canine and feline parasites ,git, fv,cestoda. nematoda
TRANSCRIPT
1. Canine and feline parasitesGIT
Cestoda Nematoda
Family: Taeniidae
The Taeniidae are usually large tapeworms. The gravid proglottids are longer than they are wide.The rostellum may be absent, but it usually present and armed witha double row of hooks.
The larvocysts ( metacestodes) are:
• Cysticercus
• Strobilocercus
• Coenurus
• Echinococcus (hydatid cyst)
Taeniidae of the carnivores
Species host size IH larvocyst______________________________________________________________Taenia hydatigena dogs,wolwes ruminants, Cysticercus
wild carn. to 600 cm pigs taenuicollis
T. ovis dogs, wild carnivores 100 – 200 cm sheep,goats C. ovis
T. pisiformis dog, fox and to 200 cm lagomorph C. pisiformiswild carn. (rabbits,hares)
T. krabbei wild carnivores, 30 cm reindeer, gazelle C.tarrandidogs
T. taeniaeformis cats, felidae 60 cm rodents,lagomorph C.fasciolaris(strobilocercus)
T. multiceps dog,fox,coyote 40 – 100 cm sheep, goats ( Multiceos multiceps) human Coenurus cerebralisT. serialis dog, fox 75 cm lagomorph,
human Coenurus serialis
Species host size IH larvocyst_____________________________________________________________Echinococcus granulosus carnivores 2 – 7 mm ungulates,man echinococcus
hydatid cyst
E. multilocularis fox, dogs, cats 1.5 – 5 mm rodents,man alveococcuspigs
E. oligarthus wild felids 1.9 – 3 mm rodents polycystic(agouti) hydatid cyst
E. vogeli bush dogs 3.9 – 5.6 mm rodents polycystic (pacas) hydatid cyst
Taenia hydatigena
Distribution: cosmopolitan
Host: small intestine of dogs, wolves
IH: domestic and wild ruminants,pigs
Morphology: up to 6 m, rostellum with 33 - 44 hooks
Taenia ovisDistribution : cosmopolitan
(higly economic important in
Australia, New Zeland)
Morphology: up to 200 cm
scolex , rostellum with hooks
IH : sheep, goats, skeletal and cardiac musculatures Cysticercus ovis, heart, diaphragm, masseters appear to the predilection sites.
Prepatent period in the dog : about 60 days
Taenia pisiformis
Distribution: cosmopolitan
Host: small intestine of dogs, wolves
IH: lagomorph, rodents
Morphology: up to 200cm, rostellum with
34 – 48 hooks
Life cycle
In the IH oncosheres develop in the liver
( 15 – 30 days) migrate to the peritoneal cavity C. pisiformis
Pathogenesis
For the IH – severe damage to the liver and death can result. Light infections may result in digestive disturbances and loss of condition.
Cysticercus pisiformis
Taenia taeniaeformis
Morphology : up to 60 cm
Urban cycle : involves domestic cat ( FH) and house and
field mice and rats ( IH)
Sylvatic cycle: bobcats ( North America) ( FH) and wild
rodent ( IH)
After 30 – 42 days Cysticercus fasciolaris
(Strobilocercus) developes
Taenia taeniaeformis
Scolex
strobilocercus
Taenia multiceps
Morphology: up to 1 m,
FH – dogs and CanidaeIH – sheep, goats, human ( till know 54 cases – Africa, France, England, USA)
Coenurus cerebralis – 5 cm and more After 6-8 months in the brain and spinal cord
Taenia serialis
Taenia serialis
• Morphology: up to 72 cm,
• FH – dogs and Canidae
• IH – lagomorph, in subcutaneous
and intramuscular connective tissues Coenurus serialis – 4 cm or larger
Life cycle
Taenia krabbei
• FH: wolves, coyotes, dogs, bobcat, lynx, black bear and grizzly bear
• IH: herbivore (red deer, moose,wapiti (elk), caribou,mule deer ) Cysticercus tarandi
Echinococcus
• Echinococcus granulosus
• Echinococcus multilocularis Echinococcus vogeli
• Echinococcus oligarthus
Echinococcus granulosus
Echinococcus multilocularis
Echinococcus multilocularis
• FH: red fox and other carnivorous
• IH: small rodents (Arvicola terrestris ), human, pig, ruminants
Prepatent periode : < 26 days !
Patent periode : 1.5 – 4 months
Echinococcus multilocularis
40 – 45 days
Alveolar cyst in IH
Treatment and preventionCarnivorous:In risk region 1x month dehelmintisation
praziquantel epsiprantel
Human: Surgical removing Long lasting chemotherapy
mebendazol a albendazol
Family: Dipyliidae
Dipylidium caninum
Localisation: Small intestine,dog, cat, fox, human
Morphology: up to 50 cm,
Life cycle
IH – 2 weeks
Prepatent periode
20 days
Dipylidium sexcoronatum - cats
Joyeuxiella
Diplopylidium
• Dog. Cat Midle East, Africa
• Eggs in capsule ( i egg)
• IH : 1. IH beetles
2. IH reptiles, small mammals
Family: Mesocestoididae• Small cestodes
• Scolex with 4 suckers, no rostellum
Life cycleMesocestoides lineatus
egg
1.IH mites Oribatidae
cysticercoid
2.IH Reptiles, amphibia, birds, small mammals tetrathyridium
Pseudophyllida
• Diphylobothrium latum
Diphylobothrium latum - eggs
eggs: 75 x 45 µm
Production of eggs: milions per day
NEMATODA
OESOPHAGUS
Spirocerca lupiMorphology: stout, spirally coiled, reddish, 3 – 8 cm long worms
found in large tumour- like granulomas in the wall of the oesophagus or stomach of dogs, wild canids and occasionally cats.
FH – Canidae ( dog, fox, wolf, coyote)occasionally cat
IH – coprophagous beetlesOntophagus sellatus, O. novaki, O. similis
Paratenic hosts – lizards,poultry, birds, rodents, reptiles
Eggs: oval, thin-shelled, small 30 – 40 um
Life cycle• egg – eaten by a beetle – L3• If a paratenic host eats the beetle the larva will encyst in some organ
of this host.
• When the dog eats the beetle or paratenic host the larva penetratesthrough the stomach wall, and migrates in the arteries, eventuallyreaching the thoracic aorta in about 3 weeks.
• After about 10 to 12 weeks in the aorta the larva will migrate to theesophagus where it forms a cystic nodule which is connected by a fistula to the lumen of the esophagus.
• Here it develops to the adult stage. Eggs are laid in the cyst, pass outto the lumen of the esophagus and pass out with the feces.
• The prepatent period is between 5 and 6 months.
Pathogenesis, clinical signs
• Infection and lesions are frequently inaparent• The migrating larvae may cause inflammation and scarring of
the internal wall of the aorta, stenosis, aneurysma, rupture of the oesophagus
• Adults worms usually cause markedly protruding granulomasof pigeon-egg or nut size with opening to the oesophageal lumen in the wall of the thoracic region of the oesophagus
• Occasionally the granuloma may cause hindered swallowing (dysphagia), vomiting, oesophageal obstruction,progressive debilitation,cachexy, death
• Secondary pulmonary osteoarthropathy
• Spirocerca lupi has been associated with aortic and oesophageal sarcoma in dogs
Spirocerca lupi granuloma adjacent to aorta Aortic aneurysms due to Spirocerca lupi
Oesophageal spirocercosisSpirocerca lupi granuloma in kidney
Spirocerca lupi granuloma next to aorta Spirocerca lupi in oesophagus
Spirocerca lupi in wall of aorta
Diagnosis• not easy. The eggs are tiny, and are only laid at irregular
intervals, and repeated faecal samples are required. If the dog is vomiting, or if saliva samples can be collected, these can also be examined for eggs.
• Direct examination, using endoscopy, or radiography as well, can show the nodules if large enough.
Treatment
» Avermectins ( min. 10 days)
STOMACH
•Ollulanus tricuspis
•Physaloptera spp
StrongylidaFamily: OllulanidaeGenus: Ollulanus
• Adult worms live in the stomach and may burrow into the gastric mucosa.
• The eggs hatch while in the female and develop to the infectious third-stage larvae (L3), which is released into the lumen of the stomach. The L3 may continue its development to the L4 and adult stage in the same cat or it may be carried into the environment in parasite-induced vomitus.
• The L3s may live in the vomitus for up to 12 days. If the L3s in the vomitus are ingested by a suitable host they will develop to adults in the stomach. The prepatent period (the time from when the L3s enter the host till the next generation of L3s is born) is about 33 to 37 days. Larvae which pass into the intestine die and are digested
Ollulanus tricuspis
• Clinical signs• Vomiting minutes to a few hours after eating is a common sign. The
females are viviparous, so massive infections can build up endogenously. Transmission is via vomitus, catarrhal gastritis in cats.
• Diagnosis is by microscopic demonstration of worms in the vomitus. The use of a Baermann apparatus enables the separation of the worms from ingesta, after which they are easier to observe.
• Therapeutic efficacy in cats has been demonstrated with fenbendazole (20-50 mg/kg, PO, sid for 3 days) and levamisole (5 mg/kg, SC, once), although these are not approved treatments.
Dg: The L3, L4 or adults in the vomitus.
Order: SpiruridaFamily: PhysalopteridaeGenus: PhysalopteraPhysaloptera spp
• Several species of these stomach nematodes of dogs and cats are
seen throughout the world.
• They are usually firmly attached to the gastric or duodenal mucosa. The males are ~30 mm and the females ~40 mm long. The eggs are
oval, 32 × 55 µm, thick-shelled, and larvated.
Life Cycle:
• The egg, containing the infective first stage-larva, is passed in the feces and eaten by a beetle larva.
• The larva develops to the infective third stage larva. The dog eats the beetle and the worm develops to the adult stage in the stomach. Eggs are laid in the stomach and pass out with the feces.
• Encysted infective larvae of Physaloptera spp have been found in several species of insects, including beetles, cockroaches, and crickets.
• Mice and frogs may be paratenic hosts. After the dog or cat ingests the intermediate or paratenic host, development of larvae to adults is direct.
• These parasites may cause gastritis or duodenitis, which can result in vomiting, anorexia, and dark feces. Bleeding, ulcerated areas remain on the gastric mucosa when the parasites move to other locations; in heavy infections, anemia and weight loss may develop.
• Gastroscopy is the most efficient means of diagnosis, and immature worms are often found in the vomitus of puppies or kittens. The eggs are difficult to find in feces because they do not readily float.
•
Treatment• In cats, pyrantel pamoate (5 mg/kg, PO, 2 doses 2-3 wk apart;
20 mg/kg, PO, once) and ivermectin (0.2 mg/kg, SC, once) can be used for Physaloptera infections.
•
• In dogs, fenbendazole (50 mg/kg, PO, sid for 3 days), pyrantel pamoate (5 mg/kg, PO, once; 15 mg/kg, PO, 2 doses 2-3 wk apart; 20 mg/kg, PO, once), and ivermectin (0.2 mg/kg, PO, once) can be used.
Lesion [Stomach of dog]
Gnathostoma spinigerum,G. hispidum
• FH - cat and carnivora „gastric tumor“
• IH1 – water crustaceans
• IH2 and paratenic host – fresh water fish, amphibians,reptiles, birds, mammals
Life cycle• In FH (pigs, cats, dogs, wild animals) - adult worms reside in a
tumor which they induce in the gastric wall
• eggs ( unembryonated) when passed in the feces • Eggs - L1 - ingested by crustacean (Cyclops, first intermediate
host) - L2
• In IH 2 ( fish, frog, or snake) L2 migrate into the flesh and develop into L3
• When the IH2 is ingested by a FH, L3 develops into adult parasites in the stomach wall
Life cycle• Alternatively, the IH2 may be ingested by the paratenic host
(animals such as birds, snakes, and frogs) in which L3 do not develop further but remain infective to the next predator
• Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops .
Life cycle
Life cycle
SMALL INTESTINE
ASCARIDARoundworm diseases of carnivores
Toxocara canis Toxocara cati Toxascaris leonina
• Most common worm parasite of dogs
– 10-40% of adults and 70% of puppies have the worm, but may show no clinical signs
– There are no specific breed susceptibilities
• 2-10% of Western Europeans have at some time been infected by this worm’s larvae
• The larva is the main cause of visceral larva migrans
• Geographic Distribution: Worldwide
• Definitive host: Dogs and foxes
• Paratenic host: Mice and other mammals (not needed), birds
• Accidental host: Humans
Alae are long and narrow, prominent in both sexes
•Males are 4-6 cm in length•Females are 6.5 to more than 15 cm in length
Morphology of Adult Worm
Morphology of Eggs
•Eggs are brownish in color and almost spherical
•They have surficial pits which make them sticky, allowing them to be transported long distances
•They are unembryonated when laid
•They can survive 2-4 years in cool, moist conditions
Toxocara canis
Life Cycle
• Toxocara canis has a complex toxocaroid life cycle. • Dogs may become infected by four routes:
• Direct transmission, by ingesting infective eggs.
• Paratenic host transmission, by ingesting infected mice.
• Transmammary transmission in which nursing pups ingest L3s in their mother's milk.
• Prenatal transmission where pups are born infected as a result of L2s migrating from tissue reservoirs in the pregnant bitch - across the placenta and through the umbilical vein to the fetal liver, where they remain until birth. They then resume migration to the lungs of the newborn pups.
Toxocara cati
Life Cycle• The lifecycle of T. cati, while complex, is different from that of T. canis in five important ways:
• Paratenic hosts, such as mice, play a more significant role in the life cycle of T. cati because of the more aggressive predatory nature of cats.
• Prenatal infection does not occur in the lifecycle of T. cati.
• A high percentage of larvae (hatching from ingested infective eggs) undefgo tracheal migration, even in older, mature cats.
• Transmammary transmission is the major route of infection for T cati in kittens. Tissue larvae and larvae acquired during pregnancy will migrate to the mammary glands of lactating queens and be available for nursing kittens throughout the entire lactiation.
• A wide range of other animals, in addition to mice, may also serve as paratenic hosts. These include chickens, earthorms, and cockroaches.
Toxocara canis life cycle Toxocara cati
Clinical signs
Deworming programme
Toxocara canis
After treatment
Hookworms
• Strongylida
• Ancylostomatidae
• Ancylostoma caninum is the principal cause of canine hookworm disease in most tropical and subtropical areas of the world.
• A. tubaeforme of cats has a similar but more sparse distribution.
• A. braziliense of dogs and cats is sparsely distributed from Florida to North Carolina in the USA.
• Uncinaria stenocephala is the principal canine hookworm in cooler regions; it is the canine hookworm in Canada and the northern fringe of the USA, where it is primarily a fox parasite.
• U. stenocephala also is seen in cats.
• A. caninum males are ~12 mm long, females, 15 mm; the other species are somewhat smaller.
• The infective larvae of canine hookworms, particularly those of A braziliense , may penetrate and wander under the skin of people and cause either cutaneous larva migrans or eosinophilic enteritis.
• The elongate (>65 µm), thin-walled, hookworm eggs in the early cleavage stages (2-8 cells) are first passed in the feces 15-20 days after infection;
• Life cycle
• Eggs complete embryonation and hatch in 24-72 hr on warm, moist soil.
• Transmission may result from ingestion of infective larvae from the environment or, in the case of A. caninum , via the colostrum or milk of infected bitches.
• Infections with either A caninum orA. braziliense can also result from larval invasion through the skin, but this
route is of little significance for U. stenocephala .
Life cycle• Skin penetration in young pups is followed by migration of the
larvae through the blood to the lungs, where they are coughed up and swallowed to mature in the small intestine. However, in animals >3 mo old
• A caninum larvae, after migration through the lungs, are arrested in the somatic tissues. Arrested development may also occur in the mucosa of the small intestine.
• These arrested larvae are activated after removal of adult worms from the intestine or during pregnancy when they accumulate in the mammary glands.
Clinical signs:
• An acute normocytic, normochromic anemia followed by hypochromic, microcytic anemia in young puppies is the characteristic, and often fatal, clinical manifestation of A caninum infection. Surviving puppies develop some immunity and show lesser clinical signs.
• Nevertheless, debilitated and malnourished animals may continue to be unthrifty and suffer from chronic anemia.
• Mature, well-nourished dogs may harbor a few worms without showing signs;
• they are of primary concern as the direct or indirect source of infection for pups. Diarrhea with dark, tarry feces accompanies severe infections. Anemia, anorexia, emaciation, and weakness develop in chronic disease.
Clinical signs:• Dermatitis due to larval invasion of the skin may be seen with
any of the hookworms but has been seen most frequently in the interdigital spaces
• U. stenocephala . Pneumonia and lung consolidation may result from overwhelming infections in pups
Ancylostoma caninum
Larva migrans cutanea
AcanthocephalaOncicola canis
• Oncicola canis are rarely found in the small intestine of dogs and cats in the western hemisphere. They are white and ~12 mm long, and their thorny heads are embedded in the mucosa. The females lay brown, thick-shelled, embryonated, wide oval eggs (45 × 65 µm).
• The life cycle is not completely known, but it is thought to include an arthropod intermediate host and paratenic hosts such as turkeys or armadillos. Most infections cause no clinical signs.
Macracanthorhynchus ingens• Macracanthorhynchus ingens , naturally a parasite of raccoons, is
occasionally found in dogs. The usual observation is of a large (8-12 cm), white, wrinkled worm passed in the feces.
• The life cycle requires a millipede as an intermediate host, but other animals may serve as paratenic hosts.
• No clinical signs have been definitively associated with the infection.
• The eggs look similar to those of Oncicola canis but are larger (~50 × 100 µm). Diagnosis of patent infections is unlikely because experimentally induced infections did not persist after 1-12 days of patency. No treatment is necessary.
Cecum, colon
• Adult Trichuris vulpis are 40-70 mm long • They commonly inhabit the cecum of dogs where they are firmly attached to
the wall, with their anterior end embedded in the mucosa. Thick-shelled eggs with bipolar plugs are passed in the feces and become infective in 2-4 wk in a warm, moist environment.
• Trichuris vulpis, egg
• Although eggs may remain viable in a suitable environment for up to 5 yr, they are susceptible to desiccation
• . • The life cycle is direct. After infective eggs are ingested, the larvae develop in
the jejunal wall, and the adults mature in the cecum in ~11 wk. They may remain for up to 16 mo.
Whipworms, Trichuris vulpis
Pathogenity• Trichuris spp. are probably blood feeder
• Trichuris spp. have a mouth stylet, projecting through their mouth opening
• The adults tunnel into the intestinal mucosa with their anterior ends and the stylet is used to enter vessels or lacerate tissues creating pools of blood which the nematodes ingest ( dogs, pigs)
Clinical Signs:
• Light infections are asymptomatic.
• Bouts of diarrhea, often with large amounts of mucus and some frank blood on the stool, are seen in heavy infections.
Treatment
• fenbendazole, flubendazole, mebendazole, milbemycin, and the combination formulations praziquantel/pyrantel/febantel, pyrantel/febantel, and pyrantel/oxantel.
• Treatment should be repeated 3 times at monthly intervals because of the long prepatent period. Finally, milbemycin oxime, milbemycin/lufenuron, and diethylcarbamazine/oxibendazole, when administered for heartworm prevention, are also approved for control of T.vulpis
Trichuris vulpis
Drug/Drug Combination
Dog Cat
Dichlorophene 200 mg/kg, PO (UK) 220 mg/kg, PO (USA) 200 mg/kg, PO (UK)
Dichlorvos 27-33 mg/kg, PO for adults (extra-label) 11 mg/kg, PO for all ages (USA)
11 mg/kg, PO (USA)
Diethylcarbamazine citrate
55-110 mg/kg, PO; repeat 10-20 days later (USA, CAN)
55-110 mg/kg, PO; repeat 10-20 days later (CAN)
Diethylcarbamazine citrate + oxibendazole (daily HW)
6.6 mg/kg + 5 mg/kg, respectively, PO (USA)
Epsiprantel 5.5 mg/kg, PO (USA, CAN) 2.75 mg/kg, PO (USA, CAN)
Fenbendazole 50 mg/kg, PO, sid for 3 days (USA, CAN, UK) 100 mg/kg, PO for adults (UK)
50 mg/kg, PO, sid for 3 days (UK) 100 mg/kg, PO foradults (UK)
Flubendazole 22 mg/kg, PO, sid for 2 days for roundworms and hookworms; sid for 3 days for Trichuris vulpisand Taenia pisiformis (UK)
22 mg/kg, PO, sid for 2 days for roundworms and hookworms; sid for 3 days for Taenia taeniaeformis (UK)
Drug/Drug Combination
Dog Cat
Ivermectin (monthly HW)
0.024 mg/kg (USA, CAN)
Ivermectin + pyrantel (monthly HW)
0.006 mg/kg + 5 mg/kg, respectively, PO (USA, CAN)
Mebendazole 50-200 mg total, PO, bid for 2-5 days; depends on age and weight (UK)
50-200 mg total, PO, bid for 2-5 days; depends on age and weight (UK)
Milbemycin oxime (monthly HW + therapy)
0.5 mg/kg, PO (USA, CAN, UK) 2.0 mg/kg, PO (USA, CAN)
Milbemycin oxime + lufenuron (monthly HW)
0.5 mg/kg + 10 mg/kg, respectively, PO (USA, CAN, UK)
Moxidectin 0.17 mg/kg, SC; 6-mo HW injectable (USA, CAN)
Nitroscanate 50 mg/kg, PO (CAN, UK)
Piperazine 55-62 mg/kg, PO for roundworms, re-treat 10 days after first treatment (USA, CAN); 80-100 mg piperazine hydrate/kg, PO for roundworms (UK); 120-240 mg piperazine hydrate/kg, PO for hookworms (UK)
55-62 mg/kg, PO for roundworms, re-treat 10 days after first treatment (USA, CAN); 80-100 mg piperazine hydrate/kg, PO for roundworms (UK); 120-240 mg piperazine hydrate/kg, PO for hookworms (UK)
Praziquantel Follow label dose PO, SC, IM (USA, CAN) 5 mg/kg, PO (UK) 5.68 mg/kg, SC, IM (UK)
Follow label dose PO, SC, IM (USA, CAN) 5 mg/kg, PO (UK) 5.68 mg/kg, SC, IM (UK) Follow label dose for topical formulation (UK)
Praziquantel + pyrantel
Follow label dose, PO (USA, CAN, UK)
Praziquantel + pyrantel + febantel
Follow label dose, PO (USA, CAN, UK)
Pyrantel 5 mg/kg, PO for dogs >2.3 kg (USA) 10 mg/kg, PO for dogs <2.3 kg (USA) 5 mg/kg, PO for all weights (USA, CAN, UK)
20 mg/kg, PO; repeat 7-10 days later (CAN) 5-10 mg/kg, PO; repeat 2 wk later (extra-label)
Pyrantel + febantel
14.4 mg/kg + 15 mg/kg, respectively, PO (UK)
Pyrantel + oxantel
5 mg/kg + 20 mg/kg, respectively, PO (CAN)