Biology 625
ANIMAL PARASITOLOGY
Fall semester lecture note outline

Updated: 05 March 2002

1. Diverse group, with monoxenous and heteroxenous species
2. Most tend to be fairly large
3. Most with simple, muscular esophagus
4. Often many papillae on male tail
5. Usually, male copulatory spicules of equal length or nearly so

Superfamily: Ascaridoidea

1. Medium to large worms
2. 3 lips
3. Generally in stomach or intestine
4. Species infected either by ingestion of eggs containing infective L2 or L3 larvae, or by ingestion of L2 or L3 larvae dormant in an intermediate or paratenic host
5. Significant confusion exists for many species whether the L2 or L3 is the infective stage in the egg. Thus, textbooks will differ concerning this point.
6. Many species heteroxenous, whereas others have a lung migration which is thought to be a residual portion of a heteroxenous life-cycle
7. Intermediate hosts, when present, tend to be vertebrates
8. Family: Anisakidae is comprised of species parasitic in aquatic animals (fish and marine mammals) or piscivorous birds
9. Family: Ascarididae is comprised of species parasitic in terrestrial hosts. Transmission may require terrestrial invertebrates, or small mammals as paratenic or intermediate hosts. Some species have eggs directly infective for the definitive hosts.

Anisakis simplex (Family: Anisakidae)

1. Definitive hosts many species of cetaceans and some pinnipeds
2. Eggs out with feces; embryonate in sea water
3. L2s emerge and drift in plankton
4. Crustacea such as shrimp are the intermediate hosts where L3s develop; fish and cephalopods serve as paratenic hosts
5. Cetaceans become infected after ingesting fish
6. Similar species
   1. Contracaecum spp. (in stomach of piscivorous birds and mammals; copepods and many other invertebrates serve as intermediate hosts; fish paratenic hosts
   2. Pseudoterranova kogiae in the pygmy sperm whale, P. ceticola in the dwarf sperm whale; P. decipiens in the stomach of pinnepeds. Life-cycle is a bit more complex than Anisakis. Basically, invertebrates serve as intermediate hosts; fish serve as paratenic hosts
7. When an abnormal host ingests one of these larval nematodes, such as a human, the larvae can often survive
   1. Non-invasive, resulting in a tingling of the throat sensation as the worms migrate up the esophagus; often coughed up (most often genus Pseudoterranova)
   2. Invasive, where larvae attach, embed, and sometimes perforate the gut (most often genus Anisakis)
8. Good review of anisakiasis (1989, Clin Microbiol Rev 2: 278-284). Sushi anyone?

Ascaridia galli (Family: Ascarididae)

1. Definitive host chickens
2. Eggs containing larvae ingested; no lung migration; direct development into adults in small intestine, however, L3s burrow into gut and molt into L4s; can be extensive intestinal ulceration

Ascaris suum (Family: Ascarididae)

1. Definitive host swine
2. Eggs containing L3 larvae ingested; undergoes lung migration; up trachea; swallowed; L4 then adults develop in gut (many articles and books erroneously give the L2 as the stage infective in the egg)
3. Similar species, Ascaris lumbricoides in humans
4. I ran across a bunch of ancient "remedies" that employed roundworms. Here are a few I jotted down
   1. in China, one remedy for eye lesions called for acquiring 1 Ascaris vomited by a child, drying it in a shaded place, grinding it into a powder, mixing it with Calomel powder, and applying it to the lesion. Sounds odd, but Calomel powder contains mercurous chloride so the power itself might serve as a disinfectant.
   2. also in China, for lip sores, acquire 1 Ascaris from a latrine. Fasten it with needles at both ends onto a wooden board. The worm is then slit lengthwise using a piece of sharpened bamboo. After washing the worm well, it is baked on a tile over a fire. Then, its' ground into a powder and camphor is added. This mixture is then applied to the wound. Hey! Camphor is derived from the Camphor tree and contains terpene, which is used today to help prevent lip sores!
   3. And, this third one from China, is just plain bizarre. A real sadist must have thought this one up. It's a recipe to cure male impotence and I wrote down the formula from this old book I was thumbing through. The author even figured out the appropriate species for the common names of the plants:
      1. 1 Ascaris baked on a tile
      2. 15 seeds of Luffa cylindrica
      3. 5 fen (1 fen=0.36 grams) of Boswellia
      4. 4 fen of Balsamodendron myrrha
      5. 7 seeds of almond, with the oil extracted
      6. 5 fen musk
      7. 5 fen camphor
      8. grind it all into a powder. Mix with grease and roll it up into small pills. Prior to coitus, insert 1 pill into the urethra of the male to help enlarge and prolong the erection. Thank goodness for viagra.

Baylisascaris procyonis (Family: Ascarididae)

1. Definitive host raccoons AND sometimes canids
2. Females produce 115,000 to 180,000 eggs per day
3. Eggs may remain viable in environment for 12 or more years
4. Life-cycle in young animals
   1. Eggs with infective L2 larvae ingested (from contaminated soil, mothers teats, or from within den)
   2. Larvae hatch and enter mucosa; several weeks of development and re-emerge
   3. Mature into adult worms in about 2 months
5. Life-cycle in immune animals and juvenile raccoons
   1. Raccoons expel larvae hatching from ingested eggs
   2. Eggs with infective larvae ingested by various mammals and birds
   3. Larvae migrate through body of these hosts, often causing extensive damage including neurological problems.
   4. Larvae in non-avian hosts become dormant often (in birds, few somatic larvae and most parasites go directly to the CNS)
   5. Infected host eaten by raccoon
   6. Worms remain in gut of raccoon and do not invade mucosa
   7. Adult worms develop in gut of raccoon, 32-38 days
6. Naturally infected raccoons normally shed 20,000 to 25,000 eggs per gram of feces per day; reports of over 250,000 eggs per gram of feces have been reported
7. In some areas, seasonal cure reported. Most worms voided January - February and new infections picked up in late Spring and Summer. Highest worm intensities September - November.
8. Pathology
   1. Usually no clinical signs in raccoons
   2. Over 1,000 worms have been recovered from a single raccoon
   3. Over 10 cases of fatal CNS disease have been recorded from children, and this is most likely a small fraction of the true number of cases
   4. Mortality in Zoos because of raccoon latrines on Zoo property. Some animals are very susceptible even to 1-2 migrating larvae. These include ratites, psittaciformes, and many other types of birds, small primates, rodents, and rabbits.
   5. Most common problem in humans ocular larval migrans
   6. Livestock, felids, raptors, shrews, and oppossum very resistant to larval migrans
   7. Extirpation of woodrats in portions of the NE USA have been linked to fatal CNS disease because of rodent foraging in raccoon latrines
   8. This is a very dangerous parasite and it is likely an increase in human and domestic animal mortality will be noted unless raccoon populations are controlled in urban areas
9. Huge numbers of eggs are concentrated in raccoon latrines, which are common areas of defecation for raccoons. These areas tend to be on large logs, stumps, tree limbs, woodpiles, old barns, decks, roofs, attics, etc. Millions of infective eggs can be found in small soil samples from these areas.
10. Similar species, Baylisascaris columnaris in skunks; Baylisascaris melis in badgers; Baylisascaris trasfuga in bear

Parascaris equorum (Family: Ascarididae)

1. Definitive host equids
2. Eggs containing L3 larvae ingested; undergoes lung migration; up trachea; swallowed; L4 then adults develop in gut; may cause gut perforation

Toxocara canis (Family: Ascarididae)

1. Definitive host canids
2. Life-cycle
   1. Adults in gut
   2. Unembryonated eggs out with feces
   3. Embryonate in environment
   4. Ingested by canid
   5. In young animals, a lung migration; larvae molt to L3 in lung; up trachea; swallowed; molt 2x and adults develop in gut
   6. In older dogs, larvae exit from eggs and cross gut mucosa; may wander through body and not complete migration; L2s can become dormant in tissues
   7. Larvae can enter offspring during lactation by being reactivated during lactation
   8. Rodents and other hosts can harbor dormant larvae and serve as paratenic hosts
   9. Unborn pups can be infected in utero; worms undergo lung migration in fetus and puppies can be born with adult worms in their intestines
3. Similar species, Toxocara cati in felids. Many isolates with no lung migration and only enter intestinal wall to molt; no prenatal infections

Superfamily: Cosmocercoidea (3 families; no need to learn)

1. In gut of amphibians and reptiles
2. Typical genera Cosmocerca, Cosmocercoides, Cruzia, Falcustra

Superfamily: Heterakoidea

1. Intestinal parasites with prominent preanal sucker surrounded by a cuticularized ring
2. Eggs embryonate in environment; infective larvae develop inside; eggs simply ingested by new host
3. Most species in birds; some in amphibia and reptiles
4. Typical species
   1. Heterakis gallinarum (Family: Heterakidae)
      1. Caecal nematode of chickens and turkeys
      2. Eggs can be picked up by arthropods, and then can infect chicken when bird ingests arthropod with eggs
      3. Eggs can harbor Histomonas meleagridis
   2. Ascaridia galli (Family: Ascaridiidae)
   3. In small intestine of galliform birds
   4. Earthworms can harbor infective eggs