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49 Cards in this Set
- Front
- Back
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Generally host disease is caused by a parasitic infection when one or all of the following occur
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There are a very large number of organisms
an exuberant tissue host response occurs (inflammation) The host does not have the ability to contain the organism The parasite mechanically enters a structure which causing mechanical obstruction/blockage |
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Principles of parasites
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Parasites are eukaryotic
-one-celled or -muti-cellular Most exhibit one or more forms of a life-cycle which can be -Simple or -Complex Many are Zoonoses Some require non-human and human hosts to complete the life-cycle |
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Parasite hosts
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Definitive host is one in which the parasite reaches sexual maturity
-i.e. Malaria, the mosquito is the definitive host -i.e. Schistosoma: the human is the definitive host Intermediate host is one which is required for parasite development but one in which the parasite does not reach sexual maturity – -i.e. Malaria, humans are the intermediate host -i.e. Schistomsoma: the snail is the intermediate host Host specificity: some parasites are highly restricted to particular hosts -Can fully mature to adult tape worm only in humans: Taenia saginata (beef tape worm), -Others can infect almost any mammalian host, eg. Trichinella Tissue tropism |
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Parasite epidemiology overview
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The greatest burden of disease in the world is developing countries
-Poor sanitation, housing -Tropical climate and local ecology -No resources for environmental control -Intimate contact with animals and the animal environment Disease does occur in the developed world -Consequence of immigration or international travel -Some parasites endemic and common -e.g: Toxoplasma, Giardia, Cryptosporidium, Enterobius (pinworm) Some a problem only for immunocompromised host -e.g.: Toxoplasma, cryptosporidium |
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Parasite stats
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Toxoplasmosis
1-2 billion infected, infection most often asymptomatic except in immune deficiency Malaria: 500 million acute clinical cases/year, causes or contributes to 3 million deaths/year 3rd largest cause of death due to an infectious disease Ascariasis 1 billion infections, deaths 20,000. Schistosoma 200 million infected; severe hepatosplenic disease <10%, about 1 million deaths/year Hookworm 800 million infected, death rare (60,000), but retardation of growth & intellectual development in children, chronic anaemia. Giardia 200 million cases of diarrhea/year |
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Blood protozoa
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Vector borne (mosquito, fly or tick)
Two host life cycle Ex. Plasmodia sp. (malaria) Ex. Trypanosoma sp. (Chagas disease and sleeping sickness) Ex. Babesia (Babesiosis: North America and Europe) |
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Tissue tropism protozoa
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Two host cycles
Ex. Toxoplasma Ex. Leishmania sp. (Leishmaniasis) Leishmania vector borne Toxoplasma food borne |
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Enteric protozoa
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Entamoeba sp. (amoebiasis)
Giardia sp. (giardiasis) Cryptosporidium parvum (cryptosporidiosis) Generally two form life cycle Trophozoite –causes disease Cyst: resists desiccation in the environment Fecal-oral spread (either direct human to human or through food/water) Desiccate easily in the environment Intestinal lumen without invasion Giardia Cryptosporidium Invade intestinal mucosa Entamoeba |
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Helminths overview
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Very prevalent in the world (billions infected)
Disease very diverse Multicellular complex organisms Adult size varies from 1 cm to 10 meters Covered by a cuticle or tegument that protects them from digestion and environmental stresses. Transmission occurs through -Ingestion -Vector by a biting insect -Direct penetration of the skin |
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Helminths life cycle
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Life cycles complex
Almost always requires an intermediate host Humans can be -The only host -The intermediate host -The definitive host -An accidental or “dead-end” host --Occurs when a helminth that usually infects another animal attempts to invade or infect a human but cannot complete the necessary stage of its life cycle --Still can cause a self limited illness/disease Usually, unless re-exposed the human infection lasts only as long as the life-span of the adult worm or the intermediate stage -Thus the intensity of infection can increase only with repeated re-exposures. |
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Helminths epidemiology, disease pathology, immunity
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Warm-moist tropical or semi-tropical areas
Seen with poverty and poor hygiene, sanitation Most infections are asymptomatic Disease caused by -Mechanical effects -Invasion of host cells or tissues -Immunologic response Immunity is very complex and NOT sterilizing Eosinophilia common -Eosinophil is integral to the immune response to parasites -Seen only in tissue invasive or migratory portions of the life cycle -Not seen with adult worms in intestinal lumen -Not seen with protozoal infections |
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Nematodes (roundworms) - intestinal
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Helminth
Ascaris (intestinal roundworm) Ancylostoma duodenale, Necator americanus (hookworms) Strongyloides stercoralis Enterobius (pinworm) |
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Nematodes (roundworms) - tisue
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Helminth
Trichinella (Trichinosis) Wuchereria bancrofti (elephantiasis, lymphatic filariasis) Onchocerca volvulus (river blindness) -Actual tissue damage in cornea of eye is not due to the parasite but due to a bacteria on its skin called “Wolbachia sp.” |
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Trematodes (flukes)
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Helminth
Schistosoma (blood flukes) Intestinal and liver flukes |
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Cestodes (tapeworms)
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Helminth
Taenia saginata (beef tape worm) Taenia solium (pork tape worm) Diphyllobothrium latum (fish tape worm) |
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Ectoparasites
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Scabies
Leeches Lice Ticks Chiggers |
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Entamoeba histolytica: transmission, similar entamoeba
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Fecal-oral: through contaminated food and water; person-to-person spread may occur
Entamoeba dispar, Non-pathogenic, morphologically indistinguishable; need isoenzyme electrophoresis or specific stool antigen tests to differentiate -Much asymptomatic infection attributed to E. histolytica is probably due to E. dispar |
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Entamoeba histolytica life cycle
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Trophozoites
-pathogenic portion of lifecycle Cyst -prevents dessication Ingested cysts (environmentally resistant) transform to trophozoites upon exposure to stomach acid that colonize and in some individuals subsequently invade intestinal mucosa. In most the infection is asymptomatic. In some it invades the intestinal mucosa causing colitis and less commonly, through hematogenous or direct spread, distant infection Trophozoites can divide and transform to infective cysts in asymptomatic carriers or symptomatic patients that are passed in the stool. What causes transformation to cysts is unclear |
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Entamoeba histolytica: virulence factors, disease pathogenesis, immunity
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Virulence factors:
-Galactosamine adherence lectin -Proteinases -Lysis of WBC’s To cause invasive disease the trophozoite must penetrate the intestinal mucosa mucous layer, thus host alterations in mucosa and mucous (such as with malnutrition) is the main host defect which allows disease to occur) (ulcerative and inflammatory lesions of colon) 3 stages for infection -Attachment to host mucosal colonic epithelium through receptors -Contact-dependent killing -Ingestion of the killed host cell Immunity: -Cell-mediated immunity |
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GIARDIA LAMBLIA: epidemiology
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Worldwide distribution
Cysts found in surface waters where mammalian reservoirs frequent (beaver the prototype) Transmission: water >> food, person-to-person, zoonosis (dog or cat) Most common enteric parasite in the USA and Canada Sporadic infection in US seen in outdoor adventurers. Small epidemics seen associated with day-care or swimming pools |
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Giardia life cycle
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Ingested cysts transform to trophozoites upon exposure to gastric acid and attach to small intestinal villi where they cause a malabsorptive diarrhea.
Some trophozoites transform to environmentally resistant cyst which are passed in the stool |
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Giardia pathogenesis and immunity, microscope appearance
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Does not invade small intestinal or colonic mucosa but does cause destruction of small intestinal mucosal microvilli
Parasite virulence factors not well understood other than receptor mediated attachment Host defense is primarily IgA immunoglobulin Trophozoites: flagellum, two (eye like) nuclei |
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CRYPTOSPORIDIUM: Cryptosporidium parvum: distribution, pathogenesis, transmission
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Coccidian parasite - acid fast
Worldwide distribution Intracellular pathogen; microvilli Oocysts move into intestine where excyst to sporozoites; Oocysts resistant to disinfection; ID50 is 130 cysts or so Pathogenesis of diarrhea unclear; microvilli atrophied and blunted. Sporozoites seen along apical surfaces of intestinal epithelial cells Transmission water>>fecal-oral>person-person |
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Cryptosporidium: Epidemiology
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Can cause disease in immunocompetent and immunocompromised host
Outbreaks seen in day-care settings, swimming pool associated, and food-borne (apple cider, fresh vegetables) A few waterborne outbreaks described that are of huge dimensions. Not eliminated by water treatment (very resistant to chlorine). Transmission through water distribution systems in these cases. Agriculture, particularly cattle implicated. Calves probably the most important shedders. Occasionally person to person or zoonotic |
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Epidemiology of Malaria
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40% of world population at risk
Tropical and subtropical regions 80% of cases occur in Africa 300-500 million cases a year 1.5 – 2.7 million deaths a year -90% in sub-Saharan Africa -½ in children less than 5 yrs of age -Also high risk in pregnant women and non-immune travelers 12 billion dollars in lost revenue/year in Africa |
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Plasmodium Species Causing Malaria in Humans
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P. falciparum
-Most dangerous P. vivax & P. ovale -Less dangerous -Can relapse because of “hidden” liver stage that can persist despite drug treatment P. malariae -Rare Different distributions of species depending on geography |
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Malaria - Transmission
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Anopheline mosquito (female only)
-Aggressive night time biter (dusk to dawn) Reservoirs of infected and uninfected humans Needs opportunity for host-vector contact Mostly tropical and subtropical, altitudes below 1500m Also can be transmitted by transfusion, needles, and transplacentally |
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Malaria life cycle
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Anopheles mosquito inoculates sporozoites into human
Exoerythrocytic schizogony: -Sporozoites infect liver cells -Mature into schizonts, then rupture and release merozoites -P.ovale and P.vivax have a dormant stage (hypnozoites) in liver and can persist for years, causing relapses when they invade bloodstream Erythrocytic schizogony (asexual reproduction) -Merozoites infect red blood cells -Ring stage trophozoites mature into schizonts -Schizonts rupture and release merozoites Sexual erythrocytic stage -Some form gametocytes -Ingested by mosquito Sporogonic cycle (in the mosquito) -Micro and macro gametocytes develop into zygotes then ookinetes -Ookinetes invade midgut wall, become oocysts -Oocysts rupture and release sporozoites which travel to salivary glands for injection into human host |
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Malaria pathogenesis
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P. falciparum causes microvascular disease
-Cyto-adherence to endothelium of brain, kidneys, other organs. Exact mechanism of tissue injury not clear but microvascular occlusion is important -Mediated by “knobs” that form on erythrocytes -Parasite toxins and resultant cytokine release with systemic inflammation -Intravascular hemolytic anemia -Tissue hypoglycemia Higher the parasite load in the bloodstream, the higher the mortality (6% or more is "severe") Almost all malaria mortality is with P. falciparum |
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Malaria host factors and immunity
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Risk of severe disease greatest in young children and travellers to area
No specific protective antibodies or cell-mediated immunity found Partial immunity develops over time Normal spleen function important -Removes parasitized RBCs from circulation because they are less deformable |
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Malaria fever pattern
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Due to erythrocytic pattern
-cytokine response to rbc lysis It takes time for fever pattern to occur |
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Malaria Prevention
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Vector control
-Limited effectiveness -Mosquitos becoming resistant to chemical pesticides Bednetting -Permethrin impregnation increases effectiveness Mosquito avoidance (clothing and repellents) Antimalarial prophylaxis |
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Babesiosis: species, vector, transmission, life cycle, location
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Etiology: protozoa (Babesia sp.)
-B. microti (most common in USA:coastal NE) -B. divergens (most cases in Europe) -WA1 strain (Washington state); MO1 (Missouri) Tick vector (Ixodid: also transmits Lyme, ehrlichiosis) Can be transfusion transmitted Emerging disease but rare (100+ cases) Life cycle requires tick, mouse and deer in proximity -Humans are dead end, cannot transmit to tick -Tick attached for 24 hours Mostly seen in Connecticut and New England offshore islands (PEARL FOR YOUR BOARDS!!!!) |
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Trypanosomiasis: species, disease, vector, life cycle, microbiology
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Africa
-Trypanosoma brucei -Sleeping sickness (encephalitis brain infection), lymphadenopathy -Vector is tsetse fly through its bite South America -Trypanosoma cruzi -Chagas disease (infection of GI tract and heart) -Vector is reduvid bug (kissing bug) through its defecation -looks like "C" in blood Two stage life cycle -Promastigote (insect stage in GI tract) -Amastigote (tissue infective stage) Promastigote enters human blood stream where it is distributed to tropic tissues |
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Trypanosomiasis: host immunity
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Main immunity is humeral
Parasite avoids this immunity by periodically changing its glycoprotein coat through antigenic variation Occurs through movement of genetic “cassettes” that code glycoprotein into portion of active genome that is being expressed |
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Toxoplasma: host, transmission, symptoms, disease, prevention
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Life cycle: Very complex. Do not memorize
Definitive host: sexual life cycle occurs only in cats, humans intermediate host Geographic distribution: anywhere cats are Transmission: Ingestion of under-cooked meat, ingestion of small amounts of cat feces. Cat gets infection from eating a mouse Symptoms: most often asymptomatic, one case of note: Martina Navritolova lost the US open in 1982 when she had toxoplasmosis Disease in immune-compromised individuals (emerged as typical opportunistic disease in AIDS) encephalitis, fever, necrotizing encephalitis, myositis, myocarditis. MOST IN AIDS IS ENCEPHALITIS AND IS REACTIVATION OF LATENT INFECTION Also, congenital infection if in the first trimester of pregnancy can cause chorioretinitis, cerebral calcifications, to disseminated disease Prevention / eradication: Fully cook meat, Avoid cat litter box during pregnancy |
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HOOKWORMS: epidemiology, risk for infection
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Species which produce human disease vary geographically:
-Ancylostoma duodenale Mediterranean countries, Iran, India, Pakistan, Far East -Necator americanus North, South and Central America, Central Africa, Indonesia, South Pacific, parts of India Common in tropics, subtropics, SE USA; rare in regions with < 40” inches annual rainfall. Globally > 1 x 109 people infected Risk for infection: skin exposures to fecally contaminated soil in endemic areas -local residents of tropics -occupational (infantry troops) -recreational (tourists walking with barefoot or with open footwear)—especially cutaneous larva migrans: see below |
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Hookworm life cycle
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Infective larvae penetrate skin that contacts soil.
Migrates through systemic venous system to lung Mature in lung, migrate up trachea and swallowed Further mature into adults in small intestine. Attach to mucosa and cause slow, chronic blood loss and iron deficiency anemia. Eggs passed into stool. Eggs hatch in soil into infective larvae Gotta have stool in soil! |
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CUTANEOUS LARVA MIGRANS AKA CREEPING ERUPTION
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Example of human as an accidental or dead-end host
Dog, cat hookworm most common cause Pathogenesis: Larvae hatch in soil after eggs pass in canine, feline feces. Penetrate, migrate in skin producing inflammatory rxn along cutaneous tract. Pulmonary involvement also occurs. Clinical disease: pruritic, serpiginous lesions develop 1 week post-contact with infected soil Prevention: shoes |
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Schistosomiasis: epidemiology
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Globally > 200-300 million people infected
Infection/disease dependent on tissue tropism of specific species Surface water exposure Infections occur in -local residents of tropics -occupational (infantry troops) -recreational (Usually peace corps and ex-patriots) |
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Schistosoma mansoni, Schistosoma japonicum:
life cycle and pathology |
Blood flukes
-Snail intermediate host release cercariae -Adult worms reside in the venous plexuses of the GI tract (intestine) -Here they mate and excrete large numbers of eggs which are transported to the liver via the portal circulation -In the venules they become entraped or experience slow transit and an immune response occurs -Pathology is that of granulomatous inflammation in the venous plexuses. This inflammation eventually results in fibrosis about the venules -Periportal hypertension results and prehepatic cirrhosis with varices of collateral circulation. Eosinophilia is seen |
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Schistosoma hematobium: life cycle and pathology
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Blood fluke
-Snail intermediate host release cercariae -Adult worms reside in the venous plexuses of the urinary tract (mostly bladder) -Here they mate and excrete large numbers of eggs which are transported to the bladder via the portal circulation -In the venules they become entrapped or experience slow transit and an immune response occurs -Pathology is that of granulomatous inflammation in the venous plexuses. This inflammation eventually results in fibrosis about the venules -Varices occur within the bladder resulting in intermittent hematuria and thickening and dysfunction of the bladder wall. Bladder cancer is a long term complication. Eosinophilia is seen |
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Schistosomiasis: Blood flukes immune evasion
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Evade immune response by:
-Absorbing host proteins onto their own on their tegument surfaces (including HLA proteins and albumin), thus masquerading as the host by displaying its antigens. Long-term chronic infections occur |
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CESTODES: species
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TAENIASIS:
-T. saginata=beef tapeworm, endemic in most of developing world -T. solium=pork tapeworm. Endemic in Latin America, Africa, Middle East, Central Asia. -Cysticercosis from T. solium larvae seizures DIPHYLLOBOTHRIASIS (fish tapeworm): -Vitamin B12 deficiency. |
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CESTODES: disease
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Adult tapeworms cause little or no symptomatic disease
Larval (cysticercal) tapeworms responsible for serious disease -Cysticercal phase usually seen in intermediate host. However if human ingests eggs rather than tissue phase cysticerci will cause result in intermediate cysticerci in muscles and brain. From brain seizures. Little or no eosinophilia |
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Cestode: morphology and function
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Strobila: linear sets of reproductive organs of both sexes packaged into segments or proglottids
New proglottids are continuously generated and differentiated from the anterior end (neck) of the worm As each segment moves toward the posterior, they become sexually mature, copulate, and produce eggs When a proglottid contains fully developed shelled eggs, it is said to be gravid When it reaches the end, a gravid proglottid will detach and pass out with the feces of the host. Individual proglottids can behave like an individual worm, crawling actively |
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Cestode: life cycle
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Embryonated eggs and/or gravid proglottids ingested by pigs
Humans ingest cycstic pig muscle Scolex attaches to intestine Adult grows and releases eggs and/or gravid proglottids -Ingested by pigs OR -If egg ingested by human, human can have cysticercosis |
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Cysticercosis
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Humans are infected with adult (gravid) worms
Somehow, eggs make it into the stomach from the intestine Infection begins with “shelled” larvae passing through the stomach and hatching in the intestine The eggs then enter the blood and can be disseminated to any organ of the body Most serious infections include the brain and eyes Mature cysticerci can range from 5mm to 20cm in diameter |
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Filaria (all nematodes)
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Elephantiasis
-Mosquito vector -Lymphatic obstruction and limb/scrotal edema Oncocerciasis -Fly vector -Lose of skin elasticity, severe pruritus, corneal scaring leading to blindness Loa loa -Tissue and conjunctiva migrant |
