing host immunity and finally ends, accumulations of zoites form true cysts and the contained zoites are known as bradyzoites as they develop slowly (Greek brady = slow). These cysts may become quite large 60µm and can survive for many years - even the life time of the host. It is these latent infections that can provide problems in humans.
The prepatent period in the cat - time from ingestion of infective material to oocyst excretion in the faeces, varies with the stage ingested. If the oocysts are ingested it is >20 days . If it becomes infected by eating mouse B that contains tachyzoites it takes >19 days, but if the infection is from eating mouse A where cysts containing bradyzoites are ingested it takes 3-10 days.
Infection: Humans normally become infected either by direct ingestion of oocysts from a cat or by eating raw or undercooked meat. Cooks or butchers that handle raw meat are particularly at risk. Man and other animals can be infected by the congenital route and acute infection in children can cause severe clinical symptoms. Children can become infected playing near cat litter trays etc.
The congenital condition can occur when a pregnant woman acquires toxoplasmosis for the first time, usually if infected at start of gestation period. The mother may show no symptoms but infection can take place across the placenta and the foetus has a 45% chance of being infected. On the infants born, about 60% will be sub-clinical, but of the remainder 30 % suffer symptoms ranging from hydrocephalus to intracerebral calcification, mental subnormality or some (9%) will die. Incidence in France and Austria of congential infection is 3-4 per 1000 births. In the UK, 91 cases were reported between 1975-1980.
In adults toxoplasmosis is almost symptomless but may result in fever and swelling. The most important factor in pathogenicity in adults is the immune status of the infected individual. About 30% of AIDs patients who have toxoplasma-specific antibodies suggestive of a past infection will develop toxoplasma encephalitis in the course of their illness - i.e. cysts develop in the brain. It is almost probable that illness in a result of a reactivated latent infection. That is, cysts with bradyzoites are present, but do no further damage in the immune competent person. Once an individual become immuncompromised then the parasite can emerge again and infect other organs etc. Prognosis for AIDS patients with toxoplasma is not good at present and therapy has not proved successful.
However, before you all rush out and abandon your cats, you should be aware that a current 3rd year project here has found no evidence of oocysts in cat faeces collected from local catteries - a study in Glasgow showed that a high proportion of cats were sero-positive for toxoplasma, but again no oocysts to match the seropositive data.
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