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449 Cards in this Set
- Front
- Back
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Types of trematodes
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1. Monogenea: ectoparasites of aquatic animals
2. Digenea: tissue or blood-dwelling endoparasites Both are soft-bodied and flattened |
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Platyhelminthes descendents
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-Turbellarians
-Cestodes (tapeworms) -Trematodes (flukes) |
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Digenea Trematodes
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-Fasciolidae
-Paramphistomatidae -Dicrocoelidae -Troglotrematidae -Diplostomatidae -Schistosomatidae |
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Monogenea
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-Type of trematodes
-Ectoparasites of fish -Hermaphrodites -Direct life cycle, have 1 host, reproduce, and move on -Pathogenesis is based on parasite burden -Feed on epidermis, blood, and mucus -Attach to skin or gill of fish |
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Gyrodactylus spp.
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-Monogenea trematode
-Ectopatasites on skin and gills of aquatic animals -Has Haptor for attachment -Big issue for aquarium fish and aquaculture -Tx: formalin, praziquantel -Complete elimination is difficult |
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Digenea
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-Type of trematode platyhelminthes
-Nearly all are hermaphrodites -Adults have oral and ventral suckers -Hangs out in bile and pancreatic ducts, small intestine, rumen, lungs, veins of digestive and urinary tract -Can also be in the circulatory system -Eggs are found in the feces, urine, and sputum |
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Digenea life cycles
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-Complex Indirect life cycle
-Has distinct developmental stages and intermediate hosts --Multiple hosts -Sexual and asexual reproduction, alternate between -Environment is important in defining the timing of disease |
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Digenean life cycle steps
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1. Eggs passed in feces, sputum, nasal mucus, urine into water
2. Hatch in fresh water, release miracidium (free-swimming form) 3. Enters snail intermediate host and develop into cercaria --go through asexual reproduction/cloning --amplify in numbers in each developmental stage 4. Cercaria directly penetrate host, are ingested by 2nd intermediate host and host is ingested by d.host, or metacercaria are encysted on vegetation and vegetation is ingested by d.host |
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Digenean ingestion by definitive host
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1. Cercaria directly penetrates host skin
2. Cercaria are ingested by 2nd intermediate host, 2nd intermediate host is ingested by definitive host --fish --crayfish --crabs --arthropods --vertebrates 3. Cercaria develop into metacercaria and encyst on vegetation --vegetation is ingested by host |
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Species with Metacercariae encysted on vegetation
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1. Fasciolidae
-Fasciola hepatica -Fasciola gigantica -Fascioloides magna 2. Paramphistomatidae -Paramphistomum cervi -Paramphistomum microbothroides |
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Fasciola Hepatica
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-Liver fluke
-Large, 3-4 cm long -Flattened body with clear "shoulders" -Oral sucker and ventral sucker |
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Fasciola hepatica egg
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-Found in feces
-Operculate -Unembryonated -Operculate eggs in feces is diagnostic stage |
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Fasciola hepatica life cycle
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-Aquatic and terrestrial stages
1. Unembryonated egg passed in feces into water, becomes embryonated 2. Embryonated egg is ingested by snail intermediate host, develops into miracidium, sporocyst, and redia 3. Redia develop into free-swimming cercaria 4. Cercaria develop into metacercaria and encyst on plants 5. Host eats plants and ingests metacercaria, excyst in duodenum 6. Excysted metacercaria penetrates intestinal wall and gets into abdominal cavity 7. Juveniles migrate around abdominal cavity and end up in liver 8. Adults end up in bile ducts, lay eggs that are carried by bile into the digestive tract |
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Fasciola hepatica Pathogenesis
Acute Disease |
-Disease is due to ingestion of large numbers of metacercariae via plants
-Juveniles tunneling within the liver cause thrombi and coagulative necrosis -Clostridium novyi anerobe can multiply in the lesions and lead to necrosis and hemorrhage --may lead to death in severe cases -Detection of a single fluke will condemn a liver in a slaughterhouse |
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Fasciola hepatica migratory tracts
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-Juveniles migrating to and through liver cause serious damage
-Acute transient disease -Direct damage to the liver parenchyma -Leads to secondary clostridium infection |
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Adult Fasciola hepatica in the Liver
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-Hang out in bile duct
-Cause bile duct hyperplasia -Feed on blood -Cause anemia |
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Pathogenesis of Fasciola hepatica
Chronic disease |
-More persistent in sheep
-Cows show acquired resistance and can eliminate flukes by 24 weeks -Associated with presence of adults in bile ducts -Causes hyperplasia, fibrosis, and calcification of liver -Hypoprotenemia, anemia, and wasting disease can result -Infectious dose is 200-800 metacercariae -Can be asymptomatic or gradual development of bottle jaw, ascites, emaciation, and weight loss |
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Fasciola Hepatica severity of pathology
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-Associated with levels of infectious dose, number of metacercariae ingested
-Acute type I: infectious dose is over 5,000 metacercariae -Acute type II: infectious dose is 1,000-5,000 metacercariae -Subacute fasciolosis: infectious dose is 800-1000 metacercariae -Chronic fasciolosis: infectious dose is 200-800 metacercariae |
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Acute type I Fasciolosis
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-Infectious dose is over 5,000 metacercariae
-Animal dies suddenly without any previous clinical signs -Ascites, abdominal hemorrhage, jaundice, pale membranes may be seen |
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Acute type II Fasciolosis
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-Infectious dose is 1,000-5,000 metacercariae
-Sheep die -Will show paleness, loss of body condition and ascites before dropping dead |
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Subacute Fasciolosis
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-Infectious dose of 800-1000 metacercariae
-Animal will be lethargic, anemic, and may die -Weight loss is the dominant feature |
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Fasciola hepatica distribution
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-Mostly in northwestern US:
--cold winter --transmission occurs in late summer --Disease is prevalent in late fall (juvenile migration) and adults present in winter --Tx: January, adults present and weather is cold -Also in eastern Texas, gulf states -Florida --drought during summer, transmission occurs during winter --Disease occurs in spring due to juvenile migration --adults present in the summer --Tx: August, adults present and weather is hot and dry Different disease patterns informs treatment strategies |
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Fasciola hepatica environmental cues
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-Miracidium develop in 9 days
-Development depends on temperature and moisture -Larvae develop in 6-7 weeks in snail --delayed by low temps -Metacercariae survive on pasture for 3 months --Resistant to freezing and drying |
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Fasciola hepatica treatment and control
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-Most drugs are only active against adults
--Triclabendazole --albendazole --clorsulon -Molluscisides to kill snails: --not really effective and have environmental issues -Movement to fluke-free pastures --gets rid of adults and prevents transmission |
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Fasciola magna
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-Deer are definitive host
-Forms cysts in liver that connect to the bile ducts -IN sheep and goats, juveniles do not mature but continue to migrate and cause disease --Cannot diagnose, no eggs! -Distribution is mostly in great lakes region, pacific NW, and gulf states |
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Paramphistomamum cervi
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-Paramphistomatidae family
-Rumen Fluke -Trematode life cycle -Adults are relatively harmless -Eggs look like Fasciola hepatica -High infective dose can lead to disease during migration from small intestine lumen to rumen -Tx: niclosamide |
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Paramphistomamum microbothroides
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-Paramphistomae family
-Oral and ventral suckers -Short, wide little flukes -Look like little beads |
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Species infecting via 2nd intermediate host of infected fish, amphibians, crayfish, crabs, etc.
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-Troglotrematidae
--Nanophyetus salmincola --Paragonimus kellicotti -Dicrocoeliidae --Platynosomum fastosum -Diplostomatidae --Alaria |
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Nanophyetus salmincola
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-Intestinal fluke
-Trematode Eggs in stool are diagnostic stage -Metacercariae are found on salmon species -Serves as host to Neoricketsia helminthoeca, salmon poisoning hemorrhagic enteritis --Acts as a parasite AND a vector --Neoricketsia helminthoeca is really the bigger deal |
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Paragonimus kellicotti
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-Lung flukes in Troglotrematidae family
-Adults are found in pairs in the lungs -Cause respiratory disease due to migration through lungs -Occasionally seen in Philadelphia, but usually west of Mississippi |
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Paragonimus kellicotti life cycle
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1. Unembryonated egg is passed into fresh water via feces or sputum
2. Miracidium develops in water, hatches and penetrates 1st intermediate host (snail) 3. Miracidium develops into sporocyst, Redia I and Reddia II in snail, hatches are cercaria 4. Cercaria are shed into water, penetrates gills or muscle of 2nd intermediate host (crustacean) and encysts as metacercaria in crustacean tissues 5. Host eats crustacean with encysted metacercaria 6. Worm excysts in gut, penetrates gut to peritoneal cavity and migrates to lungs 7. Eggs are laid in lungs, coughed up and swallowed |
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Paragonimus kellicotti eggs
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-Operculate eggs
-Have "collar" |
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Platynosomum fastosum
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-Bile and pancreatic duct fluke in Dirocoeliidae family
-Mostly in the south east US and west Indies -Metacercareae are found in amphibians, lizards, geckos -Intermediate hosts are ingested by cats |
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infection from Eating amphibian paratenic hosts
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-Family Diplostomatidae
-Complex life cycle -Many definitive hosts, usually a wildlife disease (esp. raccoons) -Uncommonly infects dogs and cats -Vertical transmission via milk ducts from mom to sucklings -Can be pathogenic |
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Alaria
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-Has Mesocercaria, larval stage found in paratenic hosts
-Migration in lungs can cause disease -Can be ingested by eating frogs legs |
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Alaria life cycle
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1. Trematode egg gives rise to free-living miracidium
2. Miracidium is ingested by intermediate host (snail), asexual reproduction amplifies parasite numbers 3. Free living cercaria are released, are eaten by tadpoles and develop into mesocercariae 4. Can either go into a paratenic host (frog, snake, mouse) OR can go right to definitive host 5. Mesocercaria in definitive host migrate to lungs, form metacercariae, are coughed up and swallowed as adults into host gut 6. Eggs can be pooped out or metacercariae migrated to mammary glands can be transmitted to offspring |
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Infection from Ingestion of Arthropod hosts
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-Dicrocoeliidae family
-Completely terrestrial life cycle -Miracidium is eaten by terrestrial snail -Cercariae escape in slime ball from the snail and are eaten by ants --ants become "robots" for cercariae -Worm develops into metacercariae in ant, make ant climb up in vegetation where it is easier to be ingested by the host |
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Dicrocoelium dentriticum
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-Dicrocoeliidae family
-Small flukes -Lancet shaped, no shoulders -Small operculate sggs -Found in bile duct of sheep, cattle, and pigs --clinical disease is associated with bile duct fibrosis and cirrhosis -No parenchymal migration -"Brainworm" due to altering the behavior of the intermediate host ant |
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Dicrocoelium dendriticum life cycle
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-Completely terrestrial life cycle
-Miracidium is eaten by terrestrial snail -Cercariae escape in slime ball from the snail and are eaten by ants --ants become "robots" for cercariae -Worm develops into metacercariae in ant, make ant climb up in vegetation where it is easier to be ingested by the host |
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Schistosomatidae
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-Blood flukes
-Infect directly via cercariae -Schistosoma bovis (cattle) -Schistosoma indium (Horses, cattle, goats) -Schistosoma nasale (cattle) -Schistosoma japonicum (Cattle) -Heterobilharzia americana (dog) |
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Schistosoma japonicum life cycle
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1. Eggs passed in feces into water
2. Ingested by snail intermediate host, develop into cercariae 3. Cercariae are ingested by host, migrate to liver |
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Family Schistosomatidae
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-Have snail as intermediate host
-Cercariae are infective -Separate sexes live together in circulatory system -Females can lay 300 to 3,000 eggs per day -Long lived, can be in the host for decades -Eggs cause chronic disease --granulomas in the liver and other tissues |
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Heterobilharzia americana
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-Dog schistosomes
-Uncommon, but need to be thought of -Dogs, rabbits, raccoons, bobcats, are all definitive hosts -Mesenteric veins are the predilection site -Eggs evoke a granulomatous response -Usually hosts are asymptomatic -Can cause lethargy, slow and chronic weight loss, diarrhea -in extreme cases can be fatal |
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Schistosome pathogenesis
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-Lay large numbers of eggs
-Are long-lived worms -Incite granuloma formation in lungs and liver --cause chronic disease --can result in portal hypertension |
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Swimmer's itch
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-Caused by avian schistosomes
-Cercariae are able to penetrate skin, but die before getting too far -Delayed-type hypersensitivity reaction in skin |
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Liver and Bile duct Flukes
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-Fasciola hepatica
-Fasciola magna -Dirocelium dendriticum -Platynosum fastosum |
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Rumen flukes
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-Paramphistomum microbothroides
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Intestinal flukes
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-Nanophytes salmincola
-Alaria marcianae |
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Lung flukes
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-Paragonimus kellicotti
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Circulatory flukes
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-Schistosoma
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How to differentiate between trematode eggs
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-All are operculate
-Fasciola and Dirocoelium are in sheep and cattle --Fasciola egg is larger -Paragonimus is found in carnivores --Egg is colored, may be present in sputum |
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Acanthocephalans
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-"Thorn heads"
-Separate sexes -No gut -High reproductive output -Males have cement glands that seal female vagina after copulation, prevents sexual competition |
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Macracanthorhynchus hirudinaceus
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-Found in the small intestine of pigs
-Also occasionally infects dogs and other mammals -Intermediate hosts are duct, water, and may beetles -Females are larger than males -Can be highly pathogenic -Outbreaks have stopped in the US due to "raising pigs on concrete" -Do not have a mouth or digestive system --cause necrosis at local site -Can see flattened villi |
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Macracanthorhynchus hirudinaceus eggs
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-Egg contains fully formed larva
-Seen in feces of birds and marine mammals commonly -Eggs are diagnostic stage -Thick brown shell |
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Macracanthorhynchus hirudinaceus diagnosis
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-Depends on presence of eggs
-Adults can be identified by presence of spiny proboscus -No gut or circulatory system |
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Macracantthorhynchus hirudinaceus pathogenesis
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-Can be asymptomatic
-Ulceration and granuloma formation at site of infection -Can cause acute peritonitis due to mechanical disruption of the intestinal wall -Chronic infection is related to worm burden -Will result in competition for nutrients -Diarrhea, wasting, failure to thrive -Control by removing contact with intermediate host -Tx: levamisole, ivermectin |
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Cestode life cycle
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1. Egg is expelled with feces and ingested by an intermediate host
2. hecacanth larva hatches in gut, develops into metacestode 3. Metacestode is either ingested by the definitive host OR ingested by 2nd intermediate host and develops into 2nd metacestode 4. 2nd metacestode is either ingested by definitive host OR ingested by paratenic host, which is then ingested by the definitive host |
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Cestode overview
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-No gut
-Absorb food through surface -Hermaphrodite: both sex organs exist in each proglottid segment -REquire at least 2 hosts to complete life history |
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Types of Cestodes
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-Cycloplyllidea
--Taeniidae --Anoplocehpalidae --Dilepididae --Mesocestoididae --Hymenolopididae -Pseudophyllidea --diphyllobothrium --Spirometra |
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Adult Tapeworm
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-Chain of independent progressively maturing reproductive units
-One end is anchored in the wall of host intestine by Scolex -When adult gets to the intestine, most of the larval body is digested away and only scolex remains with some undifferentiated tissue -Undifferentiated tissue begins to bud off segments -Oldest segments are furthest away from the scolex -All stages of development exist in linear arrangement -All segments are served by common osmoregulatory and nervous systems --rhythmic and coordinated movement -No organs or feeding or digestion --All nutrients are absorbed through the integument |
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Cestode oncoshperes
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-1st stage larva
-Infective only for 1st intermediate host -Made up of embryo (hexacanth, 6 hooks) surrounded by 2 embryonic membranes -Pseudophyllideans are surrounded by a shell -Cyclophyllideans fully developed into larva when passed in the feces --lack a true shell |
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Cyclophyllidea tape worms
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-4 radial muscular suckers on the scolex
--used for attachment and locomotion -Most scolices also ave rostellum (dome-shaped projection at apex of scolex) --often retractable and armed with small hooks -Segments are longer than they are wide -Genital pore is lateral --used for fertilization, no opening for release of eggs |
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Cyclophyllidea segments
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-Have no openings for eggs to escape
-Eggs accumulate until the segment is packed -Gravid segments detach from end of the chain and pass out with feces or crawl out of the anus of the host -Finding gravid segments on host or in environment are diagnostic for cyclophyllidean worms |
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Taenia solium and Taenia saginata life cycles
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------
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Echinococcus granulosus
Echinococcus multilocularis |
-Small tapeworms of dogs, only a few mm
-Scolex with armed rostellum and 4 suckers -Larval tapeworm of several hosts, including humans -Adult tapeworms are not usually pathogenic |
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Echinococcus granulosus Life Cycle
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1. Embryonated eggs are passed in feces and are ingested by host
2. Oncosphere hatches in intestine, penetrates the intestinal wall, and enters the bloodstream 3. Hydatid cyst in the lungs, liver and other tissues 4. Cyst hatches, forms protoscolex that is passed in feces (?) 5. Protoscolex is ingested by host, attaches to intestine and develops into adult in small intestine |
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Echinococcosis
Hydatid Disease |
-Caused by larval stages of Echinococcus cestodes
-Acts like a tumor and invades other tissues -E. granulosus: cystic (most common) -E. multilocularis: alveolar -E. vogeli: polycystic -E. oligarthrus: human |
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Anoplocephalidae perfoliata
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-Horses, donkeys
-Most important tapeworm species that people are worried about -2 inches long -Wider than usual cyclophollidians |
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Anoplocephalidae magna
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-Horses, donkeys
-10 inches long, long-ish worm -Worldwide and in NE |
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Paranoplocephala mamillana
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-Horses, donkeys
-Small and difficult to find -Present worldwide and in NE |
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Moneizia
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-Ruminants, sheep, giraffes
-Live in small intestine -Worldwide and in NE -Can get to be 20 feet long -Non-pathogenic -Gives off unique square/triangular eggs |
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Anoplocephalidae Life Cycle
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1. Mature segments come out in feces
2. Eggs are ingested by forage mites 3. Eggs mature from oncosphere to cysticercoid in mite 4. Definitive host is infected by ingesting the mite that contains the cysticercoid |
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Tapeworms of Horses
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1. Anoplocephala magna: small intestine, non-pathogenic
2. Paranoplocephala mamillana: small intestine, non-pathogenic 3. Anoplocephala perfoliata: cecum and ileum, clustered near iliocecal valve --can cause ulceration and associated inflammation --leads to serious diarrhea --Pathogenic adult tapeworm |
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Dipylidium caninum
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-Double-pored dog tapeworm
-Mainly affects dogs and cats -Occasionally found in humans -most common tapeworm in the USA -Spread by fleas and biting lice -Develops quickly in definitive host |
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Dipylidium caninum Life Cycle
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1. Gravid Proglottids containing egg packets passed in feces or emerge from perianal region
2. Gravid proglottids disintegrate and release egg packets, egg packets are ingested by larval stage of flea 3. Oncospheres hatch from embryonated eggs, penetrate intestinal wall of flea larva, and develop into cysticercoid 4. Infected larvae develop into adult fleas containing infective cysticercoid 5. Host is infected by ingesting fleas with infective cysticercoid |
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Hymenolepis nana life cycle
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1. Embryonated eggs are released in feces
2. Egg is ingested by insect (flea or flour beetle) and develops into cysticercoid OR are directly ingested by the host 3. Definitive hosts are infected when they ingest cysticercoid infected arthropods 4. Autoinfection can occur if eggs remain in the intestine --eggs release hexacanth embryo that penetrates intestinal villus and continues the cycle Can get full development in the host without intermediate host -Non pathogenic, but disturbing |
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Davaineidae
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-Tapeworms of poultry, mostly free-range poultry
-Davainea proglottina -Raillietine echinobothrida |
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Mesocestoididae
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-Eggs are ingested by mites, cysticercoid develops into oncosphere in mite
-May have a 2nd intermediate host, definitive host may ingest invertebrate directly -intermediate host is also the definitive host |
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Taenia taeniaformis
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-Tapeworm of cat, rat, and mouse
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Taenia pisiformis
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-Tapeworm of dog and rabbit
-larval stage is in the liver and peritoneal cavity |
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Thysanosoma spp.
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-Tapeworm in all ruminants EXCEPT cattle
-In small intestine |
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Pseudophyllidea
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-Diphyllobothrium and Spirometra
-Scolex has 2 shallow longitudinal grooves (Bothria) --Used for attachment and locomotion -Segments have uterine pore for release of eggs -Segments discharge eggs until supply is gone -Terminal segments become senile rather than gravid -Need at least 2 intermediate hosts -Also have aquatic stages |
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Diphyllobothrium latum
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-Found in dogs around the great lakes
-Often seen in seals and dolphins -Operculate egg becomes a free-swimming coracidium --eggs do not have have hooks until they mature in water -has multiple intermediate hosts --1: copepod --2: fish, can be infective for definitive host --3: predatious fish |
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Spirometra mansonoides
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-In dogs, cats, wild carnivores, and pigs
--more often in cats than dogs -Eggs hatch in water to coracidium, are eaten and become procercoid -Procercoid are eaten by intermediate host and become Sparganum, proercoid in tissues -intermediate host is eaten by definitive host |
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Pseudophyllidean Pattern
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Egg → coracidium → procercoid → plerocercoid → adult cestode
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Cyclophyllidean pattern
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1. Egg → oncosphere → cysticercus → adult cestode
2. Egg → oncosphere → cysticercoid → adult cestode 3. Egg → oncosphere → coenurus → adult cestode 4. Egg → oncosphere → hydatid → adult cestode |
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Arthropods
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-High reproductive potential with short germination time
-Have a huge impact as pests of vegetable crops and stored food products -Destory textiles and structural materials -Agents of blood loss and annoyance -Agents of dermatosis -Agents of myiases -Source of allergens -Cause disease by envenomization and anaphylaxis -Vectors of disease agents, transmit other diseases and other pathogens --can be a direct vector or a mechanical carrier |
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Characteristics of Arthropods
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1. Bilateral symmetry
2. Elongated segmented body, 3 segments 3. Paired jointed appendages 4. Exoskeleton is secreted non-cellular material 5. Ventral nerve cord 6. Open circulatory system --no vascular system --blood percolates around in an open body cavity --Dorsal tube keeps fluid moving around the body |
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Phylum Arthropoda Classification
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-Insecta: hexapoda, all have 6 feet
--diptera --pthiraptera --siphonaptera --hemiptera -Arachnida --sliders --acarina (mites and ticks) -Others not relevant to vet med |
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Chilopoda
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-Centipedes
-Some species can envenomize, but rare |
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Diplopoda
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-Millipedes
-Some species secrete irritating defensive substance |
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Hexapoda
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1. Diptera: true flies
2. Pthiraptera: lice 3. Siphonaptera: fleas, wingless blood suckers 4. Hemiptera: true bugs |
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Arachnida
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1. Scorpionida: scorpions
2. Araneida: spiders 3. Acarina: ticks and mites |
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Insect/Hexapoda body plan
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Head: concentration of nerve ganglia
-antennae and eyes are packed with sensory nerves Thorax: used for locomotion -3 segments, 1 pair of legs per segment -Wing pairs are on back 2 segments Abdomen: contains reproductive organs -Spiraciles are also on abdomen, transports O2 directly to the tissues |
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Arachnid Body Plan
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-Cephalothorax and abdomen
-Cephalothorax contains legs, mouth parts, and sensory structures --Head and thorax are fused -Never have wings |
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Arthropod Integument
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-Made of Chitin: sugar molecule polymer
--rich in N-acetyl glucosamine -Proteins cross-linked by phenol compounds --provide strength --cross links are not present at joints to provide flexibility -Waxy coating to prevent dessication |
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Insect digestive tract
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-Foregut= esophagus
--some have proventriculus -Midgut= stomach, expandable -Hindgut= colon --water is absorbed in colon Salivary glands can hold pathogens |
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Insect Endocrine System
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-Exists
-Important for reproduction and development |
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Insect respiratory system
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-Spiracles open directly to outside
-O2 is brought directly to the tissues |
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Insect reproductive system
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-Paired gonads
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Insect excretory system
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-Excretory products float around in the hemolymph of body cavity
-Concentrated in Nitrogen products |
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Insect CNS
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-Ganglia are concentrated in the head
-Ganglia also exist down the length of the body |
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Insect "fat body"
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Liver
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Simple metamorphosis
Heterometabolous |
-Form of insect development
-Sequential series in changes in form -Progeny are superficially similar to the adults -Progeny occupy the same environment as the parents -Feed off of same substrate in same feeding manner |
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Complete Metamorphosis
Holometabolous |
-Young look totally different from the adults
-Adult has sucking mouthparts -Larvae have chewing mouthparts -Adult lays eggs, usually in environment in feces or carrion -Eggs mature into larva --cast skin and grow through stages with molts -Larvae develop into pupae --quiescent non-feeding form -Pupae develop into adults |
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Acarine Development
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-Ticks and mites
-Life stages are punctuated by blood feedings on vertebrate hosts --MUST feed to grow -Larvae are 6-legged -Nymphs are 8-legged and sexually immature -Progeny resemble the adults -Shed skin and grow in each stage |
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Evolutionary trends leading to Vector competent arthropods
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1. Switch from chewing mouthparts to sucking mouthparts
--sucking mouth parts are more advanced, more evolved --mandible and maxilla have morphed into long piercing mouthparts 2. move from phytophagy (plant feeding) to hematophagy (blood feeding) |
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Integrated Pest Management
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-Eradication is not the goal
-Stress is on maintenance of populations below quantitative economic injury or pathogen transmission threshold -Systems approach involving multiple modalities -Can be physical or chemical barriers -Can involve environmental manipulation -Can involve chemical pesticides, but should be avoided |
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IPM methods
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1. Barriers: physical or chemical
--separate the host from the insect 2. Environmental manipulation --avoid manure or control manure --Manage wounds --Actively manage common sites for insect contamination 3. Chemical pesticides, used sparingly |
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IPM chemical pesticide geneology
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1st generation: botanicals and stomach poisons
2nd generation: neurotoxic chemicals, target neuromuscular function --synthetic organic compounds --Chlorinated hydrocarbons (DDT) --Organophosphates --N-phenylpyrazoles --Chloronicotinyls 3rd generation: target endocrine system and reproductive system --hormones and hormone analogs --metabolic inhibitors --pheromones |
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Tick Classification
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Phylum Arthropoda
Family Arachnida Genus Acarina 2 types: --argasidae: soft ticks --Ixodidae: hard ticks |
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Argasidae tick species
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-Soft ticks
-Argas -Otobius -Ornithodoros |
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Ixodidae tick species
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-hard ticks
-Dermacentor (American Dog Tick) -Rhipicephalus (brown tick) -Ixodes (deer tick) -Boophilus -Amblyomma |
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Ticks as agents of blood loss and tissue damage
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-Ticks are VERY successful pathogens
-Survive well -Have no natural predators -Account for SIGNIFICANT blood loss in hosts -Wound can be subject to secondary infection --flies can lay eggs in wound site (myiasis) |
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Tick Intoxication and Tick paralysis
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-When feeding, ticks salivate into the bite wound
-Salivations can induce paralysis --usually reversible --Respiratory paralysis causes big issues |
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Ticks as vectors of pathogenic agents
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-Lyme borreliosis
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Vector Capacity in Ticks
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-Persistent blood feeders
-Attach to host for long periods of time --5-7 days of engorgement -Wide host range and frequent contact with hosts -Longevity, have 2-3 year life cycle or longer --Ticks are a stable reservoir -Transovarial transmission --female reproductive tract is a sieve, easy transmission between generations -Host immune modulators, toxins are in the saliva |
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Tick Head layout
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-Capitulum: Entire head structures together
-Palp: sensory structure that helps tick move around on hair coat -Chelicerae: sawtooth-like cutting teeth at ends --do the work of piercing skin -Hypostome: Tongue-like with rows of teeth --holds and anchors tick to skin during piercing -Basis capituli: Base of the head |
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Tick Body Plan
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-4 pairs of jointed walking legs
-Spiracles as respiratory system --can be used to identify tick species -Genital pore and anal pore on ventral surface |
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Ixodid tick integument
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-Back is covered by hard shell/scutum
-Females have shorter shell -Male shell covers entire back |
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Argasid tick feeding habits
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-Feed rapidly
-Have short periods of attachment -Lair ectoparasites, sit in the lair of the host and wait, hide in the nest of the host -"hit and run" blood feeders -In periods of starvation, can go into hypobiosis and wait for years |
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Ixodid tick sexual dimorphism
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-Can easily tell the difference between males and females
-Male scutum covers entire dorsal aspect -Female scutum covers only half in non-engorged tick --short scutum allows female to completely engorge -Both sexes feed on blood |
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Ixodid tick feeding
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-Long feeding time
-Slow feeding and long periods of attachment -Take a long time to engorge on blood -Secrete glue-like substance that lets them stick onto host -Do not transfer from one host to another mid-meal, finish meals |
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Ixodid tick characteristics
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-Hard shell on back
-Can tell males from the females --clear sexual dimorphism --males have entire back covered by scutum --femeales have 1/2 of back covered by scutum -Capitulum extends anteriorly, visible from the dorsal aspect -Slow feeding with long periods of attachment -Relatively susceptible to starvation and dessication --need protective environment in harsh climates |
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Argasid TIck characteristics
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-Soft shell, pliable and leathery throughout
-Males and females look essentially the same -Capitulum is recessed ventrally, cannot really see from dorsal aspect -Feed quickly, "hit and run" feeders -Lair ectoparasites -Usually highly resistant to starvation and dessication --can go into hypobiosis --are very resistant to environmental factors -Life cycle contains multiple nymph stages and multiple host contacts |
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Tick Life Cycle
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-Life stages are punctuated by blood feedings
-Larvae are 6 legged, nymphs and adults are 8 legged -Nymphs are sexually immature adults -Soft tick cycles contain multiple nymph stages and multiple host contacts 1. Egg → Larva → Nymph → Adult |
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Tick 1-host life cycle
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Ex: Boophilus on cattle
1. eggs hatch, larva emerge in environment and climb onto host, feeding on blood 2. Engorged larvae molt, nymphs emerge and feed on blood 3. Engorged nymphs molt, adults emerge 4. Adults feed on blood and mate 5. Engorged female falls to the ground and lays eggs |
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Tick 2-host life cycle
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ex: Hyalomma
-Allows for spread of pathogens, transferred from one host to another -Individual tich parasitizes hosts of different species -Progression from small to large mammals, smaller stages of tick use smaller mammalian host 1. Eggs hatch in environment, larvae emerge and climb onto 1st host to feed on blood 2. Engorged larvae molt, nymphs emerge and feed on blood 3. Engorged nymphs drop to ground and molt, adults emerge 4. Adults climb onto 2nd host, feed on blood, and mate 5. Engorged female drops to the ground and lays eggs in grass |
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Tick 3-host life cycle
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Ex: Ixodes ricinus
-Progresses from smaller to larger vertebrate hosts and tick matures -"Pathogen transmitting machine" 1. Eggs hatch on ground, larva emerge and climb onto 1st host for bloodmeal 2. Engorged larva fall to the ground, molt, nymph emerges 3. Nymph climbs onto 2nd host for bloodmeal 4. Engorged nymph falls to the ground and molts, adult emerges 5. Adult climbs onto 3rd host for bloodmeal and mating 6. Engorged female falls to the ground and lays eggs |
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Argas persicus
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-Argasidae soft tick
-Fowl tick -Typical lair ectoparasite, parasite of nesting animals -Adults feed rapidly with short periods of attachment -"hit and run" feeders, get on, feed rapidly, then go hang out in lair -Can endure long periods of starvation, goes into hypobiosis --can be in hypobiosis for years! -Vector of Borrelia anserina -Feeds when bird is in the nest, with roosting birds feeds at night -Has multiple nymphal stages, all are blood-feeders --each stage progression requires a full blood meal |
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Otobius megnini
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-Argasidae soft tick
-Spinose ear tick -Has spines around the head that project off of the body -Only larvae and nymphs are parasitic -Nymphs remain attached for 120 days, 3 months of attachment -Parasitize a large range of domestic animals --dogs, cats, sheep, horses -Cause copious waxy exudate to come out of the ear -Atypical life history for a soft tick |
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Ornithodoros
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-Argasidae Soft tick
-All along west coast, mexico california oregon -Has a painful bite -Hones in on CO2 exhaled by animals -Feeds on host while they are sleeping or roosting -Pigs are an important vector for pathogens --transmit African Swine Fever |
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Lyme borreliosis
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-Emerging zoonosis
-Rapid rise in case reporting -high degree of public awareness -Also a high level of public ignorance and misinformation |
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Ixodes Scapularis
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-Ixodid hard tick
-Deer tick -Plain brown tick -Long mouthparts stick out in front --in nymph, mouthparts converge -Smaller than dermacentor variabilis, but size is unreliable due to engorgement capabilities -Has pre-anal groove as a defining feature |
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Ixodes Scapularis host relationships and pathogenesis
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-3-host tick, has to find many hosts to survive
-Pathogens are not transferred from mother to offspring, tick has to pick up pathogen in its own -Infection is maintained in the tick throughout its lifetime once infected -Pathogen enters tick when larva feeds on mouse -Larva feed on mice -Nymphs feed on birds, smammals -Adults and nymphs feed on dogs, deer, humans |
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Deer host for Ixodes Scapularis
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-Deer are main host
-"Cruise Ship" of ixodes scapularis --ticks feed, mate, and travel |
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Borrelia Burgdorferi
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-Spirochete agent of lyme disease
-Causes chronic illness -Initial dermatitis followed by joint disease, later possible cardiac and enephalitic complications -Diagnosed by Erythema chronicum migrans lesion --appears within 2 weeks of infection in 90% of cases --Circular red rash spreading concentrically from infective tick bite -Northeast seaboard, upper midwest, and PacNW are foci of high prevalence |
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Habitat for Ixodes scapularis
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-Habitat for rodent reservoir
-Woodland/meadow ecotone -"half light" areas -Ticks have negative geotaxis, climb up away from the ground -Sense the approach of host via receptors in legs |
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Ixodes Scapularis host affinities in different life stages
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1. Larvae are attracted to birds and smammals
2. Nymphs attracted to birds, smammals, dogs, horses, and humans 3. Adults attracted to dogs, horses, humans |
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Human granulocytic erlichiosis geographic distribution
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-Highest prevalence in NE and upper midwest
-Foci exists on the west coast |
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Amblyomma americanum
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-Ixodid hard tick
-"Lone star tick" -Common in southwest, gulf states, up to NY/NJ -has long mouth parts -Ornate tick, has markings on scutum --bright white patch on lower part of female scutum -Vector for Human monocytic erlichiosis |
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Human monocytic erlichiosis
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-Febrile illness with non-specific flu-like symptoms
-Caused by intracellular bacterium Erlichia chafeensis -Clinical illness is less severe, 5% mortality rate -transmitted by Amblyomma americanum -Highest incidence is in lower midwest, southwest, and mid-atlantic states --same distribution as Amblyomma americanum ticks |
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Amblyomma maculatum
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-Ixodid hard tick
-"Gulf Coast tick" -Ornate scutum with white markings |
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Dermacentor Variabilis
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-Ixodid hard tick
-"American Dog Tick" -Vector of Rickettsia rickettsi (rocky mountain spotted fever) and Erlichia chafeensis -Larva feeds off of voles and field mice -Nymph feeds off of rodents and rabbits -Adults feed off of dogs, humans, horses, or any medium/large sized animal -Woodland pathway or ecotone are typical habitats |
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Rickettsia rickettsii Transmission cycle
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1. Uninfected egg becomes an uninfected larva, feeds on an infected mouse or vole and becomes infected
2. Infected nymphs become infected adults 3. Infected adults transmit infection to eggs via transovarial transmission 4. Infected eggs become infected larvae, and cycle continues |
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Demacentor andersoni
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-Ixodid hard tick
-In western US -Transmits Colorado Tick Fever and Rocky Mountain Spotted Fever -Has rodent host -Has white markings on scutum |
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Rhipicephalus spp.
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-Ixodid Hard tick
-"Brown Dog Tick" -3-host tick -All hosts are dogs --tick drops off of hosts between blood meals -Crawls upwards on vertical substrates -Has a typically indoor habitat, esp. dogs in kennels or contained environments --Will infest households -Transmit erlichia and babesia in dogs |
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Rhipicephalus (Boophilus) microplus
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-Ixodid hard tick
-Cattle tick -Crawls upwards on substrates -1-host life cycle -Eggs land on the ground, larval stages climb up onto the cow -Larval, nymphal, and adult stages all stay on the same host -Transovarian transmission can occur |
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Borreliosis prevention
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1. Remove ticks within 24 hours
--will interrupt transmission 2. Regularly check animals and self for ticks 3. Remove tick by grabbing as close to the skin as possible and remove with gentle traction DO NOT: --grab tick by body --apply substances --burn |
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Diptera subsets
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1. Nematocera, "long-horned flies"
2. Brachycera, "short-horned flies" 3. Cyclorrhapa, "Muscoid flies" |
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Nematocera types
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-"Long horned Flies"
-Culicidae, mosquitos -Simuliidae, black flies -Ceratopogonidae, biting flies -Psychodidae, sand flies |
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Brachycera types
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-"Short-horned flies"
-Tabanidae, horse flies and deer flies |
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Cyclorrhapha types
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-"Muscoid flies"
-Muscidae, house flies -Calliphoridae, blow flies -Oestridae, bot flies -Hippoboscidae, louse flies and sheep keds |
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Diptera Characteristics
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-Antennae are long and segmented
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Mosquitos
Culicidae |
-Nematocera, Culicidae
-Tiny, delicate fly -Wings are covered in scales -Has piercing/sucking mouthparts -Larvae are filter feeders, live in still, fresh water -Pupal stages hatch into adults and lave the water -Females require a bloodmeal for egg development -Transmit arboviruses (EEE, WNV) |
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Mosquitoes as Vectors
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-Transmit malaria parasites, Plasmodium
-Vectors of microfilariae, Dirofilaria immitis (heartworm) |
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Black flies
Simuliidae |
-Nematocera, simuliidae
-Longhorn fly -Tiny little flies -Immature stages grow in fast-moving water and streams -Larvae cling onto substrates around the brook or stream -Pupae emerge from cocoon -Short piercing mouthparts allow ingestion of tissue with microfilariae -only females take blood --need blood to stimulate ovarian cycle |
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Onchocerciasis
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--Microfilariae in tissues are ingested by fly when it takes a bloodmeal
-Causes river blindness, major cause of blindness in endemic areas --tropics and subsaharan africa |
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Leukocytozoon smithii
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-Parasite of domestic birds
-Transmitted by black flies (Simuliidae) -Invades blood cells of birds |
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No-see-um's
Ceratopogonidae |
-Nematocera, Ceratopogonidae
-Wings have dappled pattern -Can develop in aquatic or terrestrial sites -Best in semi-liquid environment like wet mud and areas with a lot of organic matter -Mouthparts are short --cause pool of blood to form, lap up blood from pool |
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Onchocerca cervicalis
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-Parasite transmitted by ceratopogonid flies (no-see-ums)
-Microfilariae cause itching dermatitis on ventral midline -Flies feed on ventral area, exacerbate dermatitis and ingest MF to spread to another horse |
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Psychodidae
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-Nematocera
-Phlebotomine sand fly -Vector of leishmania -Completely terrestrial development in areas rich in organic matter -Female takes blood meal and takes in protozoa for leishmania pathogens -Acts as intermediate host AND vector |
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Canine Leishmaniasis in USA
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-Historically limited to dogs with a history of travel to Mediterranean or middle east
-More cases have been detected in foxhound kennels |
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Brachycera
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-Horse flies and deer flies
-Bog, robust, blood-feeding fly |
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Chrysops sp.
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-Brachycera Horse fly and Deer fly
-"Green head" -Irritating, painful bites -Large blood-feeding fly -All life stages are terrestrial -"Edward scissorhands" mouthparts --scissoring/cutting mouthparts lacerate skin of host --Sponge laps up pool of blood |
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Brachycera Horse Fly Mouthparts
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-Scissor-like
-Have sponging labellum to lap up pool of blood -Interrupted feeding -All promote mehanical transmission of pathogens -Introduces pathogens from one host to the next -Immediate transmission between hosts -No development occurs in the fly, not enough time -Pathogens transmitted: --EIA, protozoan parasites, anthrax |
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Cyclorrhapha
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-Muscoid flies
-"House flies" -Club-like structure to mouth parts with a feather --Feather is packed with sensors -Undergo complete metamorphosis -Egg → larvae → pupae → adult -Eggs are oviposited in feces or other decaying organic material -"Maggot" larvae -Pupae are in hardened case (Puparium) |
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Blood sucking muscoid flies
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-Glossina ("tse-tse")
-Stomoxys ("Stable fly") -Hematobia irritans ("Horn flies") |
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Glossina
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-Cyclorrhapha muscoid fly
-Blood-sucking muscoid fly -Tse-tse fly -Vector of African trypanosomiasis, sleeping sickness |
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Stomoxys
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-Cyclorrhapha
-Blood-sucking muscoid fly -"Stable fly" -Looks a lot like a house fly -Has piercing/sucking tube for bloodmeal --also has a grinding structure to create a pool of blood -Larval breeding ground in decaying/contaminated plant material -Can control fly incidence with proper manure management -Not known as a vector for any pathogens, just pests --May have an economic cost |
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Hematobia irritans
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-Cyclorrhapha
-Horn fly of cattle, cluster around the base of horns -Feed in large numbers -interrupt normal cattle feeding patterns -Account for economic losses in agriculture |
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Non-blood sucking muscoid flies
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-House flies
-Musca autumnalis ("face fly") |
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House Fly
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-Cyclorrhapha muscoid fly
-Non-blood sucking muscoid fly -Develop in accumulations of manure -Can be a total pain in the butt -Mouthparts only have sponging labellum, no piercing stylets --Sponge up liquid material |
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Musca autumnalis
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-Cyclorrhapha
-Non-biting muscoid fly -"Face fly" -Very bothersome fly, congregates around nose and eye conjunctiva -Vector of Boraxella bovis (bovine pink eye) |
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Melophagus ovinus
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-Cyclorrhapha, hippoboscidae
-"Sheep ked" -Fly that does not have wings! -Has adapted to spend entire lifecycle in the fleece of sheep -Adults are blood feeders -Very irritating to the sheep -Causes decreased productivity, decreased weight gain |
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Melophagus ovinus life cycle
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1. Eggs hatch into larvae inside female fly
-maintain relatively few larvae 2. larvae is extruded from the female and glued to wool 3. Pupa forms within a few hours 4. Adult emerges from the pupa, adult flies copulate -Adults are blood feeders |
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Lipotena cervi
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-Cyclorrhapha
-Louse fly -Briefly has wings |
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Myiasis
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-Infestation of organs and tissues of vertebrates by larval Diptera
-Larvae are endoparasites, live within the host |
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Gasterophilus sp.
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-Equine bot fly
-Obligate enteric myiasis -Causes Myiasis, lives in the stomach of horses -Adults have black/orange hair -Mimic bees |
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Cyclorrhapha types
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-Muscidae: house and stable flies
-Calliphoridae: blow flies -Oestridae: bot flies -Hippoboscidae: louse flies and sheep keds |
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Categories of Myiasis
|
1. Facultative: fly larvae can be free-living OR in living tissue
-larvae are usually found in free-living situations on decaying organic material 2. Obligatory: fly larvae are always in the host -Larvae are incapable of developing outside of a living host |
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Mode of Myiasis invasion
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1. enteric (bot fly larvae)
2. Urogenital 3. Traumatic (invade pre-existing wounds) 4. Cutaneous (invade healthy skin) 5. Nasopahryngeal |
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Facultative myiasis
|
-Calliphoridiae (blow fly) and Sarcophagidae (flesh fly) families
-Cause facultative enteric myiasis --larvae must be in the gut of the host -Ex: Dogs eat gross stuff with eggs or larvae in it --larvae hatch in gut, can exist for a while in gut --Dog passes larvae in feces |
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Phaenicia serricata
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-Cyclorrhapha, Calliphoridae
-Facultative cutaneous myiasis -"Bottle Fly," Mettalic green -Cause "fly strike" -Can parasitize tissue of dogs and sheep --big deal for sheep, can cause economic losses -Larvae are normally free-living -Eggs are laid in carrion or feces, sometimes in fecal material on dog's hair coat --Hair coat mimics the ideal laying ground --larvae start to eat feces on hair AND skin underneath the feces and hair |
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Phormia regina
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-Agent of fly strike in sheep
-Flies are not obligate parasites, can do just as well out in environment -Eggs are laid in wool of sheep, esp. in soiled area around the anus --can also be laid in wounds, on carrion, or on feces -Larvae feed on debris and wool, then drop to the ground and pupate -Pupae form in loose soil, emerge as adults -Adults feed on food, garbage, or feces -Tx: shave the area and give ivermectin |
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Gasterophilus life cycle
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1. Eggs are oviposited in grass and around the mouth of the horse
--eggs containing L1 are cemented to hairs of horses 2. Larvae hatch and get into the horse's mouth or larvae hatch in stomach -migrate through mucosa to stomach 3. L2 and L3 are in stomach of the horse, L3 attach to the mucosa of the stomach and the intestines 4. Larvae let go and are passed out in feces 5. Pupae are in the soil, develop into adults and mate -Entire cycle requires a full year -Migration occurs in the fall -Seasonality is important for treatment --can treat with strongyles |
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Gasterophilus ulcers
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-produced by migrating L1 and L2 from external areas to the stomach
-Can be seen on mucosa of mouth and tongue -Larvae can form peridontal ulcers between teeth |
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Gasterophilus mature larvae in equine stomach
|
-attach to mucosa of stomach and mature into pupae
-Maturation takes place over winter, takes a full year -Can give broad-spectrum anthelmintics in the fall to control for strongyles AND gasterophilus |
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Gasterophilus pathology
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-Obstructions
-Mounds to gastric mucosa --can cause erosions and ulcers -Large bowel irritation with larvae passing in feces |
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Cochliomyia hominivorax
|
-Primary screw worm fly
-Females are monogamous, only mate once --can save sperm in reproductive tract -Oviposit eggs in open wounds -Eggs hatch out o wound, give rise to hundreds of larvae that feed on flesh -Larvae eat tissue, tear and lacerate -Can destroy tissue -Have to control infestation by controlling wounds and hazards --avoid wounds, avoid infestation |
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Cochliomyia hominivorax Control
|
-Best control is to keep wounds clean and avoid hazards
-Insecticide isn't practical -Have mass-reared pupae for sterile male release --Sterile males out-competed normal males --Non-insecticidal, reproductive strategy for fly control -Very effective control! reduced infective areas to just southern texas |
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Obligatory cutaneous myiasis
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-Pre-existing wound is not required for infestation
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Hypoderma bovis
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-Adult female warble fly
-Obligate cutaneous myiasis -Adult has bee-like appearance -"Heel flies" or "Gad flies" -Mature larvae are BIG, barrel-shaped things -Female oviposits on hairs, eggs are stuck onto hair shafts --most often on hocks or heels of cow --Oviposition is a quick hit and run type of deposition -Cows have "gadding behavior" to avoid flies |
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Hypoderma bovis life cycle
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1. Eggs are laid on hairs on hocks or heels of cattle
2. Larvae hatch out of eggs and penetrate into skin of host --form "warble" in skin --In summer, larvae pop outof warble and drop to ground 3. Larvae migrate directly straight up through cow abdominal viscera --migrate dorsally |
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Hypoderma bovis Warbles
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-Warbles leave wounds for infection or screw worm fly infestation
-Results in economic losses --decreases hide value --decreases normal grazing behavior while cows are trying to get away from the flies, results in decrease in milk and meat production -Wounds are in tissue under the skin along dorsal midline -treat with broad-spectrum approach |
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Cuterebra sp.
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-Causes obligate cutaneous myiasis in small mammals
-flies lay eggs around entrances to rodent/rabbit burrows -Larvae form warbles, can be proportionally HUGE compared to the mouse or cat or rabbit |
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Oestrus ovis
|
-Nasopharyngeal myiasis
-Nasal bot of sheep -Very pathogenic and uncomfortable for the sheep -Early migrating stages are susceptible to treatment |
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Oestrus ovis life cycle
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1. Larvae are deposited in or around sheep nostrils
2. Larvae crawl up nasal passages to nasal and frontal sinuses where immature larvae attach to mucus membranes 3. Larvae grow for 8-10 months in the host, then migrate down nasal passages and are sneezed out 4. Pupae form in loose soil 5. Adults emerge from pupae and copulate but do not feed |
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Fleas
|
-Ectoparasites of companion animals
-hexapoda: Siphonaptera -Small, wingless ectoparasites -Laterally compressed, adapted for moving in haircoat -Tall, skinny, and flat -Legs modified for jumping, have lots of muscle --jump from environment onto host -Males and females suck blood |
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Flea external morphology
|
-Incredibly distinctive morphology
-Terminal segments have features that can be used for taxonomy -Foregut/midgut junction has inward pointing spines --spines can be clogged with RBCs and RBC products, contributes to contamination |
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Flea life history
|
-21 days cycle with continual host
-Can arrest in pupal stage for months waiting for an appropriate host -Eggs are laid on host -Females constantly lay eggs on the host -Eggs fall off, develop into larvae off of the host --eggs need cooler ambient temps to develop --must fall into the environment -Eggs are not sticky, just fall off -heavily infested host is showering environment with eggs all of the time -Eggs falling off of host makes control difficult -Egg → larva → pupa → adult -Eggs hatch and larvae develop in the environment |
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Flea Larvae
|
-hatch from flea eggs in the environment
-Feed on organic matter -Eat adult fecal pellets in environment --"flea dirt" |
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Flea pupae
|
-Enclosed in silken cocoon
-Exist in environment -Flea is fully-formed (Pharate) within the pupal case --ready to erupt can cause damage -Can remain quiescent for months in pupal cocoon --without viable host, will remain viable in the pupal stage for months |
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Flea Adult
|
-Jumps out of the cocoon when ready and onto host
-Not host-specific, will much on whatever it can -Most species move freely about in the host hair coat, very mobile adults |
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Siphonaptera Types
|
1. Loose host association, adults move around freely between hosts
--Ctenocephalides --Xenopsylla --Pulex 2. Long-term attachment --Echidnophaga 3. Skin penetration, forms sub-dermal pocket --Tunga |
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Flea transmission
|
-Major route of transmission is from an infested environment to the host
-Once on the host, adult fleas do not really leave -Main route of transmission is through the environment |
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Echidnophaga gallinacea
|
-"Stick tight" flea
-Affects poultry (chickens and turkeys) -Flattened head, flat nose -Attaches to the skin of birds, mostly around the face -Long-term attachment -Forms dermal ulcers in the host |
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Tunga penetrans
|
-"Chigoe flea"
-Penetrates skin and forms sub-dermal pocket |
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Ctenocephalides felis
|
-"Cat flea"
-has facial combs and prodronal combs |
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Ctenocephalides canis
|
-"Dog flea"
-Disappearing species of flea! -Ctenocephalides felis is taking over |
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Flea allergy dermatitis
|
-Chronic dermatosis
-Induced by hypoallergic response to flea saliva --animal is allergic to flea saliva -Big concern with flea infestations -Usually in hindquarters and under belly of the animal |
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Ctenocephalides felis and canis as intermediate hosts
|
-Intermediate hosts for Dipylidium caninum (double-pored tapeworm)
-Egg packets are ingested in the larval stage -Cystercercoids of tape worms mature at same time as flea reaches adult stage -Infected fleas are ingested during grooming, cystercercoids are also ingested and hatch in definitive host intestine |
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Xenopsylla cheopis
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-Oriental Rat flea
-Vector for plague and murine typhus -transfers diseases from rats to humans --since flea is non-specific for hosts, easily transmits diseases between hosts -Have caused numerous outbreaks of plague |
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Yersenia pestis in fleas
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-Oriental rat flea acts as vector
-Yersinia organisms from infected host get clogged in the spines in the digestive tract of the flea -Flea regurgitates Yersinia organisms into bite wounds of next host |
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Cycles and pathways of plague transfer
|
-Fleas transmit plague to ground squirrels and prairie dogs
-Wide host preferences allows fleas to jump from rodents to humans -Bubonic plague exists in SW USA |
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Flea Control
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1. Treat and prevent infestation on the host
--Main priority 2. Break life cycle in the environment 3. Control immune response to flea salivary antigens --Immunize hosts to flea feeding, prevent scratching |
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21 day timeframe for flea life cycle
|
-Critical 21 day cycle!
-treatment that lasts only a few days will not work -Residual activity in hair coat needs to last more than 21 days |
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Pthiraptera
Lice |
-Wingless
-Dorsoventrally flattened ectoparasites --"squashed flat" -legs are modified for grasping hairs --tarsal claws grasp hairs -Paste eggs (nits) onto host hairs, eggs stick onto hair -Vestigial eyes and no wings |
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Lice tarsal claws
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-Modified for grasping hair
-Big lobster claws -Adapted for grasping -Hold onto hosts -Works like a thumb and forefinger |
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Pthiraptera family tree
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-Anoplura (sucking lice)
-Mallophaga (chewing lice) --Ischnocera --Amblycera |
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Anoplura lice types
|
-Sucking lice
-Haematopinus -Linognathus -Solenopotes -Pediculus -Pthirus |
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Mallophaga lice types
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-Chewing lice, have opposing mandibles
-Ischnocera --Damalinia --Felicola --Trichodectes -Amblycera --Menopon --Menacanthus |
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Anoplura Lice
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-Blood sucking lice
-Stylet retracts back into head when not feeding -Head is narrower than thorax |
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Mallophaga lice
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-Chewing lice, biting lice
-Big chewing teeth -head is wider than thorax -Antennae may be recessed on head |
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Lice life cycle
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-Simple metamorphosis, adults and nymphs look alike
-All life stages occur on the host -VERY host specific -Need constant temperature that host provides, cannot survive off of host for very long -Life cycle is constant, produces 1 generation every 21 days -Potential for explosive population growth on the host exists! -Primary transmission is host-host contact -Egg → 1st nymph → 2nd nymph → 3rd nymph → adults |
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Lice population growth
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-Potential for EXPLOSIVE population growth on the host
--all life cycle stages take place on the host! --Lice seldom leave the host -In a 6 month timeframe, can boom from 2 lice to over 23 million |
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Lice transmission
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-Direct host-host contact
-Lice rarely leave the host |
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Lice host specificity
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-VERY host specific
-Physiologically not adapted for multiple hosts |
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Lice on Cattle
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-3 species infest cattle
-Chewing and sucking lice -Cause pediculosis |
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Pediculosis
|
-Chronic louse infestation in a cow
-Hair coat is damaged -Not gaining weight -Anemic |
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Haematopinus
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-Louse
-Important parasite of cattle and swine |
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Pthirus pubis
|
-Human crab louse
-Sucking lice -Not associated with pathogens -Very uncomfortable -Transmitted via direct host-host contact |
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Pediculus humanus
|
-Sucking louse
-Transmits diseases --Epidemic Typhus --Trench fever --Relapsing fever -Causes dermatitis or pediculosis in cattle -Infests entire body -Can live on clothes -Prevalent during high-stress periods of time when people are living very close to each other --war, famine, upheaval, relocation |
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Menopon gallinae
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-Chewing louse
-Feather shaft louse -Affects chickens, damages feather shafts -Antennae are recessed |
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Damalinia bovis
|
-Chewing louse of cattle
-Antennae stick up |
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Trichodectes canis
|
-Chewing louse of dogs
-Acts as intermediate host for Dipylidium caninum --dogs eat lice with dipylidium oncospheres |
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Lice control
|
-Flea control will kill all lice infestations
-Occurrence has plummeted due to current flea products -Lice still exist, but are pretty easy to control |
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Mites
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-Phylum arthropoda, Order Acarina
-200 families of mites -Relatively few mite species are medically significant -Many could be construed as "beneficial" -Ecologically diverse --aquatic to terrestrial to parasitic niches -natural parasites of invertebrates -Range of feeding habits from phytophagy to blood or tissue --all feed on some type of cellular fluid from an organism -Scavengers, break down plant material and carrion -Control populations of mosquitoes and biting flies |
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Medical importance of mites
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-Can cause loss of blood or other tissue fluid (poultry mites)
-dermatitis and tissue damage (mange) -Allergic responses (house dust mite allergen) -Transmission of pathogens as vectors or intermediate hosts |
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Arachnida body segmentation
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-Loss of overt body segmentation
-Scorpions are most ancestral, have clear body segmentation -Highly specialized mites and ticks have lost all evidence of segmentation --Body is basically a sac-like globe with feeding parts |
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Mite generalized external morphology
|
-Features are similar to ticks
-Sac-like body -Anterior portion has feeding apparatus --capitulum, lateral palpae, chelicerae -Plates on underside have taxonomic significance -Terminal segment of leg (pretarsus) gives species |
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Mite pretarsus
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-Last segment of the mite leg
-Important for taxonomic identification --varies in form -Can be a long stalk, claw, suction cup -Used to grasp on to skin or hair coat of hsot |
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Mite types
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-Burrowing vs non-burrowing
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Burrowing mites
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-Sarcoptes
-Notoedres -Knemidokoptes -Demodex |
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Non-burrowing mites
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-Psoroptes
-Otodectes -Dermanyssus -Ornithonussys -Chyletiella -Trombicula |
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Sarcoptidae mite
|
-Burrowing mite
-Agent of mange or scabies -Globular body shape, very round -Short, stubby legs -Legs II and III are widely separated on the body, not close to each other -Long, stalked pretarsi have terminal suckers -Females burrow into epithelium and lay eggs --Burrowing causes sarcoptic mange/scabies and itching dermatitis -Obligate parasite in skin of the host -not able to survive for long periods off of the host --susceptible to dessication and temp. fluctuations -Transmitted via host-host contact |
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Sarcoptidae life cycle
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1. Eggs are deposited in skin as they burrow and tunnel in skin
2. Eggs hatch and release larvae 3. Larvae molt into nymphs in molting pouches in skin 4. Mating occurs after male penetrates molting pouch of adult female |
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Sarcoptes variants
|
-Variants are based on host species
-Variants can reproduce and make fertile offspring -Different varieties cannot establish well on different hosts --can cause transient, self-limiting dermatitis --Cannot set up multi-generational established infection on host -Dog sarcoptic mange will not cause an outbreak of scabies in humans |
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Sarcoptic Mange
|
-Sarcoptes var. canis
-Important dermatosis in dogs -Don't see lesions on the trunk, concentrated on the extremities -Distribution gives clue that it is sarcoptes -Itchy, puritic lesions -Confirm Dx with skin scraping, will see active mites |
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Sarcoptes var suis
|
-Sarcoptic mites on pigs
-Cause really terrible dermatitis -Lesions are red, itchy, and encrusted with scabs due to serous exudate drying on surface of the lesion -Starts on face and ears and moves backwards |
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Sarcoptes scabei transmissibility
|
-Different variants are not really transmissible
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Notoedres cati
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-Burrowing mite
-Sarcoptes scabei in cats and rodents -Looks a lot like Sarcoptes, anus is positioned differently -Can cause similar mange in cats and smammals |
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Knemidokoptes mutans
|
-Burrowing mite
-Agent of "scaly leg" in poultry -Has exeptionally short, stubby legs -Lives in skin under scales of birds -Results in edema, inflammation, and swelling in sin under scales --causes scales to stick up -Important ectoparasite in birds |
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Demodex folliculorum
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-Burrowing Mite in Demodicidae family
-Human follicle mite |
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Demodicidae family of mites
|
-Every mammalian species has own version of demodex
-Common in all animals -Part of normal skin microbiota of any normal mammal, harmless commensal --healthy skin has demodex -Route of transmission is not related to where mites came from, is related to underlying immunosuppression that allowed outbreak to occur |
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Demodex canis
|
-Burrowing mite of dogs
-Commensal in healthy dogs -Agent of mange in immunocompromised individuals --Immunosuppression can lead to increased numbers of burrowing mites |
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Consequences of Demodex canis infestation
|
-Can be commensal relationship in host with normal immune system
-Can be localized: small lesions on face or forepaws --usually resolves spontaneously -Can be generalized: lesions spreading over entire body --poor prognosis if left untreated |
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Genrealized Demodicosis
|
-Demodex all over body
-Generally a result of underlying immunnosuppression --allows mite populations to grow uncontrolled -Lesions spread from small foci to cover entire body --usually start on extremities and spread to trunk -Can get secondary bacterial infection or pyoderma -May be fatal |
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Demodex bovis
|
-Demodex in large animals
-Cows, goats, sheep -Nodular swelling under the skin |
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Dermanyssidae
|
-Non-burrowing mites
-Spider-like or tick-like in appearance -Legs radiate out from body -Classic lair ectoparasites --live down in next between blood feedings --feed on host at night, while animals are roosting -Parasites of birds and nesting mammals -Transmit from nest to bird, not really from bird to bird --source of infestation is infested environment -Can live for long time in nest without a host |
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Dermanyssus gallinae
|
-Non-burrowing mite
-Chicken mite -Feed at night -Can actually exsanguinate nestling chicks -Can be annoying, but can also be extremely dangerous |
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Ornithonyssus sylviarum
|
-Northern fowl mite
-Biologically similar to Dermanyssus, nesting mite -Can live for months without a host -Infested environment is source of infestation for naive birds -Can be moved around by birds, transmit infestations --wild passeriform birds -Will bite humans! give nasty itching bite |
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Pneumonyssoides caninum
|
-Non-burrowing mite
-Tracheal mite of dogs -Lives in nasal passages and trachea -Causes chronic sniffing, coughing, and nose-bleeds |
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Psoroptidae family of mites
|
-Non-burrowing mites
-Issue with livestock |
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Chorioptes bovis
|
-In Psoroptidae fammily
-Agent of hock mange in cattle and horses -Feed on surface of the skin -Inject proteolytic enzyme to cause liquefaction necrosis in skin -Can only ingest fluids, have to inject proteolytic enzyme to liquefy tissues |
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Psoroptes ovis
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-Non-burrowing mite
-Causes sheep scabs, wool hangs off in mats or tags -Causes itchy, puritic lesions, damages skin surface --Will have serous exudate from lesions -Lesions are primarily on the trunk where fleece is thick |
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Otodectes cynotis
|
-Psoroptidae mite, non-burrowing mite
-Common ectoparasite in dogs and cats -Ear mite -Extremely irritating in heavy infestations -Animal will have dark-brown exudate from skin -Feeds on the surface of the skin, causes serous exudate -Can move out of the ear onto general hair coat -Tx: macrolide endectocides --ivermectin, milbomycin |
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Chyletiella mite
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-Non-burrowing mite
-Common ectoparasite on cats and caged rabbits, and smammals --can be an issue in lab animals -Lair ectoparasite -Feeds intermittently on host, lives in nesting material -Stout spines on palpae -Pretarsus is a little comb |
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Trombiculidae family of mites
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-Non-burrowing mites
-"Chiggers" -Itchy, red wheal on skin -Cause liquefactive necrosis of skin, suck up tissue, and immediately drop off -Free-living life cycle -Only larval stage is parasitic (can see 6 legs), nymph and adult stages (8 legs) are free-living |
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Neotrombicula whartoni
|
-larval trombiculid
-Non-burrowing mite -Orange-red in color -Common ectoparasite of cats -Cause itchy, papular lesion |
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Chemical control of mites
|
1. Sarcoptidae and Psoroptidae:
--Avermectins --Milbemycins 2. Demodicidae: --Amitraz, Mitaban --Will also respond to macrocyclic lactones (ivermectin) 3.Chyletidae and Dermanyssidae: --Organophosphates --Carbamates |
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Protozoa
|
-Unicellular animals
-contain 1 more more nuclei -Covered by unit membrane that is usually modified to provide structure or rigidity -Pellicle: membrane and underlying structures (microtubules) -Glycocalyx: secreted layer covering membrane --glycoprotein or mucopolysacccharide |
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Protozoa taxonomy
|
-Sarcomastigophora
-Apicomplexa -Ciliophora |
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Protozoal reproduction
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1. Binary fission, splits nucleus and cytoplasm to form 2 progeny
2. Schizogony (multiple fission), nucleus divides multiple times before cytoplasmic division --forms many progeny 3. Endodyogeny, internal budding --new daughter cells are formed within mother cell |
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Binary fission
|
-Form of asexual reproduction
-Used by many protozoan species -Chromosome attaches to plasma membrane and is replicated by an enzyme --both chromosomes are attached to membrane -Chromosomes move apart, membrane grows inwards, and cells separate |
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Schizogony
|
-Multiple fission
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Tritrichomonas foetus
|
-Protozoa → sarcomastigophora → mastigophora
-Venereal disease of cattle -3 anterior Flagella is attached to body wall -1 anterior flagella, associated with undulating membrane -basal body gives rise to flagella -Axostyle provides structural support -20-30 micrometers long -Transmitted via sexual interactions, natural breeding -Trophozoites hang out in vagina and uterus of cow, preputial cavity of the bull --reside on mucosal surface -Mostly occur in beef-growing regions of the US |
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Tritrichomonas transmission
|
-Sex (natural breeding)
-Protozoa lives in folds of the penis and sheath, in perpuce -Older bull has deeper crypts in prepuce, provides site for trichomonas replication -One infected bull can infect 80-90% of partners -Can survive process for freezing semen --samples should be tested before AI -Dx involved culture of vaginal or preputial washes and ID of trophozoites |
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Bovine trichomoniases
|
-First observed as increased in open cows
-Following initial herd exposure, may see up to 50% decreased in pregnant animals -Under chronic conditions, may see smaller increase in open cows (10-15%) -Signs of vaginitis or pyometra are less common -No clinical signs in bull |
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Clinical outcomes of Tritrichomonas foetus infections in cattle
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-Infertilty or early embryonic death (60%)
-Abortion after 70 days (5%) -Pyometra (5%) -Infected with no disease (20%) -Not infected (10%) Histologically will have marked lymphocytic infiltrate and thickened epithelium |
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Tritrichomonas pathogenesis
|
-Disease mechanism is unclear
-trophozoites can bind to vaginal epithelial cells in vitro, will lyse cells -Infection in reproductive tract induces inflammation associated with vaginitis, endometritis -Inflammation of uterine tissue or placenta may induce abortion -Developing fetus dies early in pregnancy -Parasites may invade placenta or fetal tissue --not a major cause of disease |
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Tritrichomonas infection in the cow
|
-Cow is infected during breeding
-May show subtle mild vaginal discharge -Pyometra may develop 1-3 weeks pst-infection -Protozoa attach to the lining of the reproductive tract --induces inflammatory response that results in death of embryo -Inflammation in reproductive tract |
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Tritrichomonas infection resolution in cows
|
-Cows are good at getting rid of infections, resolve infection
-Infected cows normally eliminate infection within 3-4 months --parasites may persist in some cows for over 18 months -Elimination of infection leads to a degree of protection against re-infection --immunity decreases after 1 year -Infection does not cause permanent damage to the reproductive tract -Most cows can conceive normally during the next breeding season |
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Tritrichomonas infection of Bulls
|
-Bulls are chronically infected
-Younger bulls are much more resistant to infections --no deep preputial crypts to let parasites survive -Older bulls remain infected throughout lifetime -Constant source of transmission to susceptible cows |
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Tritrichomonas Treatment
|
-Cows naturally resolve infection, are not normally treated
-Bulls are difficult to treat -Acriflavine ointment solution for bulls younger than 4, less effective in older animals -Unless bull is valuable, treatment does not usually happen --Culling is "treatment" |
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Tritrichomoniasis control
|
1. Breed virgin bulls to virgin cows
-avoid intial infection 2. Use AI with uninfected bulls 3. Test and remove infected bulls from herd 4. Cull open cows 5. Use bulls younger than 4 for natural breedings 6. Vaccinate |
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Bovine trichomoniasis vaccine
|
-Trich guard: available as a monovalent vaccine or polyvalent vaccine
--will also vaccinate for leptospira and Campylobacter -Induces immune response -Vaccinated cows are protected against the disease but may still become infected -Provides reasonable prevention to infection -Vaccine has no effect on bulls |
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Trichomomads
|
-Common commensals of the GI tract of large animals
-Sets up in large intestine, colon, and cecum --sit in intestinal crypt, sometimes in lamina propria tissue -Occasionally noted in fecals from dogs -Occur and commensals in mouths of humans and small animals -Pathogenesis is generally limited to trichomonas foetus in cattle, trichomonas vaginalis in humans, trichomonas gallinae in birds |
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Tritrichomoniasis in Cats
|
-Causes severe diarrhea in young cats (first reported in NC)
-Parasite is morphologically identical and genetically similar to T. foetus -Can treat with Flagyl (metronidazole), fenbendazole --other drugs can improve symptoms but will not eliminate infection |
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Tritrichonomas foetus in cats
|
-31% of cats are positive internationally
-10% of cats in US -Usually occurs in young cats from breeders -Disease is associated with protracted diarrhea, can last up to a year -Affects distal ileum and colon, sometimes cecum -Diarrhea characterized by semi-formed feces --Can be severe --blood and mucus are sometimes observed -Most cases are associated with breeding facilities and catteries or homes with multiple cats |
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Tritrichmonas foetus transmission in cats
|
-Trichomonas stages can't survive long in external environment
--no long-term resistance -transmission is usually fecal-oral and requires close or direct contact between cats -Infections are almost always associated with cat colonies or houses with multiple cats -No evidence for transmission from other animals --pigs or cattle |
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Trichomoniasis in cats clinical signs
|
-Normal appearance
-Affects distal small intestine and proximal large intestine -Diarrhea of the large bowel -Semi-formed, stinky feces with fresh blood and mucus -Dribbling feces is common -Anus is red, swollen, painful -Apart from diarrhea, cats are generally healthy |
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Trichomoniasis prognosis in cats
|
-Most cats will eventually recover
-Average duration of clinical infection is 9 months -Cats that resolve disease may still shed parasites in feces for several months or longer |
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Trichomonad Diagnosis
|
-Common commensal organism that also causes disease
-May be seen in normal direct fecal smear -Dx usually involves culture of parasites -Direct smear is 15% effective -Cultures are 55% effective -PCR is 95% effective, HIGHLY effective |
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Trichomoniasis treatment in Cats
|
-Ronidazole 2x daily for 2 weeks can cure cats
--may also cause reversible neurological toxicity |
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Giardia
|
-Protozoa → Sarcomastigophora → mastigophora → Giardia
-Parasite of small intestine -Flagellated parasite -2 nuclei -Many flagella -Cyst provides resiliency in external environment -Cyst in fecal float is diagnostic stage |
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Giardia life cycle
|
1. Cysts and trophozoites expelled in feces, only cysts can survive outside of the host
--can survive for weeks to months in cold water 2. Dormant cysts are ingested by host 3. Excystation, trophozoites emerge to an active state and undergo asexual reproduction within intestine 4. Encystation occurs during transit towards colon |
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Giardia trophozoites
|
-Teardrop shape
-2 nuclei -Multiple flagella -2 adhesive discs -Axostyle -Sits on surface of villi in intestinal tract |
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Giardia cysts
|
-Trophozoites secrete a cyst wall consisting of multiple glycoprotein layers
-Cyst can survive for months in the environment, exact survival time is unknown -Cyst is very susceptible to drying, chlorine, ammonia compounds, boiling, and freezing --needs to stay moist to stay viable -Killed by most household disinfectants -Very small compared to ascarid egg |
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Giardia species
|
-Giardia duodenalis:
--Giardia lamblia and Giardia intestinalis --in humans, dogs, cats, cattle, and other mammals -Giardia agilis: amphibians -Giardia muris: rodents -Giardia psittaci: birds |
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Giardiasis and young animals
|
-Giardiasis is a disease of young animals, mostly in puppies and kittens
-Associated with diarrhea, may be sufficiently severe to cause weight loss or decreased weight gain -Young animals are also susceptible to re-infection -Infection can persist for many months -Older animals may be asymptomatic carriers -Resistance is associated with production of anti-Giardia IgA antibodies --individuals with IgA deficiencies appear to be more susceptible to giardiasis |
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Giardiasis in domestic animals
|
-in cows in NY:
--20% of cows younger than 6 months --3.5% in cows 6-24 months -0.2% infection in cows older than 24 months -15-30% of foals in ohio were infected -29% of cattle in Canada -38% of sheep in canada -9% of swine in Canada |
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Giardiasis and Disease
|
-Giardia is NOT an invasive parasite!
-Lives on surface of intestinal villi -Causes diarrhea without blood -Does not cause tissue damage --some other concurrent infection can -Wight loss accompanies severe infections, esp. in young animals |
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Giardiasis Disease mechanisms and Pathogenesis
|
-Trophozoites cover surface of microvilli, adhere to villi
-Mechanically damages epithelial cells --decreased enzyme activity leading to malabsorption -Causes malabsorption of glucose, Na, water, and reduced disaccharidase activity -May lead to secretion of electrolytes and fluid accumulation in intestinal lumen -Can induce enterocyte apoptosis, linked to altered gut formation -Immune response may alter gut pathology --villus blunting |
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Giardiasis as a Zoonosis
|
-Humans are usually infected with A and B assemblages
-Other animals can also be infected by A and B -Dogs are usually infected with C/D assemblage parasites, have also been found with A and B -Cats generally have assemblage F, can also have A and B -Giardia is a potentially zoonotic infection |
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Genotypes of Giardia duodenalis found in mammals
|
-Assemblage A: humans, livestock, deer, cats, dogs, ferrets, beavers, muskrats, voles, guinea pigs
-Assemblage B: Humans, livestock, chinchillas, dogs, beavers, muskrats, voles, rats, marmoset -Assemblage C/D: Dogs, coyotes -Assemblage E: Aplaca, cattle, goats, pigs, sheep -Assemblage F: cats |
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Giardia diagnosis
|
-Cysts on fecal exam
--ZnSO4 flotation with centrifugation -More than one exam may be required, cyst output is highly variable --concentration of cysts varies -Salt distorts shape of cysts, cannot use salt -Commercial ELISA kits are available -Animals negative for fecal cysts are often positive by elisa |
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Giardia Treatment
|
-Metronidazole (Flagyl)
-Fenbendazole is drug of choice currently --use for both small and large animals --Blocks polymerization of tubulin into microtubules -Fenbenazole use in dogs is off-label --50mg/kg for 3 days |
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Giardia control
|
-Can be a sever problem in kennels and catteries
-Treat all animals in a closed facility -Clean surfaces with chlorine or ammonia products -Dry surfaces thoroughly -Bathe animals, cysts can stick to fur of an animal |
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Giardia immunity
|
-Trophozoites don't invade tissue, have limited contact with many components of the immune system
-Humans and dogs with IgA deficiencies suffer more severely from giardiasis -Immunity is likely to involve production of IgA --inhibits parasite mobility or membrane uptake of nutrients --IgA does not fix complement |
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Giardia Variant-specific Proteins
|
-Antigenic variation
-Provides protection from host enzymes -Host adaptations -Strong homology between VSPs in one human isolate capable of infecting mice and VSPs from Giardia muris |
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Antigenic variation in Giardia
|
-Expresses a family of genes encoding immunodominant cysteine-rich surface protein antigens
-Approximately 150 VSP genes -Surface proteins are highly resistant to host proteases --may allow trophozoites to reside in intestine --resist digestion by host enzymes |
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Giardia control
|
-Vaccine: Giardia Vac
--useless -Vaccine is not recommended -not a life-threatening parasite or disease |
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Protozoa: Apicomplexa
|
-Coccidia
-Hemosporidia -Piroplasmidia |
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Apicomplexa: Coccidia
|
-Eimeria: intestinal parasites of large animals and poultry
-Cystoisospora: parasite of small animals -Isospora: swine -Cryptosporidium: GI coccidian in multiple animals, opportunistic pathogen in association with HIV -Toxoplasma: Intestinal parasite of cats that can cause serious disease in immunocompromised individuals -Sarcocystis: infects many animals, most important in horses -Neospora: parasite of dogs, newly discovered |
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Apical Complex
|
-Characteristic of apicomplexan protozoans
-Present in all coccidia -Spends most of life cycle in cells and used apical complex to enter cells -Has polar ring, micropore, nucleolus and nucleus, Mt, and posterior ring |
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Invasion of a cell by merozoite/sporozoite
|
1. Recognition
2. Attachment 3. Entry 4. Invasion |
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Schizogony
|
-Multiple fission
-AKA merogony -Crucial in ability of parasites to cause disease -Multiply from one organism to 8 exceptionally quickly -TONS od merozoites are produced from one sporozite |
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intestinal coccidia life cycle
|
1. Unsporulated oocysts are excreted from intestine
2. Oocysts sporulate, beomce mature, and are ingested by the host 3. Mature oocyst becomes sporozite within the host, sporozite is infective for the host 4. Sporozite undergoes schizogony (multiple fission) and gives off multiple merozoites 5. Merozoite is capable of invading the cell, gets into host intestine and undergoes schizogony again -can cycle in merozoite/schizogony producing large numbers 6. Merozoites in cells mature to form microgametocytes and macrogametocytes (male and female gmetes) 7. Gametes fertilize to form zygote, zygote secretes cyst wall and forms oocyst |
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Sporulation
|
-Multiplication of zygote to form sporozoites
-Unsporulated oocyst → sporulated oocyst → sporozoite → merozoite (via schizogony) → microgametocyte and macrogametocyte → zygote (via fertilization) → unsporulated oocyst |
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Generalized coccidia life cycle
|
Infection → merogony I → merogony II → merogony III → gamogony → sporogony → infection
Limited life cycle Number of oocysts ingested correlates with severity of disease |
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Eimeria
|
-Protozoa: Apicomplexa: Coccidia
-Highly host specific -Most are parasites of the intestinal tract -All undergo a limited number of cycles of schizogony before gamete development --usualyl 2-4 rounds of schizogony -Many species are highly pathogenic |
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Eimeria oocyst
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-Unsporulated oocyst is passed in feces
-Sporulation and development of infectious sporozoites occurs in external environment -Sporulation takes 48-72 hours -Oocyst contains large embryonic mass -Unsporulated oocyst is not infectious, sporulated is -Can survive in environment for 2 years -Have thick wall and are highly resistant to disinfectants -Can be killed by freezing, drying, high temps, or ammonia solution --none are practical for control in commercial operations |
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Bovine coccidiosis
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-Important infection in beef cattle
-One of top 3 disease problems in feed lots, major problem in feed lots! -Cattle are infected with different Eimeria species --Eimeria zurnii and Eimeria bovis are most important --widespread and highly pathogenic -Patterns of infection vary between beef and dairy cattle -2-3 million cattle are infected each year -200,000 cattle die each year from infection |
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Bovine coccidiosis pathology
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-Bleeding of large intestinal wall
-Whole sections of intestinal wall may slough off -1 oocyst → 8 sporozoites -1 sporozoite infected cell → 120,000 merozoites -Each infected cell produces 30 merozoites Infection with 1 oocyst can lead to destruction of over 28 million cells Infection with 1000 oocysts can lead to death of 28 billion cells |
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Bovine coccidiosis clinical signs
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-Diarrhea, usually with blood
-Tenesmus -Dehydration -Weight loss -Animals may exhibit reduced weight gain, even after recovery |
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Feed lot Coccidiosis
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-Difficult situation with high-turnover
-Many animals entering feedlot are likely infected -Feedlot itself is likely contaminated -Oocysts build up in feed lot until cattle are ingesting sufficient numbers of produce disease --usually occurs within 1-2 months of entering feed lot --cattle have to ingest a sufficient number of become infected -Stress contributes to susceptibility --shipping stress, new environment, new food, overcrowding |
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Coccodiosis on a ranch
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Any conditions that lead to accumulation of large numbers of oocysts in a confined area can lead to an outbreak or coccidiosis
-Control by keeping food and water off of the ground and uncontaminated |
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Bovine coccidiosis
Susceptible populations |
-Young cattle are more susceptible
-Mature cattle can build resistance and mount immune response -Maure cattle can develop disease if no previous exposure -Outbreaks are more common in the winter due to stress --can occur at ant time throughout the year -Disease outbreaks occur when non-immune animals are exposed to high numbers of oocysts |
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Nervous coccidiosis in calves
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-Neurological syndrome associated with coccidiosis
-Need high levels of infection to get neurological signs -Results in up to 10,000 deaths per year -Muscle incoordination, twitching, loss of balance, salivation, irregular respiration, seizures -No evidence of neurological lesions -May be due to gut pathology that leads to loss of Ca and Mg --electrolyte imbalance? |
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Coccidiosis in Dairy cattle
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-Disease outbreaks occur when calf pens are contaminated with oocysts
-Can occur when infected calves are housed with uninfected calves -Stress of weaning, cold weather can contribute to outbreaks |
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Coccidiosis control
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-Sanitation: prevent fecal contamination of food and water
--put food troughs above ground level -Anticipate stress in young animals -Provide prophylactic drugs -Treat cattle with drugs for 28 days, allow immunity to develop -Tx: amprolium (thiamine antagonist) therapeutic --Decoquinate: interferes with cellular respiration |
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Eimeria in swine, sheep, and goats
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-IN pigs, Eimeria infection is common but disease is rare
--not highly pathogenic -Very important pathogen in sheep and goats -Sheep: disease may be severe --industry is small so it isn't a big deal -Goats: infection and disease are common --industry is increasing in size, getting more important |
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Eimeria in goats
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-Kids are more prone than adults
-Most prone when starting to eat solid food (3-4 weeks old) -Weight loss can be substantial and sometimes chronic -Effect on growth is irreversible due to damage to intestinal lining, compromising food absorption -Advanced cases can result in diarrhea with blood and mucus |
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Eimeria leukarti
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-Eimeria in horses
-Very large oocyst -Oocyst does not float, not seen on fecal -Generally thought to not be pathogenic -Oocyst is occasionally seen on fecal exams, esp on young animals |
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Eimeria in Rabbits
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-Common intestinal coccidia:
--E magna, E. media, E. perforans -Bile duct coccidia: --E. stiedae -Will see diarrhea and weight loss in heavily infected young animals -Schizogony occurs in cells of bile duct can cause severe disease --anorexia, diarrhea, constipation -May be fatal in young animals -Tx: sulfamethoxine |
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Coccidiosis in Poultry
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-Poultry industry is huge and spends TONS on anti-coccidial drugs
-Economic losses due to coccidiosis is huge, 100-200 million dollars yearly -Anti-coccidial drugs have dramatically contributed to fast, fat chickens and development of poultry industry -Disease depends on number of oocysts ingested and species ingested --is directly related to level of destruction of intestinal cells -Infected birds will be lethargic, have ruffled feathers, diarrhea with or without blood -Laying hens will produce fewer eggs -E. tenella produces blood in feces -E. acervulina invade epithelial cells, no blood |
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Chicken coccidia
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-Chickens are susceptible to at least 9 species of Eimeria
-Eimeria tenella: highly pathogenic, causes infection in cecum --thickening of cecal wall -Eimeria necatrix: in small intestine first, then cecum -Eimeria acervulina and Eimeria maxima: upper part of small intestine |
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Most pathogenic chicken coccidia
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-Eimeria tenella
-Eimeria necatrix -Responsible for most chicken fatalities -Host specific and site specific |
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Coccidia development in broilers
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-Usually develops several weeks after birds enter growing houses
-INtroduction of young, susceptible birds into oocyte contaminated environment -Birds become infected, shed oocysts -Oocysts build up to pathogenic levels -Stress due to over-crowding can contribute to susceptibility |
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Control of Chicken coccidiosis
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-Hygiene and moisture control
-Cull sick or infected birds -Segregate young birds and older birds -Raise birds on wire -Use drugs --drug resistance is growing, cycle drugs to avoid resistance |
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Coccidia live cycle
Eimeria vs. isospora |
-Eimeria: unsporulated oocyst divides into 4 sporocysts with 2 sporozoites each
--ends up with 8 sporozoites total -Isospora: unsporulated oocyst divides into 2 sporocysts with 4 sporozites each --ends up with 8 sporozoites total -Unsporulated oocyst → sporulated oocyst → sporocyst → sporozoite → trophozoite → schizont → merozoites → gametes → unsporulated oocyst |
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Isospora infections
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-Sporulated isospora oocysts contain 2 sporocysts, 4 sporozoites each
-Schizogony occurs in small intestine -Sporulation takes 2-3 days -Oocysts are passed in unsporulated form -Most isospora are host-specific -As oocysts produlates over 48 hours, can see development of 2 sporocysts |
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Isospora suis
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-Affects neonatal pigs, nursing pigs
-20% of cases of diarrhea in nursing piglets are due to Isospora suis infection -Diarrhea decelops at 7-14 days -Low mortality, death increases if more oocysts are ingested by piglets -If blood is present, suspect concurrent infection -Clostridium perfringens can exacerbate isospora suis infection --will lead to decreased weight loss and increased mortality |
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Isospora suis diagnosis
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-Neonatal diarrhea, not responsive to antibiotic therapy
--watery or pasty diarrhea -Diarrhea occurs before oocysts are detected in feces -Fecals may need to be done after start of diarrhea -Histology can confirm infection |
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Isospora suis transmission
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-Route of infection for neonatal pigs is unclear
-Neonatal infections occur with little infection in sows -Incidence of infection in sows is very low compared to infection in pigs -Environmental contamination is source of oocysts, not sow -Must ingest an oocyst to become infected, source is not known -Farrowing crates may allow for buildup of oocysts in confined area |
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Isospora suis Treatment and Control
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-Tx: difficult because piglets are nursing
--cannot be given treatment in food or water -Anti-coccidial drugs have minimal activity against Isospora suis in piglets -Toltrozuril (20mg/kg) is effective as a single dose to 3-5 day old piglets --halts infection -Control with improved sanitation |
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Cystoisospora characteristics
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-"Carnivore" Eimeria
-Some stages invade tissue and arrest (Hypnozoites) --do not divide in tissue but survive for prolonged periods --Initiate intestinal infections when definitive host eats paratenic host -Oocysts contain 2 sporocysts with 4 sporozoites each - |
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Cystoisospora Hypnozoites
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-Stage of Cystoisospora that invades tissue and arrests
-Quiescent stages in gut wall -Do not divide in tissue -Can survive for long periods of time in tissue -When ingested by definitive host, development re-starts -Initiate intestinal infections when paratenic host is eaten by definitive host |
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Cystoisospora felis Life cycle
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1. Unsporulated oocyst is passed in feces, goes through sporoblast stage to become a sporulated oocyst
--Temperatures above 40C and below 20C inhibit development 2. Sporulated oocyst is ingested and encysts in tissues of paratenic host (rodent) 3. Paratenic host is ingested by Cat definitive host 4. Hypnozoites "wake up" and move into small intestine of the cat and continue development |
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Canine coccidiosis
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-Cystoisospora canis (lareg oocyst)
-Cystoisospora ohioensis (small oocyst) -Infection can occur at any age, disease is usually seen in younger animals -Infection is usually mils, but death can occur due to massive infections |
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Feline coccidiosis
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-Cystoisospora felis (large oocytes)
-Cystoisospora rivolta (small oocysts) -Infection can occur at any age, younger animals more often infected -Generally mild disease, but deaths may occur from massive infections |
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Clinical coccisiosis in dogs and cats
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-Infections are asymptomatic in most animals
-In puppies and kittens usually presents as diarrhea -May have blood in stool, but rare -Prevalence decreases with age |
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Cystoisospora as a primary pathogen
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-Poorly studied parasite
-Cystoisospora infection is common, but disease is not -Treatment for cocidiosis in young animals does eliminate clinical signs -Has been possible to experimentally produce disease in young animals -Disease may be severe in immunocompromised dogs -Strains may have varying pathogenicity -Clinical disease may be associated with concurrent infection of other pathogens (parvo, distemper, etc.) |
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Endodyogeny
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-Internal budding
-Form of reproduction -Division of parasite into 2 new parasites -Slower division than schizogony Number of progeny produced is less than the number produced by schizogony --less pathogenic parasite? |
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Cystoisospora diagnosis, treatment, and control
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-Dx: isospora oocysts in fecal
--dogs and cats may be infected with other coccidians that pass through intestine (esp. sarcocystis and eimeria) -Tx: Sulphadimethoxine --Albon, Bactrovet for 10-14 days -Control: Sanitation! Keep environment clean! |
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Cryptosporidiosis life cycle
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1. Oocyst hatches to sporozoite and invades cell
2. Sporozoite develops to trophozoite, develops into type I meront and merozoite --asexual cycle that can be continued 3. Merozoite develops into type II meront and enters sexual cycle 4. Undifferentiated gamont develops into microgamont or macrogamont, forms zygote 5. Zygote develops into a thin-walled sporulted oocyst that participates in autoinfection OR thick-walled sporulated oocyst that exist host -Infection is not self-limiting |
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Cryptosporidium interaction with cells
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-Cryptosporidium sits right on top of epithelial cells in small intestine
-Cryptosporidium is enclosed by the host membrane -Buds off of host surface -Modifies the zone of attachment to the host, draws nutrients from the cell -Polar rings allow feeder organelle to draw nutrients -Can have many many cyrptosporidia that bud off of the surface from one cell --looks like many little zits on the cell |
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Cryptosporidium infection
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-Parasites are present in ileum and jejunum
-Very disruptive to villus architecture, destroys intestinal villi -Appears are small dots on the surface of villi |
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Cryptosporidium oocysts
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-Infectious when passed in feces
-Do not need to sporulate in the environment, are immediately infective -highly infective, as few as 30-40 oocysts can cause infections in humans -Highly resistant to disinfectants (chlorine) --takes forever to kill with chlorine, lots ot nime needed! --hard to get out of water supply -Small and hard to identify, only 5-6mm |
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Cryptosporidium diagnosis
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-Oocysts are tiny, resemble yeast
-Cannot see on unstained blood smear -Appear red after acid-fast staining, staining is necessary -Oocysts float with ZnSO4 or saturated sugar solution -Oocytes are immediately infective after passage! |
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Cryptosporidium species
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-C. hominis: humans (sheep, cattle)
-C. parvum: humans and ruminants (deer, mice, pigs) -C. Andersoni and C. bovis: cattle (sheep) -C. muris: rodents (humans, mountain goat) -C. baileyi and C.meleagridis: birds (humans) -C. suis: swine (humans) -C. felis: cats (humans and cattle) -C. canis: dogs (humans) Not host specific! |
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Human Cryptosporidium infections
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-Most large outbreaks are due to C. hominis
-Most individual outbreaks are due to C. parvum, usually associated with ruminants -Species from dogs and cats occasionally infect humans -C. meleagridis from birds can also infect humans -Zoonotic disease! --isolates from dogs, cats, birds, and large animals can be transmitted to humans |
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Cryptosporidiosis
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-Disease occurs almost exclusively in young animals, except in humans
-Immune response limits infection -Occasionally very heavy infections can lead to severe disease or even death -Immunocompromized individuals develop severe, chronic, and often fatal infections |
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Human cryptosporidiosis
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-First recognized in AIDS patients
-Waterborne epidemic disease -80% of humans have antibodies to Cryptosporidum -Is out there, exists! -Recent outbreaks in Georgia, PA, Oregon, Milwaukee |
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Calves as source of Cryptosporidium infecction
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-Veterinary students from edinburgh became ill after visiting calves infected with cryptosporidium
--didn't was hands! -Calves are common source of infection |
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Cryptosporidium in AIDS patients
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-All kinds of cryptosporidium are found in AIDS patients
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Cryptosporidium in dogs and cats
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-Infected dogs with oocysts from a calf can pass oocysts for over 2 months
--Numbers of oocysts will be low -3% of cats in NY -2% of stray dogs in Ca shed oocysts -Mild diarrhea reported in puppies and kittens infected with cryptosporidium parvum |
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Large animal Cryptosporidiosis
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-Clinical signs: fever, watery diarrhea, weight loss, dehydration
--occasionally may see blood in feces in very severe infections -Can cause disease in young cattle, sheep, goats, pigs, probably horses -Cattle seem to be most susceptible -Intestinal lesions: Villus atrophy and fusion --mostly in ileum, cecum, and upper colon --site of infection depends on species -Infections usually occur in neonates, 1-2 weeks old --May be seen in animals up to 6 months old -infections last for 2 weeks |
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Cryptosporidiosis in Calves
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-Most severe infections are in young calves
-One calf can pass 1-10 billion oocysts per day for 1-2 weeks (holy crapballs) -Detected in 59% of calves on 23% of farms during recent national survey -in WI, kills 20,000 calves per year, causes $3 million in loss |
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Cryptosporidia treatment and control
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-No effective treatments
-Control is difficult due to resistance to disinfectants -Resistant to chlorine, dessication, freezing, salt water -No drugs that work -Nitazoxanide, paromomycin, azithromycin have some activity -Fluid and electrolyte therapy to young animals with severe diarrhea and dehydration |
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Enterocyte effector responses to cryptosporidium
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-IFN-gamma plays important role
--produced by intestinal lymphocytes --can stimulate, kill, inhibit reproduction of intestinal coccidians -Resistance may involve NO production --may also be due to mechanisms that limit intracellular pool of Fe needed for parasite growth -Immunity to most intestinal coccidians develops slowly and is effective once developed |
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Cryptosporidiosis summary
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-C.parvum is a common cause of self-limiting diarrhea in cattle
-Known to infect humans also -Dog and cats have own species of cryptosporidium --may also harbor parasites that can infect humans -Young puppies and kittens may develop signs, disease is rare -Rarely transmitted from pets to owners, but can happen -Immunocompromised pet owners are at most risk, but even then risk is low |
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Sarcocystis
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-Obligatory 2 host life cycle
-Carnivore is usually the definitive host -Herbivore or bird is usually the intermediate host -Disease is rare in definitive host, but may occur in intermediate host -Infection is widespread in large animals in US |
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Sarcocystis life cycle
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1. Unsporulated oocyst becomes sproulated oocyst in intestine of definitive host and is passed in feces as sporocyst
2. Sporocyst is ingested by cow intermediate host, penetrate into lamina propria and become sporozoite 3. Sporozoite matures into 1st generation schizont in arteries of intermediate bovine host, becomes merozoite 4. merozoite matures into 2nd generation schizont in capillaries, gives of more merozoites 5. Merozoites get into blood stream and encyst in muscle and nerve cells, stay encysted for the life of the intermediate host 6. Bovine intermediate host tissues are eaten by definitive host (fox, raccoon, dog, coyote, wolf) and immediately become sexual stages in small intestine -microgametes and macrogametes mature in intestinal epithelium and form Zygote |
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Types of sarcocystis
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-S. cruzi: Cattle (IH), Dog (DH), pathogenic for both
-S. hirsuta: Cattle (IH), Cat (DH), pathogenic for IH -S. hominis: Cattle (IH), human (DH) -S. tenella: Sheep (IH), Dog (DH), pathogenic for both -S. gigantea: Sheep (IH), Cat (DH), not pathogenic -S. capricanis: Goat (IH), Dog (DH), pathogenic for both -S. moule: Goat (IH), Cat (DH), unknown pathogenicity -S. miesheriana: Pig (IH), Dog (DH), pathogenic -S. procifilis: Pig (IH), Cat (DH), unknown pathogenicity Over 100 species of Sarcocystis in mammals and birds |
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Sarcocystis infection in definitive host
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-Carnivore eats muscle tissue from intermediate host
1. Bradyzoites penetrate mucosa and usually enter lamina propria 2. Macrogametes and microgametes develop 3. Flagellated microgametes produced, exit and penetrate macrogamete 4. Zygote forms resistant wall and undergoes endogenous sporulation 5. Oocyst or sporocysts are gradually liberated in feces over weeks |
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Sarcocystis sporocysts
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-Oocysts have thin walls, easily break down
-Sporocysts are usually seen in the feces, not oocysts -Sporocysts are often fully sporulated when passed in feces from definitive host |
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Sarcocystis infection in intermediate Host
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1. Sporocysts or oocysts are ingested by intermediate host
-excyst in the gut, penetrate mucosa and invade endothelial cells 2. Invade larger cells and larger blood vessels, divide, then move onto smaller vessels -2 generations of schizogony occur in endothelial cells of small blood vessels and capillaries 3. Merozoites invade striated muscle fibers, form sarcocysts (encyst) -each sarcocyst is filled with numerous slow-dividing bradyzoites 4. Sarcocysts gradually increase in size, bradyzoites increase in number 5. Sarcocyst ingested by carnivore or scavenger |
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Sarcocystis infection
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-Parasites divide in endothelial cells via schizogony
-Leads to tissue damage and inflammation -Can infect WBCs also --will see merozoites within lymphocytes |
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Sarcocystis cyst
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-Bradyzoites are within cysts in muscle tissue
-Bradyzoites are infective for the carnivore definitive host -Some sarcocysts are macroscopic and may lead to meat condemnation --Sarcocystis hirsuta -Sarcocysts can be large and visible to naked eye -Can create macroscopic lesions in the wall of the esophagus |
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Sarcocystis pathogenesis
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-Common infection and less common disease
-Disease is associated with schizogony within endothelial cells of small arteries and capillaries in intermediate host -Damage to endothelium leads to petechial hemorrhages --acute inflammation and multiple organs can follow --kidneys, heart, lungs, liver, and muscle affected -Disease is most acute when 2nd generation of schizonts rupture --day 28-40 -Can give multitude of symptoms |
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Sarcocystis signs
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-Main signs: Fever, anemia, weight loss, abortions, reduced milk production
-Death -Abortion, stillbirth -Anorexia, inappetence, weight loss, poor growth -Muscle atrophy -Hair loss around neck, rump, tail -Hypersalivation, nasal discharge -Fever -Anemia -Signs depend on weeks after infection -Most infected animals do not show signs of disease |
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Sarcocystis tenella
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-In sheep
-Causes severe necrotizing interstitial pneumonia -Can see necrosis in parenchyma |
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Sarcocystis disease considerations
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-May cause clinical disease following ingestion of very large numbers of oocysts or sporocysts
--fever, anorexia, anemia, death -Most cattle become infected with lower number of parasites, develop immunity instead of disease -Abortion or decreased milk production is not common --most cows develop resistance before breeding age -Impact of infection may be subtle (reduced weight gain) |
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Sarcocystis diagnosis and treatment
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-Difficult to diagnose, overt clinical disease is rare
-Most animals are seropositive -Clinical signs are very generic and non-specific -Ingestion of large amounts of sporocysts can lead to disease signs -Histology of representative animals in a herd can help with diagnosis -Tx: amprolium --can control outbreak --Disease is treatable if recognized |
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Most important species of sarcocysts
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-Sarcocystis cruzi: cattle
-Sarcocystis capracanis: goats -Sarcocystis tenella: sheep All cause damage to endothelial cells in multiple organs |
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Sarcocystis control
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-Do not feed raw meat products from large animals to dogs or cats
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Sarcocystis in abnormal hosts
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-Infection is not common in normal intermediate hosts, but can cause issues in dead-end hosts
-Sarcocystis nneurona can produce severe effects in abnormal/accidental hosts -Causes Equine Protozoal Myeloencephalitis (EPM) |
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Equine Protozoal Myeloencephalitis
EPM |
-Sarcocystis neurona infection in abnormal/dead end host
-33,000 cases per year -Exposure rates vary widely from region to region, are generally high -40-45% of horses in PA have antibodies to Sarcocystis neurona, widespread exposure -EPM-like disease has been noted in skunks, raccoons, cats, dogs, mink, seals, sea otters --unclear if any are natural intermediate hosts -Lesions in brainstem or spinal cord destroy tissue and cause inflammation -Usually unilateral lesions |
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Sarcocystis neruona
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-Virginia opossum is definitive host
-20-25% of opossums may be infected --Sheds sporulated sporocysts -Can infect horses, causes equine protozoal myeloencephalitis -40-45% of horses in PA have antibodies to Sarcocystis neurona, widespread exposure |
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Sarcocystis neurona life cycle
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1. Sporocyst is shed in feces of opossum definitive host and is ingested by a horse
2. Horse is aberrant host, sporocyst enters neuronal tissue -lesions occur most often in the brainstem or spinal cord -Are usually but not always unilateral -Location of parasite in CNS gives damage and disease |
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EPM pathogenesis
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-Parasites present in CNS cells and tissues
-Mostly in neurons, mononuclear cells, and glial cells -Parasites get into cells, multiply, and destroy cells --cause inflammation -Tissue damage is due to parasite damage and inflammation |
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EPM clinical signs
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-Neurological disease
-Varies greatly in severity -main signs are incoordination and hind-end lameness, usually unilateral -Infection of cerebrum causes depression or seizures (not common) -Infection of brainstem or spinal cord causes gait abnormalities, loss of coordination, paralysis -Loss of muscle tone -Head tilt, paralysis of face or tongue, muscle atrophy, difficulty swallowing can also occur -Neurological signs are usually asymmetrical -Direct effect on muscles innervated by direct nerves from spinal cord -Signs are based on damage to neurons on one side of CNS -Untreated, can be fatal |
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EPM diagnosis
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-Diagnosis is difficult, tests are only suggestive
--Infection is limited to CNS, hard to biopsy or detect organisms in CNS tissue -Most exposed horses are seropositive -Have to rely on clinical signs --asymmetrical muscle atrophy, altered, gate, ataxia, hind limb paralysis -western blot assay can detect anti-S. neurona antibodies in CSF --90% of horses with CNS signs have antibodies in CSF -Can use PCR to detect parasite DNA --questionable value, few intact parasites in CSF and DNA is rapidly degraded |
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EPM summary
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-If a horse exhibits clinical signs compatible with EPM and no other easy explanation for neurological signs, TREAT
-EPM is most common cause of neurological signs in horses -Assumptive diagnosis based on clinical signs Unilateral lameness or hind end paralysis |
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EPM Treatment
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-Pronazuril every day for 1-2 months, long treatment
-Sulfadiazine/pyrimethamine every day -NSAIDS --inhibit inflammation to neurological tissue --can be VERY effective! -Early treatment can lead to recovery -If treatment began after development of clinical signs, will most likely be ineffective or only partially effective --neurons cannot regenerate |
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EPM prognosis
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-60-70% of treated horses show improvement
-15-20% of horses return to normal -10-25% of horses relapse after treatment -horses with advanced neurological diseases are less likely to show improvement -Tx is against parasite, not for neurological damage --cannot repair damage to CNS |
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EPM-like disease in other hosts
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-Mink, cats, raccoons, skunks, pacific harbor seals, ponies, zebras, lynx, dogs, sea otters
-Has caused MAJOR outbreaks in sea otters along california coast --cysts washed into ocean? |
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Sarcocystis neurona in cats
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-5% of free-roaming domestic PA cats have antibodies
-7% of VA cats have antibodies -may cause EPM-like disease in cats |
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Sarcocystis summary
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-Apicomplexan parasite
-2-host life cycle, hosts have predatory-prey relationship -Disease is rare in definitive host (carnivore) -Mild/subclinical disease in natural intermediate host (herbivore) -Prevalence of infection in herbivores is high -infected aberrant hosts (horses and marine mammals) can how very severe neurological disease |
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Besnoitia
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-Newly emerging parasite of donkeys
-Known to be a parasite of multiple animals in Africa and Asia -Increasing number of cases noted in cattle in Europe over past 5 years -Outbreaks in donkeys observed over past few years in US -Becoming more widespread |
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Besnoitia types
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-Besnoitia besnoiti: Africa, Asia, Europe
-Besnoitia tarandi: Canada, Scandinavia, Russia -Besnoitia caprae: Africa, Iran -Besnoitia bennetti: USA, Africa |
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Besnoitia bennetti in USA
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-Affects Donkeys
-Found in PacNW, MT, TX, East Coast -Definitive host is unknown --cats, rodents, rabbits have been found to be definitive hosts in other Besnoitia species -Infections occur in spring --based on mating behavior and fly vectors |
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Besnoitia life cycle
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-Mostly unkown!
-Acute phase: Tachyzoite proliferation -Chronic phase: Bradyzoites in tissue cysts -Mechanical transmission by biting insects --insects feed on dermal cysts -Direct transmission from cow-cow via close contact --natural mating --dermal cysts rupture -Wildlife reservoirs? -Host can ingest oocysts to become infected -Parasite invades endothelial cells -invades other cells and forms cysts mostly in dermal tissue |
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Common Besnoitia dermal cyst locations
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1. nares
2. sclera 3. larynx 4. Epiglottis Lesions are pathogonomic for infection -Mucosal tissue lesions are most common |
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Besnoitia dermal cysts
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-Parasite invades endothelial cells and other cells to form cysts
-Cysts form in dermal tissue -Flies can feed on dermal cysts, act as vectors for transmission -Dermal cysts can rupture with direct contact --rubbing of wounds on animals may cause transmission -LOTS of bradyzoites exist in cysts on skin |
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Besnoitia clinical disease
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-Disease is highly variable
-Some animals show no signs, others lose weight and become cachectic -Diagnose by finding cysts on biopsy --can also do serology -No treatment -Difficult to control since life cycle is greatly unknown -Causes damage to endothelial cells |
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Babesia
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-Protozoa → Apicomplexa → Piroplasmidia → babesia
-Blood parasite of cattle -Occurs in many parts of the world -Occasional parasite of dogs in US |
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Piroplasms
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-Intracellular blood protozoans
-Transmitted by ticks -Babesia: blood parasite of cattle, occasional parasite of dogs in US -Theileria: African cattle, causes "east coast fever" -Cytauxzoon: parasite of cats, all cases have been fatal |
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Babesia bigemina
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-Pear-shaped parasites in RBCs of host
-Can be large (4-5micrometers) or small (1-2.5 micrometers) -only stage in the host is trophozoite --divides within RBCs -Rhipicephalus (Boophilus) annulatus is the tick vector -Infection was eliminated from US in 1940's by control of ticks -Much of southern Tx is under tick quarantine due to Babesia bigemina transmission |
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Canine Babesia
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-Strictly within erythrocytes
-Divides within RBCs -Never get more than 4 parasites per cell -RBCs taken up by tick, mature, and reproduce within tick -Zygote migrates into the ovary or saliva of ticks -Transmitted to canine host when tick feeds on dog -Original babesia found in US, now broken into sub-species |
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Canine Babesia in US
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-Changing situation due to multiple sub-species
-Babeisa Canis: original babesia identified in dogs in US, now broken into sub-species -Babesia canis vogeli -Babesia canis canis -Babesia canis rossi -Babesia gibsoni |
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Babesia canis vogeli
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-Least pathogenic babesia canis variant
-Dominant babesia canis species in US -Rhipicelpahus sanguineus vector -Most infections are sub-clinical -Chronic infections are occasionally noted --intermittent fever, decreased appetite, weight loss -Acute infections are more rare, occur mostly in puppies or dogs with infected blood transfusion --lethargy, fever, severe hemolytic anemia -Infected dogs stay carriers of infection -Splenectomy can exacerbate disease, will not get phagocytosis and removal of infected RBCs -Occurs mostly in southern US, survives year-round due to climate -Common greyhounds |
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Babesia canis canis
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-Babesia canis variant in Europe and parts of Asia
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babesia canis rossi
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-Most pathogenic babesia canis variant
-Found in south africa |
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Babesia gibsoni
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-Babesia canis variant found worldwide, including US
-More pathogenic than babesia canis vogeli -Endemic to India, northern Africa, southern Asia, Middle East -Mostly in pitbull terriers and staffordshire terriers --fighting leading to transfer of blood and parasites? -Small babesia -Severe anemia and thrombocytopenia are more common -Unknown vector |
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Babesia canis voglei presentation
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-Mostly Subclinical infections or mild infections
--associated with fever, lethargy, or mild anemia -More severe infections in transfused dogs -High % of greyhounds infected --greyhounds often used as blood donors -Recovered dogs remain carriers |
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Babesia canis gibsoni presentation
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-Parasites usually detected in blood 1-4 weeks after infection
-Parasitemia reaches 2-6%, low-level infection -Fever, lethargy, throboccytopenia, anemia in young puppies -Anemia involves lysis of RBCs and increased erythrophagocytosis -Disease is more severe in immunosuppressed, blood transfused, or splenectomized dogs --conditions exacerbate disease -Most dogs develop chronic infections with few clinical signs, intermittent fever, and lethargy -parasites stay in blood and cause chronic infections -IN US, most cases are in pitbulls or dogs bitten by pitbulls |
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Babesia canis gibsoni disease
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-Severe hemolytic anemia
-Thrombocytopenia -Icterus -Fever -Spelnomegaly -Lymphadenopathy |
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Babesia geographic distribution in US
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-Most states have had positive samples
-7 out of reporting states had no samples -Out of 673 dogs, 144 positives for Babesia gibsoni, 10 positive for Babesia canis --129 pitbulls positive for Babesia gibsoni --6b greyhounds positive for Babesia canis |
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Babesia conradae
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-Originally thought to be babesia gibsoni, now is own species
-More pathogenic than other Babesia species in US -High parasitemia, anemia, thrombocytopenia, hemoglobinuria, lethargy -Half of studies dogs died of infection --several relapsed after Tx -No cases seen in last 10 years until this year in CA -Rhipicephalus vector? -New form of Babesia, lots of unknowns |
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New Babesia species
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-new species identified in NC
-Dx: parasites in blood smears and PCR |
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Babesia Risk Factors
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-Babesia infects all dogs, individual babesia species more commonly seen in certain breeds
--Babesia canis: greyhounds --Babesia gibsoni: Pitbulls -Kennels with high Rhipicephalus populations and transmission -Fighting dogs and Babesia gibsoni transmission |
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Babesia clinical disease
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-More common in south and midwest
-Affect any age dog, more severe in young animals -Signs: lethargy, depression, pale mucus membranes, jaundice -Fever -Lymphadenomegaly -Splenomegaly |
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Babesia diagnosis
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-See parasites on blood smear
-Serology will not always show antibodies, and will not always have cross-reactivity between species -Positive PCR indicates infection --hard to get PCR |
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Babesia treatment
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-Berenil: not available in US
-Babesia canis: imidicarb, diproprionate --possibly cures -Babesia gibsoni: Atovaquone with azithromycin --reduces morbidity and mortality --may not actually cure infection |
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Equine Prioplasmosis
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-Babesia caballi and Thileria equi
-Parasites present in RBCs, looks like babesia -Multiple tick vectors, including: --dermacentor --rhipicephalus --Boophilus --Hyalomma |
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Equine babesiosis
Equine Perioplasmosis |
-Endemic worldwide except for US, Canada, Australia, England, Ireland, Japan, and Iceland
-Major cause of equine disease in US in 1960's --eliminated in 1988 -All horses entering US are tested -Reportable disease to both state and USDA -Strict control to keep disease out of US |
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Equine perioplasmosis recent outbreaks
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-2008: 20 horses in FL
-2009: Kansas -2011-2013: 400 cases in TX and 12 other states --most linked to ranch in TX |
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Theileria equi
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-Lymphoma-like disease, affects lymphocytes
-Acute infection causes fever, malaise, anorexia --depression and tachycardia accompanied by anemia --Death may occur due to severe anemia -Subacute: intermittent and less severe signs of acute infection -Chronic infection: mild anemia with variable fever and weight loss --Infections may resolve clinically, parasites will persist -Animals remain as carriers |
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Cytauxzoon felis in Cats
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-Parasite of bobcats
-May be transmitted to domestic cats, more rural infection -First reported in domestic cat in MO in 1976 -Most reported infections are in southern US -Transmitted by Amblyomma americanum -Anemia, fever, anorexia, splenomegaly, lympadenomegaly --signs can be very severe -Originally thought to be 100% fatal in domestic cats, some cats do survive --recovered cats remain infected -Have found some sub-clinical cases -Death occurs within days of clinical signs -No effective treatment |
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Cytauxzoon felis in RBCs
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-Tiny little inclusion bodies in RBCs
-Can also have macrophages with Schizonts --schizogony occurs in macrophages |
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Cytauxzoon felis pathology
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-Due to tissue schizogony
--Schizont-infected macrophages are thought to block small blood vessels -results in multi-organ ischemia, infarct, failure and death |
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Cytauxzoon felis Diagnosis and Treatment
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-Blood smear exam, should see parasites within RBCs
-PCR -Tx: euthanasia --imidocarb with aggressive supportive therapy --IV fluids and heparin to prevent DIC |
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Hepatozoon americanum
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-First seen in dogs in TX in late 1970s
-Amblyoma maculatum is vector (Gulf Coast tick) -Cases so far limited to TX, GA, OK and gulf states -Severe disease -Gametes circulate in blood, mostly in neutrophils and monocytes --gets into WBCs -Parasites divide within cysts in skeletal muscle |
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Hepatozoon americanum Life Cycle
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1. Dog ingests tick, sporozites penetrate dog gut
2. Sporozites undergo merogony, release merozoites from mature meronts --can either go into secondary merogony, or penetrate leukocytes and go through gametogony 3. Tick takes up gamonts during blood meal 4. Gametogenesis and fertilization 5. Sporogony, mature oocysts develop in haemocoel |
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Hepatozoon americanum infection and disease
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-parasites cross intestine, enter blood and hang out in macrophages
--mostly in skeletal muscle -Multiply in large cysts that can rupture --rupture causes pyogranuloma and inflammation -Infections persist for years -Disease is associated with division of parasites within muscle |
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Hepatozoon americanum clinical signs
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-Fever, weight loss, loss of appetite
-Severe muscle pain, weakness in limbs, lameness, cannot move without pain -Neutrophilia and anemia may be observed -Dogs usually die within a year if not treated -Treated individuals can live for 5-6 years longer -Reinfection is usually fatal -Disease is usually not curable |
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Hepatozooon americanum Diagnosis and treatment
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-Parasites in blood smear
--difficult due to low numbers -Parasites in muscle biopsy (more reliable) -Serology -Tx: trimethoprim, sulfadiazine, clindamycin, pyrimethamine --long-term administration of decoquinate |
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Balantidiases
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-Occasional parasite of animals
-Ciliate organism with 2 nuclei --large macronucleus and small micronucleus -Has food and contractile vacuoles -Large flagellate -Uses cilia for locomotion -forms cyst wall |
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Balantidium coli Life Cycle
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1. Cyst infective stage is excysted in small intestine
2. Multiplies via transverse binary fission, becomes trophozoite in lumen of colon 3. Trophozoites live in large intestine, encyst |
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Balantidium coli
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-Uses cilia for locomotion
-Trophozoites live in large intestine, encyst -Form ulcerating lesions, cause diarrhea or dysentery -Are largest protozoans -Commonly found as a commensal in the large intestine of pigs -Rarely trophozoites invade the gut wall of humans and domestic animals |
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Amoebiasis
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-Common in humans in tropical and sub-tropical areas
-Not endemic in US, but is in other areas -Cysts formed during infections of humans and primates --Cysts may be infectious to other animals -Infections in dogs and cats have been reported but are rare -No cysts formed during canine or feline infection --not reservoir hosts -"imported" disease |
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Amoebiasis Life Cycle
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1. Cyst is excreted in feces and ingested by human via contaminated food or water
2. Excystation in small intestine, trophozoite forms -trophozoite can either become asymptomatic, can be invasive and cause amoebic colitis, or can cause liver abscesses 3. Trophozoite encysts in the colon and is excreted in the feces |
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Entamoeba histolytica
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-trophozites reside in large intestine
--May invade the gut wall --Results in necrotic lesions -Trophozites may travel through portal system to liver --forms liver abscesses -Trophozoites may invade lungs or CNS and cause serious disease -Acute infection: diarrhea or dysentery -Parasites kill and ingest other cells --get into cells and cause damage |
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Entamoeba trophozoites
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-Trophozoites can invade lungs, liver, and large intestine
-15-30 micrometers in diameter -Live in large intestine -Migrate to liver via portal system and form liver abscesses -Migrate to lungs and CNS to cause serious disease -Acute infection is due to trophozoites invading cells |
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Entamoeba cysts
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-contain 1 or more nuclei
-Often have chromatin bodies of aggregated ribosomes |
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Entamoeba invadens
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-Liver infection in a snake
-highly pathogenic in stakes and turtles -Causes similar disease to Entamoeba hystolytica --includes liver invasion -Tx: flagyl |
