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19 Cards in this Set
- Front
- Back
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What is the morphology of Toxoplasma gondii? What hosts does it infect?
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✩MORPHOLOGY:
-only one parasitic species (T. gondii) -tissue cysts variable in size, surrounded by primary cyst wall -small (faecal) oocysts containing 2 sporocysts, each containing 4 sporozoites (1-2-4 configuration) ✩HOSTS: -carnivores, herbivores, insectivores, rodents, pigs, primates, and occassionally birds -particularly important in sheep, goats, and humans DEFINITIVE HOSE: feline (oocyst formation) |
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What are the sites of infection & lifecycle of Toxoplasma gondii?
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✩SITES
-in the ca, the parasite undergoes asexual and sexual mutiplication in intestinal epithelial cells, culminating in the formation of oocysts 3-5 days post infection -in all other vertebrate hosts, parasite undergoes asexual multiplication in a wide range of extra-intestinal tissues (in any cell except non-nucleated erythrocytes) -during the acute phase of infection, the parasite divides rapidly forming small groups of 8-32 tachyzoites which lyse host cells -as an infection becomes chronic, the parasites divide slowly forming accumulations (cysts) of bradyzoites, particularly in the brain, heart & skeletal muscle -these tissue cysts are surrounded by a thin wall and can persist for months or even years -cyst formation appears to coincide with the development of host immunity ✩LIFECYCLE -infections are transmitted by the ingestion of sporolated oocysts from cats, by the ingestion of fresh or undercooked meat which contains viable zoites or transplacentally -the oocysts are excreted in the cat faeces & require sporolation in the environment for 2-4 days before they are infective to the next host |
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What is the pathogenesis of Toxoplasma gondii?
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-most hosts exhibit age related resistance to the disease
-most infections in adults and weaned individuals are asymptomatic -acute infections by proliferating tachyzoites cause non-specific, flu-like symptoms (lymphadenitis, fever, muscle pain, and anemia) -symptoms generally subside with the development of immunity but may sometimes persist, producing subacute disease characterized by lesions in the lung, liver, heart, brain and/or eyes -chronic infections by encysted bradyzoites usually cause no clinical signs, although degenerating cysts have been associated with hypersensitive inflammatory reactions, resulting in, for example, encephalitis, myocarditis and/or chorioretinitis -infections also may be reactivated by immunosuppressive therapy or acquired immunodeficiencies -infections may also be transmitted transplacentally -if the mother/dam contracts infection during pregnancy, parasites may cross the placenta and infect the fetus causing spontaneous abortion, stillbirth, or congenital abnormalities, such as hydrocephalus, brain calcification, chorioretinitis, and mental retardation -nonetheless, if the mother/dam is infected prior to pregnancy, her immunity is transferred to her fetus which is consequently protected |
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What is the diagnosis & control of Toxoplasma gondii?
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✩DIAGNOSIS
-parasites may be detected in autopsy or biopsy material by histology, immunolabelling, or by inoculation of rodents with infected tissue(s) -most infections, however are diagnosed serologically -elevated IgM antibody titres are considered to indicative of recent infection -acute infection is indicated by a 4-16 fold increase in specific antibody titre over a 2 week period ✩CONTROL -chemotherapy can be successful when pyrimethamine and sulphonamides are given together as they act synergystically -clindamycin & spiramycin -the toxic side effects of bone marrow depression can be relieved by administering folinic acid -the risk of transmission can be reduced by maintaining high standards of hygiene, particularly where cats are involved (emptying of litter trays; using gloves while gardening), by thoroughly cooking or deep freezing meat prior to consumption, and washing potentially contaminated food-stuffs -vaccines are being developed and a live vaccine (Toxovax) is available to protect sheep against toxoplasmosis |
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What is the morphology, hosts, & sites for Neospora?
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✩Morphology
-tissue cysts indistinguishable from toxoplasma, although the cyst wall is slightly thicker -the parasites are serologically distinct and do not cross-react with Toxoplasma gondii antisera -oocysts (from feces) are morphologically the same as those of T. gondii (and Hammondia) ✩HOSTS -detected in North Ameria, Australiasia and Europe -mainly in DOGS, but also in calves, lambs and foals ✩SITES -cysts have been detected in various tissues, particularly brain, spinal cord, and muscles ✩LIFE CYCLE -studies have demonstrated that trans-placental transmission can occur in dogs (infected puppies born to infected bitches) -dogs can become infected with tissue cysts and subsequently excrete oocysts in feces ✩PATHOGENESIS -infections have been associated with HINDLIMB PARESIS or paralysis in dogs -cutaneous neosporosis has also been reported -abortion (and associated neonatal mortalities) mainly in cattle (sometimes sheep and horses) ✩DIAGNOSIS -parasites detected in histological sections of autopsy/biopsy material by immunolabelling ✩CONTROL -not clear yet -clindamycin can be used for the treatment of clinical cases |
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What is the morphology & hosts of Sarcocystis?
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✩MORPHOLOGY
-tissue (muscle) cysts vary in size from microscopic to macroscopic, depending on parasitic species -thick cysts walls containing species-specific protrusions (zoites arranged into compartments; undifferentiated cells (metrocytes) found at periphery of cyst) -small Isospora-like (thin walled) oocysts produced in the intestine of the definitive hosts (sporocysts released) ✩HOSTS -tissue cysts in a wide range of mammals, birds and reptiles, world-wide -infections are particularly prevalent in wild and domestic herbivores which are preyed upon by carnivores -up to 90% of sheep and 60% of cattle have been found to be infected in many countries, including Australia -most parasite species have been found to be specific for both their intermediate and definitive hosts, and multiple species may occur in a host |
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What are the sites & lifecycle of Sarcocystis?
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✩SITES
-in intermediate hosts, parasites first undergo several cycles of asexual proliferation (schizogony) in the endothelial cells of the vasculature (arterioles & capillaries), followed by tissue cyst formation usually within skeletal and heart musculature -in definitive hosts gametogony and sporogony occur in the small intestine, resulting in the excretion of infective sporocysts ✩LIFECYCLE -definitive hosts become infected by consuming meat containing tissue cysts, whereas intermediate hosts become infected by ingesting oocysts excreted in the faeces of the definitive host -gametogony (no schizogony) takes place in the definitive host (carnivore); schizogony and cyst formation in the intermediate host (herbivore/omnivore); oocysts usually sporulate within the intestines of the definitive host, and free, infective sporocysts are excreted |
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What is the pathogenesis of Sarcocystis?
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✩PATHOGENESIS
-intestinal infections in definitive hosts are usually asymptomatic -systemic infections in intermediate hosts have been associated with both acute and chronic disease, but not all parasite species are pathogenic -first and second generation schizonts lyse host endothelial cells, causing petechia hemorrhage throughout most tissues -heavy infections cause acute, transient disease characterized by anaemia, fever, and sudden mortalities (e.g. Dalmeny disease, feedlot outbreaks in cattle) -acute infections in pregnant animals an cause reproductive losses through abortion and stillbirth -subclinical infections have also been associated with weaner illthrift, reduced weight gain poor wool growth, and reduced milk production -acute clinical disease is rarely seen under field conditions -however, early, low-dose exposure usually generates good protective immunity (premunition) to subsequent infectin & disease -chronic infections by tissue cysts have been associated with muscle atrophy, myositis, and myocarditis -macroscopic cysts are also classified as carcass lesions by meat inspection services in some countries, thereby limiting the marketability of meat and resulting in significant economic losses (e.g. S. gigantea) |
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What is the diagnosis & control of Sarcocystis?
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✩DIAGNOSIS
-sporocysts may be detected by the coprological examination of faecal material from definitive hosts, whereas tissue cysts are detected by histological examination of autopsy or biopsy material from intermediate hosts -serological tests have been employed for the detection of some infections in livestock; some lack specificity ✩CONTROL -intestinal infections in carnivores respond well to treatment with coccidiostats -several coccidiostats also appear to be partially effective against tissue cyst infections in herbivores -in many instances, control may be inappropriate because hosts with light infections are protected against acute disease |
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Describe the morphology & hosts of Babesia
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✩MORPHOLOGY
-intraerythrocytic stages appear as small round, ovoid, or elongated trophozoites, in pairs or as pear-shaped merozoites, or in tetrads as cruciform merozoites ✩HOSTS -infections have been detected in most domestic animals (cattle, sheep, goats, horses, pigs, dogs, cats), and numerous wild animals and humans -some parasite species are not host specific and can be transmitted among different mammals; some are zoonotic -all species are limited in their distribution according to that of their tick vectors -in Australia, important cattle (Babesia bovis and B. bigemina) and in dogs (B. canis vogeli and B. gibsoni) |
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Describe the sites & lifecycle of Babesia
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✩SITES
-parasites infecting host erythrocytes undergo transformation to form trophozoites which divide by (binary) shizogony and undergo differentiation to form merozoites -the host cell is destroyed by rupture and the merozoites infect new cells, repeating the cycle of development ✩LIFE CYCLE -infections are transmitted by ixodid (hard-bodied) ticks which may be one-, two- or three-host ticks -Boophilus (Rhipicephalus) microplus acts as the intermediate host for Babesia bovis -ingested parasites develop into large motile vermicules which migrate through the body of the tick and then undergo sporogony -parasites may undergo trans-ovarian transmission and infect developing eggs -eventually hundreds of small pyriform bodies (sporozoites) are formed within salivary glands and are injected into mammalian hosts upon feeding |
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Describe the pathogenesis of Babesia
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✩PATHOGENESIS
-infected animals develop a high persistent fever, becoming dull and listless -erythrocyte destruction may be as high as 75% in fatal cases, and even milder infections produce severe anemia -hemoglobin clearance mechanisms become overloaded, resulting in jaundice and red discoloration of the urine ("red water" in bovine babesiosis) -chronically infected animals remain weak, thin and suppressed for several weeks before recovery -animals which recover are usually immune for life (premunition) -bos taurus is more susceptible to infection than bos indicus (zebu) -young cattle are less susceptible than older cattle (inverse age resistance) |
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Describe the diagnosis & control of Babesia
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✩DIAGNOSIS
-detection of intraerythrocytic stages in smears of peripheral blood -specific serological and PCR tests can also be used ✩CONTROL -chemotherapy with imidocarb and related drugs (amidocarb, dimidin) can facilitate recovery, resulting in latent infections or cure -however, elimination of all parasite may also eliminate premunition -anti-tick vaccine partially effective -tick control (dipping) programs have been relatively effective in several countries in controlling or eliminating infections in domestic livestock -live, attenuated vaccines (produced in splenectomised calves) can be used to protect cattle against babesiosis |
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Describe the morphology, hosts, sites, lifecycle, pathogenesis, diagnosis & control of Theileria
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✩MORPHOLOGY
-intraerythrocytic stages appear as small rod, oval, ring or comma-shaped bodies ✩HOSTS -infection have been recorded in domestic and wild ungulates (hoofed animals) in Africa, Asia and southern Europe as well as in wild and domestic felids in North America -infections are confined in their distribution to that of tick vectors ✩SITES -parasites first infect lymphocytes within lymphoid tissues where they form 2 types of schizonts macro- and micro-schizonts -merozoites from both can undergo further schizogony in lymphocytes whereas only those from micro-schizonts invade erythrocytes to become typical piroplasms ✩LIFE CYCLE -infections are transmitted by ixodid ticks -gametogony occurs in the gut of nymphal ticks resulting in the formation of kinetes which migrate to the salivary cells and undergo sporogony to form infective sporozoites -transovarian transmission does not occur but trans-stadial infection does occur between nymphs and adults -asexual development first in lymphocytes then in erythrocytes of the vertebrate host ✩PATHOGENESIS -clinical signs such as high fever (1-2 weeks after infection) may be rapidly accompanied by nasal discharges, runny eyes, swollen lymph nodes, weakness & emaciation, diarrhoea and occasionally by haematuria and anemia -calves are more resistant to disease tan adults (ie. inverse age resistance), and survivors develop a solid protective immunity to subsequent infection, without premunition ✩DIAGNOSIS -detection of characteristic stages in erythrocytes or schizones in leucocytes, macrophages and other cells in blood or tissue smears ✩CONTROL -no drugs are known to be effective once symptoms appear, although some tetracyclines prevent disease if given during the incubation period -control depends on tick control (dipping) and strict quarantine regulations -live attenuated vaccines have shown some success for some parasite species |
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Describe the morphology & hosts of Plasmodium
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✩MORPHOLOGY
-intraerythrocytic forms include small, round trophozoites (ring forms), multinucleate schizonts; macro- and micro-gametocytes (size & shape characteristics for many species) ✩HOSTS -130 species have be classified into different subgenera which occur in mammals (primates & rodents), birds and reptiles -humans are hosts for 4 main species (Plasmodium falciparum, P. malariae, P. ovale, and P. vivax), although they can occasionally become infected with other species from non-human primates -most species are confined to tropical and subtropical regions, depending on the distribution of their insect vectors |
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Describe the sites of Plasmodium
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✩SITES
-sporozoites injected by mosquitoes undergo asexual exoerythrocytic schizogony in liver cells (some sporozoites undergo arrested development, forming hypnozoites, which relate to malaria relapses) -merozoites then invade erythrocytes and undergo further schizogony, followed by gametogony -macro- and micro-gametocytes ingested by the female mosquito during feeding, fuse to become a motile ookinete which migrates into the haemocoel and transfors into an oocyst -the oocyst then produces hundreds of sporozoites which then migrate into the salivary glands (once infected, mosquitoes remain infected for life) |
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Describe the pathogenesis of Plasmodium
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✩PATHOGENESIS
-vague clinical signs may develop prior to parasitaemia, including headache, anorexia, and mild fever -thereafter, predominant clinical manifestations include anaemia caused by destruction of erythrocytes and characteristic fever parapoxssms (rapid change from cold-chills to hot sweats) produced by inflammatory responses -these parapoxysms usually coincide with the intraerythrocytic cycle and may be accompanied by dizziness, nausea, vomiting, delirium, hepato/splenomegaly, leukopenia, and thrombocytopaenia -depending on the parasite species involved, severe complications may arise including splenic rupture, cerebral signs, haemolytic anaamia, cardiac, pulmonary and renal failure |
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Describe the lifecycle of Plasmodium
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✩LIFECYCLE
-extraerythrocytic schizogony in hepatocytes, then intraerythrocytic schizogony and gametogony -infections are transmitted by female mosquitos, mainly Anopheles, Aedes, Culex spp. |
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Describe the diagnosis and control of Plasmodium
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✩DIAGNOSIS
-made by a combination of clinical symptomatology and detection of parasites in stained smears of peripheral blood -immunological and PCR techniques can also be used ✩CONTROL -antimalarial drugs such as primaquine, chloroquine (despite emergence of chloroquine-resistant strains), sulfadoxine, pyrimethamine, mefloquine, quinine, and tetracycline -multidrug resistance is now wide-spread in Plasmodium falciparum -vector control programs have had variable success, mainly depending on the degree of insecticide resistance encountered |
