Lagochilascaris minor Leiper, 1909
(Figures 4-39 through 4-43)
ETYMOLOGY:Lago (Hare) + Chil (Lip) + Ascaris; along with major (due to being larger than the previously described Lagochilascarisminor).
HISTORY: In 1909, Leiper described a new genus and species of ascaridoid nematode based on worms collected from subcutaneous lesions from the necks of two human patients in Trinidad. Sprent (1971) reviewed the genus and reviewed the 11 cases that had been reported from humans in Trinidad, Surinam, Tobago, Costa Rica, and Brazil. In these cases worms had been recovered from subcutaneous tissues of the neck, the mastoid porocess, from tonsils, and passed from the nose. In 1991, it was reported that there had been a total of 62 cases from around the world, and that 46 of these cases were from Brazil (Costa and Weingrill, 1991). Since that time additional cases have been reported from Surinam (Oostburg,, 1992); Brazil (Aguilar-Nascimento, 1993; Bento et al., 1993); Bolivia (Olle Goig et al., 1996); and Mexico (Vargas-Ocampo and Alvarado-Aleman, 1997). Lagochilascarisminor infection has been associated with fatal encephalopathy (Rosemberg et al., 1986; Orihuela et al., 1987). Volcán et al. (1992) performed experimental infections that incriminated the cat as a potential final host of this nematode.
GEOGRAPHIC LOCATION: All reports of natural infections have been in humans. Sprent (1971) summarized 11 cases from Tinidad, Tobago, Surinam, Costa Rica, and Brazil). More recent cases have included: Brazil (Bento et al., 1993); Bolivia (Olle-Goig et al., 1996); Mexico (Vargas-Ocampo et al., 1997); Surinam (Osostburg, 1992); Colombia (Botero and Little, 1984); and Venezuela (Orihuela et al., 1987). Two female worms recovered from the larynx of a bush dog (Speothosvenaticus) in Venezuela appeared to be Lagochilascarisminor (Volcán and Medrano, 1993). A species of Lagochilascaris was also found in the larynx of an ocelot (Felispardalismearnsi) in Costa Rica (Brenes-Madrigal et al., 1972).
LOCATION IN HOST: In humans, the worms have been recovered from subcutaneous abscesses in the neck, the inner ear, the mastoid process, the tonsil, and in the parenchyma of the brain. In the cats that have been experimentally infected worms have been recovered from the lungs, cervical region, larynx, pharynx, rhinopharynx, and in sacs at the base of the tongue. Eggs are passed in the feces of these experimentally infected cats. In the North American opossum, Didelphisvirginiana, the related species Lagochilascscarissprenti, is foun in excavations under the mucosa of the stomach (Fig. 4-38)
PARASITE IDENTIFICATION: Adults of Lagochilascaris tend to be rather small worms with the total length of the males being around 17 to 20 mm and the length of the females being around 18 to 21 mm. The worms are cream colored. The vulva of the female is located at or slightly behind midbody. The lips are a distinguishing feature in that the dorsal lip and each of the subventral lips have a deep central cleft in the anterior border that gives them the typical “hare-lip” appearance. The anterior end of the worm is constricted between the base of the lips and the body of the worm, and there is an inflation of cuticle on the anterior of the worm behind this indentation that has been termed a collar. Extending anteriad from the collar are prolongations called interlabia that protrude foward between each of the three lips. The eggs of Lagochilascaris are the feature that can most easily be used to distinguish Lagochilascaris major from Lagochilascarisminor. Although the eggs are similar in size (around 60 μm in diameter) and general appearance having a thickened brown shell, the eggs of Lagochilascarisminor have approximately 15 to 25 pits around the circumference while those of Lagochilascarismajor have approximately 33 to 45 pits around the circumference. It appears that the collar is more apparent on the anterior end of Lagochilascarisminor and that the lips of Lagochilascarisminor tend to be the same width or narrower than the collar while those of Lagochilascarismajor appear wider than the collar.
LIFE CYCLE: Volcán et al. (1992) and Campos et al. (1992) showed that the cat could be infected by being fed mice that had been infected for 40 days; both sets of workers also reported that cats were not infected when simply fed eggs containing infective-stage larvae (Fig 4-49). In the work of Volcán et al. (1992) eggs first appeared in the feces beginning 17 days after infection, and 9 of the 10 cats fed mice were positive by 40 days after infection. Campos et al. (1992) found that 9 to 20 days after the feeding of mice that adult worms were present within the esophagus, pharynx, trachea, and cervical lymph nodes. Also, in one cat that had been infected for 43 days that the lesion in the lungs and cervical region contained adults, eggs containing developing larvae, and hatched third-stage larvae in various stages of development; and they postulated that the auto-infective cycle that is characteristic of human lesions may occur in the cat (figs 4-40 to 4-43).
Freire-Filha and Campos (1992) found that some of the larvae given to mice in infective eggs were capable of developing to adults within cysts in the muscles. Similar growth of larvae to adults in cysts in the muscle of mice was reported for the related species Lagochilascarissprenti when eggs of this parasite of the opossum (Didelphisvirginiana) were fed to mice. The morphology of the larva of Lagochilascarissprenti that is typically found in the muscle of mice was described by Bowman (1987). The fact that Lagochilascarissprenti is typically found in the stomach wall of the opossum may indicate that the final host of Lagochilascarisminor has actually yet to be found.
CLINICAL PRESENTATION AND PATHOGENESIS: Cats show some signs of infection beginning nine days after being fed experimentally infected mice, i.e., slightly decreased motor activity, weak vocalizations, and frequent sneezing (Volcán et al., 1992). One of 10 experimentally infected cats developed a fistula in the posterior wall of the pharynx. A second cat developed destructive lesions at the based of the tongue with sacks that had inflamed walls and which contained mucus, eggs, and adult worms.
TREATMENT: Infections of humans with Lagochilascaris minor have proven refractory to treatment with anthelmintics. In humans the lesions may persist and living worms may be removed from the lesions for periods of several years. Treatment with high doses of diethylcarbamazine have apparently worked (de Leão et al., 1978), but have also been unsuccessful (Draper, 1963). Worms were recovered from this lesion for up to 10 years after the firfst diethylcarbamazine treatment (Sprent, 1971). Thiabendazole has worked in some cases (Oostburg, 1971), but has failed in other cases (Oostburg and Verma, 1968; Mondragon et al., 1973). Levamisole has apparently also worked on occasion (Santos et al., 1990) and failed on other occasions (Aguilar-Nascimento et al., 1993). Ivermectin has apparently has successfully treated one human case of infection (Bento et al., 1993).
EPIZOOTIOLOGY: The cat is probably not the normal final host of either Lagochilascarisminor or Lagochilascaris major. Interestingly, cats have not been reported as naturally infected with Lagochilascarisminor, infections in cats have been described as due to Lagochilascarismajor. The difference in pits on the circumference of the egg is a fairly easily discernable taxonomic character, suggesting that most diagnoses have been correct. Cats are probably acquiring their infections with these nematodes by the ingestion of intermediate hosts.
HAZARDS TO OTHER ANIMALS: Mice and agouti rats (Dasyproctaleporina) have been experimentally infected by the feeding of the eggs of this Lagochilascarisminor. In some mice, the larvae go onto develop into adults in abscesses within the musculature (Freire-Filha and Campos, 1992); similar growth of adults of Lagochilascarissprenti in the muscles of mice has also been described (Smith et al., 1983). The eggs passed in the feces require a period of days to become infectious, and thus, pose no threat when passed in the feces.
HAZARD TO HUMANS: Humans are considered the host most at risk for infections with Lagochilascaris minor. At this time, it is unclear how humans are becoming infected. They may be obtaining their infections by the ingestion of some improperly cooked meat and are mimicking a final host in a manner similar to the cat when fed the larvae of an infected mouse. On the other hand, humans developing lesions may be serving as some form of intermediate host, and like the mouse where worms develop to the adult stage in abscesses after the ingestion of eggs, the human may have acquired their infections by the ingestion of eggs containing infective-stage larvae.
CONTROL/PREVENTION: This infection will be prevented preventing cats from hunting.
REFERENCES:
Aguilar Nascimento JE, Silva GM, Tadano T, Valadares Filho M, Akiyama AMP, Castelo A 1993.Infection of the soft tissue of the neck due to Lagochilascaris minor Trans Roy Soc Trop Med Hyg 87:198.
Bento R F. Mazza C, Motti EF, Chan YT Guimaraes JRR, Miniti A. 1993. Human lagochilascariasis treated successfully with ivermectin: a case report. Revista do Instituto de Medicina Tropical de Sao Paulo 35:373-375.
Bowman D.D. 1987 Diagnostic morphology of four larval ascaridoid nematodes that may cause visceral larva migrans: Toxascaris leonina, Baylisascaris procyonis, Lagochilascaris sprenti, and Hexametra leidyi. J Parasitol 73:1198-1215..
Costa VR, Weingrill EC. 1991. Lagoquilascaríase. Report of the 12 Congress of the Brazilian Society of Parasitology, Encarte 13:5.
Campos DMB, Freire-Filha LG, Vieira MA, Paçôm JM, Moacir AM. 1992. Experimental life cycle of Lagochilascaris minor Leiper, 1909. Rev Inst Med Trop São Paulo 34:277-287.
Campos DMB, Freire-Filha LG. 1992. Consideraçoes sobre o desenvolvimento de Lagochilascaris minor Leiper, 1909 em camundongos isogênicos da linhagem C57B1/6. Rev Pat Trop 21:219-233.
Draper JW.1963 Infection with Lagochilascaris minor. Br Med J 1:931-932.
de Leão RN, Leao-Filho J, Brago-Dias L, Calheiros LB 1978. Human infection with Lagochilascaris minor Leiper, 1909. A case history from Para State. Rev Instit Med Tropde Sao Paulo 20:300-306..
Leiper RT. 1909. A new nematode worm from Trinidad: Lagochilascaris minor sp. n. Proc Zool Soc Lon 4:35-36
Mondragon H, Cano MR, Botero DR. 1973. Primer caso de infecciíon humana por Lagoichiascaris minor en Colombia. Antioquia medica 23:463-464.
Ollé-Goig JE. 1996. First case of Lagochilascaris minor infection in Bolivia. Trop Med Int Heal 1:851-853.
Oostburg BFJ. 1992. Thiabendazole therapy of Lagochilascaris minor infection in Surnam, a report case. Am J Trop Med Hyg 20:580-583.
Oostburg BFJ, Verma AAO. 1968. Lagochilascaris minor infection in Surnam, a report case. Am J Trop Med Hyg 17:548-550.
Orihuela R, Botto C, Delgado O, Ortiz A, Suarez JA, Arguello C. 1987. Human Lagochilascarisis infection in Venezuela. Description of a fatal case. Inst Med Trop, Venezuela 20:217-221.
Vargas-Ocampo F, .Alvarado-Aleman J. 1997. Infestation from Lagochilascaris minor in Mexico. Int J Dermatol 36:37-58.
Rosemberg S, Lopes MBS, Masuda Z, Campos R, Vieira Bressan MCR. 1986. Fatal encephalopathy due to Lagochilascaris minor infection. Am J Trop Med Hyg 35:575-578.
Santos VM. 1990. Relato de caso de infecçao humana por Lagochilascaris minor. An Bras Dermatol 65:189-192.
Smith JL, Bowman DD, Little MD. 1983. Life cycle and development of Lagochilascaris sprenti (Nematoda: Ascarididae) from opossums (Marsupialia: Didelphidae) in Louisiana. J Parasitol 69:736-745.
Sprent JFA. 1971. Speciation and development in the genus :Lagochilascaris. Parasitol 62:71-112.
Volcán GS, Medrano CE, Payares G. 1992. Experimental heteroxenous cycle of Lagochilascaris minor Leiper, 1909 (Nematoda:Ascarididae) in white mice and incats. Mem Inst Oswald Cruz, Rio de Janeiro 87:525-532.
Volcán GS, Medrano CE, Quiñones D. 1991. Infeccion natural de Speothos venaticus (Carnivora: Canidae) por estadios adultos de Lagochilascaris sp. Rev Inst Med Trop São Paulo 33:451-458.
FIGURES:
Figure 4-38. Lagochilascarissprenti. Section through the wall of the stomach of an opossum, Didelphisvirginiana, showing the adult worms living in the typical submucosal excavation.
Figure 4-39. Lagochilascarissprenti. Infective third-stage larva expressed from an embryonated egg. Note the pedunculated knob at the end of the tail.
Figure 4-40.Lagochilascarissprenti. Section through the muscle tissue of an experimentally infected mouse showing the larva within an eosinophilic granuloma.
Figure 4-41.Lagochilascarissprenti. Large cyst that developed on the cheek of a mouse experimentally infected with this worm.
Figure 4-42.Lagochilascarissprenti. When the lesion from the cheek was opened, it was found to contain an adult nematode.
Figure 4-43.Lagochilascarissprenti. Section through another large cyst in an experimentally infected mouse showning the presence of both a large cyst containing an adult female and two sectons through smaller cysts containing larvae.