| Capillaria hepatica | |
|---|---|
 | |
| One of the plates published with the original description of the species, showing the masses of eggs in the liver of the host (above) and free alive eggs (below). | |
Scientific classification | |
| Kingdom: | Animalia |
| Phylum: | Nematoda |
| Class: | Enoplea |
| Order: | Enoplida |
| Family: | Capillariidae |
| Genus: | Capillaria |
| Species: | C. hepatica |
| Binomial name | |
| Capillaria hepatica Bancroft, 1893 | |
Capillaria hepatica is a parasiticnematode which causeshepatic capillariasis in rodents and numerous other mammal species, including humans.[1] The life cycle ofC. hepatica may be completed in a single host species. However, the eggs, which are laid in theliver, must mature outside of the host body (in the environment) prior to infecting a new host.[1] Death and decomposition of the host in which the adults reach sexual maturity are necessary for completion of the life cycle.
This species was first described in 1893, from specimens found in the liver ofRattus norvegicus, and namedTrichocephalus hepaticus.[2] Various authors have subsequently renamed itTrichosoma hepaticum,Capillaria hepatica,Hepaticola hepatica andCalodium hepaticum.[3][4] Currently it is usually referred to as eitherCapillaria hepatica or, less often,Calodium hepaticum.[citation needed]
Adults are often found in dozens of rodent species, but also occur in a wide variety of other wild and domestic mammals, and occasionally humans.[5][6]C. hepatica has been found in temperate and tropical zones on every continent and infestation rates of wild-caught rats of up to 100% have been reported.[1][7]
Usually,Capillaria hepatica is found in rodents, monkeys and other animals.Capillaria hepatica is rarely found in humans and at least 40 cases have been reported. There are no endemic areas of infection withC. hepatica and human infection primarily results fromzoonotic transmission.[8]
Of the human infections, most have been found in children under the age of 5.[9]
The tissueniche of this parasite is theliver. The adult females will deposit eggs in theparenchyma of the liver. Occasionally in humans larvae will migrate to the lungs, kidneys and other organs.[1]
Adult worms take the shape of a slender nematode, with the anterior part of the body narrow and the posterior part gradually swelling.[10] The females measure about 53–78mm x 0.11–0.20mm, but the males are approximately 24–37mm x 0.07–0.10mm.[10] The adult worms are rarely seen intact, as they mature and die in the parenchyma of the liver.[11] The adult females lay eggs that are about 48-66μm x 28-36μm.[10] The shell of the eggs is striated with shallow polar prominences at either end. Numerous mini-pores can be seen in the outer shell as well. Unembryonated eggs may be ingested by a carnivore, in which case they are harmless and pass out in the feces. Eggs will embryonate in the environment, where they require air and damp soil to become infective. Under optimal conditions this takes about 30 days. Larvae are juvenile versions of the adult worm.[1]
Hosts ingestC. hepatica eggs (from sources outlined below) which hatch into first stage larvae (L1). The L1 larvae bore through the intestinal wall and are carried to the liver by thehepatic portal vein. Development from the L1 stage to sexually mature adults occurs in the liver within 18–21 days.[1] Eggs are laid in the liver parenchyma of the host throughout the adult worm's life span, which lasts for about 30–40 days.[1] Up to 938,000 eggs have been reported from the liver of a single rodent host.[12]
The eggs in the liver exist in a state of arrested development – they are unable to develop into larvae until they spend some time outside of the host, in the environment. Escaping from the liver tissue may be accomplished either by the death and decomposition of the host's body, or by the consumption and digestion of the host by apredator orscavenger.[1] If the host is eaten, the eggs will pass into the environment in the feces of the predator or scavenger. In the environment, eggs require 4–5 weeks to develop, and may remain viable in a dormant state for several more months.[13] Once these "environmentally-conditioned" eggs are eaten by a suitable host, the first stage larvae (L1) hatch in the intestine and continue the life cycle. Humans are usually infected after ingesting embryonated eggs in fecal-contaminated food, water, or soil.[1]
In humansCapillaria hepatica causes hepaticcapillariasis, a serious liver disorder.[14] The nematode wanders through the host liver causing loss of liver cells and thereby loss of function.[8] However, as the adultC. hepatica begin to die in the liver tissue, their decomposition accelerates the immune response of the host.[15] This response leads to chronicinflammation andencapsulation of the dead worms incollagen fibers, and eventually to septalfibrosis (abnormal connective tissue growth) andcirrhosis of the liver.[16] The eggs that are left behind can become encased bygranulomatous tissue, with large sections of theparenchyma replaced by these egg masses.[14]C. hepatica can also causehepatomegaly. Infections ofC. hepatica can present with several clinical symptoms, including abdominal pain in the liver area, weight loss, decreased appetite, fever and chills,hepatitis (liver inflammation),ascites (excess fluid in the peritoneal cavity) andhepatolithiasis (gallstones in the bile ducts).[14]
This parasite can be fatal in humans, as transmission and survival of the parasite depend on death of thedefinitive host in order for the eggs to reach soil and water to embryonate.[8]
Diagnosis is made by finding eggs or adults ofC. hepatica in liver tissue from biopsy ornecropsy samples.[1] The encapsulated eggs and adults may appear as white nodules which measure 2–3mm in diameter on the surface and interior of the liver atautopsy.[17] Key identification features of this parasite are a double-layered,[18]: 941 striated shell and shallow polar prominences of the egg and a narrowing at anterior end and gradual swelling at posterior end of the adult worm. Identification ofC. hepatica eggs in the stool does not result from infection of the human host, but from ingestion by that host of livers from infected animals, the eggs will then pass out harmlessly in the feces.[1] Most cases have been determined after death because clinical symptoms resemble those of numerous liver disorders.[1]
Successful treatment of human cases withthiabendazole[19] oralbendazole (with or withoutcorticosteroids)[9] have been reported. Albendazole must be taken with food because a fatty meal will increase thebioavailability of the drug.[1]
Two ways of preventingC. hepatica infections in humans are to institute effective rodent control programs and to prevent dogs and cats from eating rodents.[8]
The firstpaleoparasitological record of human hepatic capillariasis was published in 2014.[20] Twocalcified objects recovered from a 3rd to 4th-century grave of an adolescent inAmiens (NorthernFrance) were identified as probablehydatid cysts. By using thin-sectionpetrographic techniques, probableCapillaria hepatica eggs were identified in the wall of thecysts. The authors claimed that hepatic capillariasis could be expected given the poor level of environmentalhygiene prevalent in this period. Identification of tissue-dwelling parasites such asC. hepatica inarchaeological remains is particularly dependent on preservation conditions andtaphonomic changes and should be interpreted with caution due to morphological similarities withTrichuris sp. eggs.[citation needed]
The selective liver damage byC. hepatica in rodents has been used in model systems to study the extensive regeneration capabilities of the mammalian liver,[21] and for testingantifibrotic drugs.[22]
C. hepatica has attracted interest for use inAustralia as abiocontrol of the house mouse,Mus musculus.[23] It has been moderately successful inSouthern Australia.[24]