----start parasit 9.9.97---- parasitology 9.9.97 Dr Jorge Guerrero lecture #7 "The Lungworms" Dr. G is the senior director for veterinary professional services at Merck AgVet. Class: Nematoda Order: Stongylida Superfamily: Metastrongyloidea Genera: metastrongylus, mullerius, aleurostrongylus, et al Generalities: slender worms with a rudimentary or absent buccal cavity. predilection site is lungs, trachea, or adjacent vessels. these are mainly parasites of carnivores, ungulates, rodents, and primates. Typical life cycle: indirect (with one exception), requiring intermediate host which is generally the snail or slug (with one exception being an earthworm). All of these parasites have L1 with kinked or crimped tail. L3 gets into the intermediate host by ingestion or direct penetration. these worms may produce lesions in lung parenchyma or bronchial tree. slide: L1 with crimped/kinked tail. Protostrongylus rufescens: lungworms of sheep and goats rufescens == red these are small, reddish worms, 1.5-3 cm in length. these worms are embedded in tissue of the bronchioles, which should give an idea of the pathology they cause. intermediate host: snail, slug (molluscan host REQUIRED) L1 hatches in the bronchioles and is coughed up, swallowed, and passed in feces. L1 then penetrates the foot of the snail or is ingested by the snail. L1 grows into L3 in 2-10 weeks. L3 retains TWO sheaths and is the infective stage for the definitive host. L3 can survive beyond the life of the invertebrate host - well protected by sheaths. life cycle: infected snail eaten by host. L3 released in intestinal lumen and migrates to mesenteric LN, molts to L4, moves in blood to heart and lungs, molts to L5. prepatent period 5-6 wks. adult worm lays eggs for 2 or more years (which hatch to L1 in lung and are coughed up and swallowed and passed). may be vertical transmission. heavy worm burdens produce unthrifty animals. they are less productive compared to uninfected animals. this report was about a natural infection in an experimental sheep flock in MD.USDA reports infection of this flock with signs of diarrhea, wt loss, and respiratory signs. other investigators report this parasite predisposes host to secondary bacterial infections (secondary to destruction of lung tissue). is widely distributed in temperate areas. no specific pathognomonic signs. may be underreported. controversy over exactly what pathology it causes. cause of considerable morbidity and mortality in Big Horn Sheep. Dx: L1 in feces, extracted by baermann technique. L1 is characterized by the kinked tail. Also, postmortem exam: lung nodules containing adult worms, eggs, and L1s Tx: fenbendazole (FBZ), ivermectin (IVM), oxfendazole, albendazole, levamizole. Ivermectin is used at 400 micrograms/kg MUELLERIUS CAPILLARIS small parasite 1.2-2.3 cm. Is present in alveoli but NOT bronchioles. slugs and snails are intermediate hosts. widely distributed in temperate regions including eastern US. dx: L1 in feces, kinked tail, small spherical lesions on lung surface. Tx: FBZ, IVM (400 micrograms/kg) slide: L1 of m.capillaris, showing kinked tail. slide: affected sheep lung with round 5 mm diameter vesicles. this worm is more common than protostrongylus rufescens in domestic sheep/goats. histologically you see the larvae in lungs, and a huge cellular infiltrate in surrounding tissue. METASTRONGYLUS APRI (there are two other spp, but we're talking about this one) common parasite of grazing pig large nematodes, up to 6 cm, predilection site == bronchi/bronchioles esp of posterior lobes. eggs laid in bronchi, coughed up, swallowed, expelled in feces. Eggs have thick shell and are resistant to environmental conditions - can live up to a year outside. larvae hatch in feces. L1 or eggs are ingested by earthworms, which are the intermediate host. L1 molts twice to L3 in about 10 days, inside of the earthworm. L3 is the infective stage. slide: heavy infection of metastrongylus. looks like spaghetti slide: larvae within earthworm, present in large number. L3's found in walls of esophagus of earthworms for up to SEVEN YEARS! (who knew earthworms lived that long?) pigs are infected by infected earthworms. L3 is liberated in pig intestine, migrates to mesenteric LNs, molst to L4, migrates to bronchioles via blood, molts to L5 in bronchioles. prepatent period about four weeks. this is typical life cycle of all metastrongylus spp. these parasites induce inflammation in lungs...cause bronchitis and bronchiolitis with secondary overinflation of related alveoli in 4-6 mo old pigs. we see enlarged mesenteric LNs at necropsy. this is most commonly seen in pigs on pasture, due to intermediate host requirement. pigs raised on concrete do not have as much exposure to earthworms. but some swine farmers are moving to partial pasture systems. older animals develop an immunity and don't have as much of the clinical signs. infected pigs may exhibit poor growth, hacking cough if chased, shortness of breath (SOB), nasal discharge, and complications from secondary bacterial infections (staph.) slide: section of a bronchiole containing a transverse section of nematode, and a lot of inflammatory infiltrate and mucous in the area. dx: thick shelled, rough, larvated eggs in feces. The egg is very characteristic for this species. eggs are also very dense (MgSO4 required for flotation). light infections are usually asymptomatic. tx: BZM, LVS, or IVM injectable or in feed. control: house the animals away from dirt so they don't eat earthworms Lungworms of white tailed deer: PARELAPHOSTRONGYLUS TENUIS adult parasite occurs in the cranial venous sinuses and subarachnoid spaces (CNS). it is considered a lungworm since L1s are found in the lung. this parasite is very prevalent in deer - prevalence from 68-96% depending on age group. we find mean 3.2 worms per host in the deer, and worm is nonpathogenic in this host. worm is big - 4-10 cm in length. problem- this parasite can be spread to domestic animals. some eggs hatch in the venous sinuses (jugular veins) L1 and eggs are carried to the lungs in the blood L1s are coughed up and swallowed L1s are expelled with feces and they penetrate the foot of a grazing snail or slug. larvae molt twice to L3 in the intermediate host in 3-4 weeks. L3 is the infective stage. definitive host is infected by ingestion of infected intermediate host. in the new host, L3 is liberated and migrates through intestine to the spinal cord in 10 days. they develop within the dorsal horns of gray matter for 20-30 days, molting twice. then adults migrate in subdural space to the cranium, penetrate dura mater, and enter venous sinuses. the prepatent period is three months. why is this parasite interesting if not pathogenic in normal host? well...infected snails and slugs are eaten by other animals. then there are major problems. there can be fatal neurological disturbances in elk, moose (moose dz) caribou, sheep (rare), goats (more common), and llamas there is no treatment - it is fatal to these animals. so you do not want your domestic animals hanging out with white tailed deer!!! clinical signs in aberrant host: circling, head pressing, loss of fear of humans, incoordination, abnormal gait, paralysis, recumbency and death. this is highly pathological, and an obstacle to repopulation efforts (moose and caribou) where white tailed deer live. moose and caribou used to be present in NE USA, and now there are so many deer, the moose and caribou are gone, and we can't repopulate because of this parasite. slide: section of the CNS showing cross sections of the nematode. again - no pathology in deer. deer have a good host/parasite relationship with this nematode. they get along together. Lungworm of cats: Family: Angiostrongylidae Genus: Aelurostrongylus SP: AELUROSTRONGYLUS ABSTRUSUS found in lungs of about 5% of cats in USA. this seems to be small, but when you compare it to that of say FIP, or FIV, it is at about the same or sl higher level than that of those two diseases. these are delicate parasites, fine, small - about 7-10 mm in length, and are found deeply embedded in lung tissue. males have a very short bursa. adults are found in terminal bronchioles and alveolar ducts. eggs and larvae are produced by the adults and are found in the lung tissue as well. the females produce eggs. egg masses in alveoli form nodules. (eg, they induce the production of nodules by the host). L1 hatches from egg, travels up tracheal elevator, is coughed up, swallowed, and shed in feces. In environment, L1 penetrates snail/slug, molts 2x, L3 is infective stage. mollusk is eaten by rodents or birds (paratenic host) and L3 remains within paratenic host. cats are infected by eating rodents or birds or infected mollusks. then L3 penetrates mucosa of GI tract, and goes to lungs via bloodstream. prepatent period is 31-51 days. eggs laid by adults for up to 7 mos. cat sheds up to 50000 larvae/day. clinical signs usually slight, coughing after exercise. in heavy infxns, will see chronic cough, gradual wasting, dyspnea, and death. pathology: solidified grey raised nodules 1-10 mm in diameter. nodules with eggs, larvae and cellular infiltrate seen histologically. also hypertrophy of smooth muscles of pulmonary vessels. diagnosis as in previous cases can be done by ID of L1 in feces - remember the kinked tail. also can find L1s in tracheal wash. chest xray supportive of clinical signs can also be diagnostic. it's also interesting that this parasite has caused some cross reactions with the heartworm, dirofilaria immitis. this caused some confusion initially. treatment: LVS, FBZ, IVM (at high levels in cats, ivermectin can be "surprising" so you use small doses). Lungworm of dogs: FILAROIDES SPP OSLERUS OSLERI is the one we're talking about, not FILAROIDES OSLERI!!!!! small, slender parasite found in lungs of dogs. bursal lobes greatly reduced in males. adults in trachea (esp bifurcation) and bronchi. DIRECT LIFE CYCLE no intermediate host! prepatent period 6-7 mos. oviparous females shed larvae surrounded by thin transparent membrane. transmission occurs through ingestion of regurgitated stomach contents, feces, or tissue containing L1 or L1 in saliva. L1-L5 takes about 34 days in lung tissue. adult worms found at bifurcation of trachea 70 days post infection. usually seen by bronchoscopy or tracheal wash. also can find L1 in feces. autoinfection by grooming or cophrophagy. clinical signs: spasmodic hard dry cough at exercise or exposure to cool air. NOT induced by pressure on larynx. usually seen in young 4-6 mos old animals. slide: nodes in bifurcation of trachea - raised red ones. pathology: grey or red nodules at tracheal bifurcation the larvae have the kinked tail tx is hard. can use sodium caparsolate like in HW, must check for HW first. need to tx dailly for 21 days. can use LVS sid 10-30 days, or ivermectin offlabel. control: c-sections, hand rearing, screening of new dogs in kennels. ------BREAK---- 9.9.97 Dr. Schad 2-3 INTRODUCTION TO NON-BURSATE NEMATODES AND RHABDITOIDEA (i.e., Strongyloides spp) this is an introduction to the nonbursate nematodes - nematodes OTHER than Strongylida Now we are dealing with Class: nematoda Order: Rhabditida Superfamily: Rhabditoidea Genus: Strongyloides - the threadworms Spp: a whole bunch :) in fact, if any of us go into parasitology, this is a huge genus that we'll work with. there are species in birds, reptiles, fish, etc. but we won't cover those. General Features of STRONGYLOIDES spp: * they are intestinal parasites (eg, adult worms found in intestines) * a small, thin-shelled, embryonated egg is found in host feces (may look like strongyle type eggs but are smaller and invariably embryonated, with tadpole appearance) * freeliving larvae found on soil/grass etc * infection usually by ingestion of L3 or skin penetration by L3 * transmammary transmission is common. many species have this- s.ransomi (pig), s.westeri (horse), s.venezuelensis (rodents) * skin penetrating larvae migrate to gut, we think, via pulmonary/tracheal route. lately, however, it seems that pathogenesis suggests pulmonary route isn't as predominant as might be suggested by textbooks. using radiolabelled larvae, about 35% migrate via lungs. in heavy infestations this can cause dz, but you shouldn't think this is some kind of canonical route. the rest of larvae may wander or move in a more random fashion and get to the intestine another way. * L3 grows to adult in the gut. * adult worms have no buccal capsule. are long and thin, and the main features of adult female worms are long esophagus, about 1/4 of length of worm, and very large eggs relative to diameter of worm * no intermediate hosts, no known paratenic hosts but hey, generalities are not prudent... UNIQUE, EXCEPTIONAL features of STRONGYLOIDES spp * adult parasite - FEMALES ONLY!! how do they reproduce? parthenogenesis. * freeliving stages-- include adult males and females. so, reproduce internally (by parthenogenesis) and externally (sexually)!! OMAR: if it is outside the host, it isn't a parasite...it's living on its own not parasitizing anything :) * infective L3 is NOT ensheathed, so won't last long outside host. after 6 days, loses some of the chemotactic behavior. L3 also has very long esophagus. * freeliving stages look very different. females are chubbier. if you leave feces sitting in lab, you may see development into this stage. Also may find L3 in feces - and this is infective to human (dog form is, anyway) * S.Stercoralis parasitic female adults produce larvae that may develop precociously in the host, and reach infectivity and autoinfect the host - they never leave this host, in other words. this is only S. stercoralis, not other spp. this happens particularly in immunosuppressed hosts, causing large buildup of parasite load. * autoinfection is very rare among metazoan parasites STRONGYLOIDES spp: * s.papillosus - ruminants, rabbit (may contribute to parasitic gastroenteritis PGE in ruminants; usually not a major parasite of ruminants, although can see mass migrations causing problems in young calves) * s. ransomi - swine. this species is more of a problem. piglets exposed to heavy infection, by transmammary transmission, can get massive diarrhea, dehydration, and rapid death. massive migration also can result in sudden death. * s. westerni - horses - diarrhea in young foals is seen if they get heavy transmammary transmission * s.stercoralis - dog, cat, man, other primates. used to cause death of newborn higher primates in zoos, now more controlled. unless you wind up practicing overseas will not see it in cats. the US strain isn't infective in cats as far as we can tell. * s. fuelleborni - primates morphology of adult worm: long esophagus, big eggs. can tell apart some kinds of females because some spp have spirally wound ovaries around the intestine, as in hemonchus. TWO KINDS OF FREELIVING LIFE CYCLES POSSIBLE * direct (homogonic) - no freeliving adults * indirect (heterogonic) - with freeliving adults HOMOGONIC CYCLE: the egg is passed in host feces, hatches into L1 on pasture. L1 molts to L2 which molts to L3 which is infective and NOT ensheathed, and which is eaten by host. HETEROGONIC: parthenogenetic female in host lays eggs as before, passed in feces, hatch into L1, molt into L2, molt into L3, molt into 4, molt into L5 male and females. then, the females lay eggs which hatch and go on as above in the direct cycle. we don't see more than one freeliving cycle happening. there is one species in the cat, seen in Puerto Rico. Omar, this is for you. S. planiceps can have multiple freeliving cycles. putting these together with migratory pathways it becomes complex, but if you look at the back of your handout, you'll have a lovely picture of it all. (it's on p 5 actually) now, remember we said there is transmammary transmission - we're not sure how the larvae get into the subcutaneous fat around the mammary tissue, but they do. somatic migration or percutaneous entry, I guess. then they enter the piglet because they are passed in milk. re: prepatent period (PPP) it depends on host immunity, age, etc. runs about 5-10 days. route of entry can also influence the PPP. Q: is there always a freeliving part of the cycle, or do some go solely via direct pathway? (eg, must they take the green road or can they only take the red road?) well, you can select for a mostly homogonic strain in the lab, that will rarely take heterogonic route. there are genetic and environmental factors which affect the life cycle. in early infections, shortly after animals have been experimentally exposed to this parasite, most larvae passed go directly to infectivity. as the infection ages, andhost is getting more resistant, increasingly the larvae go indirectly - entering freeliving cycle. this is strategic for the worm - to go into heterogonic cycle, extending life cycle outside the host, increasing the population, making it more likely to get into naive, more susceptible hosts. this reasoning is speculation, but if true is pretty sophisticated stuff. PATHOGENESIS: * due to larval penetration as in hookworms, so we see some foot rot and so forth. * due to migration. migration of larvae in skin is big deal in people but not animals. sudden death is seen in calves and piglets * due to presence of adults in intestine in young animals * due to migration after autoinfection (s.stercoralis only) CLINICAL FEATURES: skin- penetration and subq migration of larvae - local erythema, macules, papules, tracks - people only see chart in handout. slide: histological skin prep. larval form is seen. some species spend some time in skin. slide: dog with pulmonary petechial hemorrhages on lungs - can see lots of hemorrhage in lungs histologically in some infected animals slide: adult worm in the small intestine. these worms will, if abundant, undermine the mucosa, and you see mucous, hemorrhage, mucosal sloughing. these are skin penetrators, and when they penetrate the feet can predispose to secondary bacterial foot rot. often these infections are self limiting. Strongyloidiasis during intestinal phase of infection is a spectral disease. a few worms is subclinical. a heavy load can cause sloughing of intestinal mucosa and bloody diarrhea. slide: experimental infection given to dog. dog started to clear it about 8 wks post infection. was given more larvae, but still cleared the infection totally by week 15. at week 18 dog was treated with prednisolone. at that point, the infection recredesced. so, what's going on? well apparently the host is kicking out worms and also suppressing the fecundity of the worms. eg, some worms remain in host but do not shed. if host immune system is suppressed, infection flares up. we see this with renal transplants - recipients can die when their immune systems are suppressed, because of parasitic infections flaring up. s.westeri is seen in very young horses, and is cleared rapidly pigs - experimentally induced infxn in one pig is causing awful watery diarrhea, and stunted growth. diagnosis/signs: early signs when lungs are involved: coughing, anorexia, diarrhea heavily infected animals: wt loss, dehydration, death eggs in feces have very thin shell. in most species we see eggs that are uniformly embryonated. in S.stercoralis eggs develop so rapidly that larvae have already hatched when feces are passed. so you see L1 in feces. in dog, a number of species may appear as larvae. one thing to use to ID this worm is the genital rudiment which is very prominent in this larva. also called genital primordium. it pushes the gut aside and is bean shaped. also, a rhabditiform esophagus, which has a characteristic bulge at the distal end, and is pretty short. has a tiny dimple of a mouth. yesterday we stopped short of control when we spoke of hookworms. since this is another geohelminth we'll discuss control for both now. control is similar, anyway. also for ascarids although eggs are more resistant than larvae. most important: most likely to be concerned about - chemotherapy. treatment not to worm one animal for its sake, but to interrupt the life cycle and to limit the number of transmission into environment (eg herd health). also environmental sanitation - removal feces whenever practical. often manure removal is not practical or financially acceptable, but it is helpful. these larvae are susceptible to drying, so removal of shade and creation of dryness is important. remember - grass can provide shade for a larva that's this small. so, say, on a feedlot, you want to stop dripping taps, make better drainage, etc. provide appropriate dry bedding. destruction of larvae in environment, though, usually not an option - resistant to chemicals. but textbooks say to control hookworm larvae you can put out borax, 10 lbs/100 feet, raked into soil and watered in. that will kill the lawn, though, so that's a tradeoff. heat - in zoos, steam generators can be used which is very effective even against ascarid eggs. also horticultural devices can flame the surface. finally, if dogs are on heartworm prophylaxis, eg ivermectin plus pyrantel or milbemycin, that will kill hooks, ascarids, strongyloides as they enter the host. ---end----