Larval migration in oral and parenteral Toxocara pteropodis infections and a comparison with T. canis dispersal in the flying fox, Pteropus poliocephalus.

When eggs of T. pteropodis were fed in large doses to juveniles of a definitive host, Pteropus poliocephalus, larvae hatched throughout the gastrointestinal tract. The majority penetrated the mucosa of the distal half of the intestine, to reach the liver via the portal circulation. A few entered the lymphatics to eventually reach the liver by passing through the lungs and migrating tracheally or continuing in the systemic circulation. Patent infections did not develop. Eggs inoculated subcutaneously also hatched and larvae again reached the liver, travelling via the circulation through the lungs and often other tissues; again, some underwent tracheal migration. Infective larvae of T. canis, identical in size with T. pteropodis, passed through the liver and lungs and dispersed mainly to skeletal muscles, but with time gradually accumulated in the brain. These findings indicate that Toxocara larval distribution is not primarily influenced by larval dimensions but reflects goal-directed behaviour.

Observations on egg production by Toxocara pteropodis.

Studies in juvenile Pteropus poliocephalus showed an average daily egg production by Toxocara pteropodis of 25,000 per female, with concentrations of up to 16,000 epg. regardless of whether eggs were fertile or infertile. Production commenced as early as 35 and as late as 48 days post-partum and rose to plateau average levels over about 10 days. For 23 days one bat passed infertile eggs which, over 2 days, were then replaced completely by fertile eggs. The implicit delay in maturation of a male nematode suggests that transmammary passage of larvae to suckling bats may persist for at least 3 weeks. Patency was terminated by the spontaneous expulsion of worms. If male worms were lost first, the egg output converted from fertile to 100% infertile within 48 h and the females were devoid of spermatozoa, suggesting that T. pteropodis copulate at least once daily. In prolonged infections, worm fecundity and egg fertility diminished, so that females with stored spermatozoa were producing mixtures of fertile and infertile eggs.

Pathological and haematological responses of cats experimentally infected with Toxocara canis larvae.

Responses of eight adult cats to one or two infections with larvae of Toxocara canis were studied up to 39 days post infection (DPI). Clinically, all cats remained normal throughout the study. The major necropsy finding was multifocal, white to grey nodules mainly within the liver, lungs and kidneys; live larvae were found in liver nodules. Histologically, the nodules were eosinophilic granulomas. Granulomas containing a larval section were observed mainly within the liver. All infected cats had variably severe, eosinophilic arteritis and bronchiolitis and medial hypertrophy and hyperplasia of the pulmonary arteries. No inflammatory eye lesions were detected. Circulating eosinophil levels increased in all infected cats; peak values of 15,790 and 10,050 eosinophils microliters-1 were observed at 25 or 32 DPI in cats receiving a single or double infection, respectively. Bone marrow of all infected cats exhibited marked eosinophilic hyperplasia which did not correlate with the level of circulating eosinophilia. Thus, infection of cats by the larvae of T. canis causes disseminated eosinophilic and granulomatous disease with marked pulmonary artery and airway lesions.

Experimental infection of mice with Toxocara canis larvae obtained from Japanese quails.

The migration and distribution of Toxocara canis larvae in the tissues of Japanese quails, infected orally with 5 x 10(3) infective eggs, were studied, as well as the re-infectivity of these larvae in mice, inoculated with 50 larvae obtained from the liver of these quails. Post-infection, the highest concentrations of larvae were found to be present in the liver of quails while only a few migrated to other tissues like lungs, heart, muscle and brain. The migration and distribution of the larvae in the tissues of mice were studied by necropsy on days 6 and 12 post-infection. On both days the highest number of larvae, 11 and 10, were recovered from the carcase followed by six and seven from the leg muscles and four and eight from the brain, respectively. A few larvae were recovered from the liver, lungs and viscera. This implies that the larvae had a special affinity for the muscle and brain tissue of mice, unlike in the quails. The role of these larvae in relation to paratenism is discussed.

The life cycle of Toxocara vitulorum in Asian buffalo (Bubalus bubalis).

A procedure for labelling hatched Toxocara vitulorum larvae with 75 selenium is described. Labelled larvae are infective when administered into the small intestine and portal vein of buffalo of all ages. Only very young calves are infected after oral administration. The labelled larvae are used with an enhanced fluorographic autoradiographic procedure to study the dynamics of the infection in non-pregnant and pregnant buffalo. Larvae penetrate the wall of the small intestine between 2 and 8 h after administration. Most larvae go straight to the liver via the portal vein but a few enter the mesenteric lymph nodes. Over the next 90 h some larvae migrate to the lung and a few to muscle, brain, kidney and peripheral lymph nodes. Most remain in the liver. Over the next 3-7 weeks the larvae grow by about 10% and no moulting is observed. In a pregnant host larvae grow to 500-600 microns in liver and lung 1-8 days before parturition and migrate to the mammary gland around the time of parturition. In the mammary gland they grow to about 1200 microns and pass into the milk during the 7 days after parturition.

Immunodiagnosis of parasitic zoonoses: sensitivity and specificity of in vitro lymphocyte proliferative responsiveness using nematode antigens purified by affinity chromatography.

The sensitivity of in vitro lymphocyte proliferative responsiveness using antigens purified by affinity chromatography, was greater than that of three serological tests and allowed the specific identification of Dirofilaria immitis, Toxocara canis, Angiostrongylus cantonensis and Ascaris lumbricoides in animals sensitized with parasite antigens, and the diagnosis of natural (D. immitis, T. canis and Angiostrongylus cantonensis) and zoonotic nematode infections. Lymphocytes remained viable in whole blood suspensions in RPM 1640 in a polystyrene insulation box at air temperature for at least 12 hours and reacted in the cell-mediated immunity test (CMIT) without loss of response. The CMIT proved useful in the early immunodiagnosis of nematode infections and showed that parasite antigens purified by affinity chromatography retained a high degree of specificity and sensitivity in both the CMIT and serological tests.

The egg production of Toxocara vitulorum in Asian buffalo (Bubalus bubalis).

The egg production of Toxocara vitulorum in Asian buffalo has been studied. Eggs were first present in the faeces of calves when they were 22.3 +/- 1.6 days old. In calves treated with pyrantel when 3 days old, the age at first patency was extended by 3.5 days indicating that there was no pre-natal transmission. Calves on only half the milk of the cow had a significantly longer prepatent period of 27.7 +/- 2.2 days. The peak egg output occurred in calves 35.7 +/- 2.6 days old and had a duration of 5.5 +/- 2.5 days with 98,000 +/- 63,700 eggs g-1 of faeces. The duration of the patent period was 35 +/- 12 days. The average lengths of populations of mature female parasites from different hosts at the time of peak egg output or older, ranged from 15.0 to 31.0 cm and was correlated with those of the males in the same populations (10.6-20.4 cm). The size of females was not affected by intraspecific competition. The proportion of males in the populations was 0.39 +/- 0.11. The egg output per female per day at the peak was 110,000 +/- 58,000 and was correlated with the size of the females at autopsy, but the egg output per female per day at the time of autopsy was lower and was not correlated, so it was concluded that the drop in egg counts was the result of reduced fecundity. The fertility of the eggs from faeces was greater than 92% throughout.(ABSTRACT TRUNCATED AT 250 WORDS)

Canine toxocariasis and the associated environmental contamination of urban areas in eastern Nigeria.

The prevalence of canine toxocariasis in pet dogs in two urban towns in eastern Nigeria and the associated environmental contamination were studied through examination of 262 faecal and 400 soil samples. Infection rates in dogs varied from 6.67% to 42.35%, the prevalence rate being inversely related to the age of dogs. Sex and breed of dogs had no significant influence (P greater than 0.05) on the prevalence of infection. There was no evidence of widespread contamination of public places, as Toxocara ova were recovered only from some private premises, namely, those of a dog owner and the kennel of a veterinary hospital.

A critical look at the importance, prevalence and control of toxocariasis and the possibilities of immunological control.

The visceral infection of humans with Toxocara canis is particularly prevalent in children and may cause a variety of symptoms that commonly persist for 6-24 months. The ocular infection usually causes permanent loss of visual acuity. Human infection is acquired by ingestion of embryonated T. canis eggs with contaminated dirt. Review of recent reports indicates that patent T. canis infection is widely prevalent in the general population of dogs all over the world (3-81%) and results in a substantial contamination of the ground (0.3-87%). The results of sensitive and specific serological tests suggest that about 7% of the clinically healthy human population of the United States, about 5% of that of Canada, and about 4% of that in Great Britain is infected with the parasite. Control of transmission of the parasite to man is often attempted by eliminating the infection in dogs, reducing the population of dogs and the environmental contamination with their feces, and educating the public about the zoonotic potential of toxocariasis. The evidence reviewed indicates that these methods are only marginally effective. Because T. canis relies on congenital and lactogenic transmission to persist in nature, only a procedure that effects the sustained killing of the reservoir larvae in the tissues of the bitch, or of newly-acquired parasites, is expected to be successful. Research with mice, rabbits and dogs demonstrated that prior infections of the host induce the development of protective immunity to reinfections. This procedure, however, leaves remnant populations of larvae from the immunizing infections that are resistant to anthelmintics and to the effect of prior irradiation. Hyperimmunization with partially-purified extracts of T. canis larvae induced 37% resistance to a challenge in mice when the extract was administered alone, and 76% resistance when administered with lipopolysaccharide adjuvant. Production of complete resistance, however, will probably require the prior control of the immunosuppression induced by the parasite. T. canis infections inhibit the production of homologous protective immunity and antibody responses to heterologous antigens, probably by interfering with the activity of helper T-cells, competing with protective antigens, and suppressing antibody synthesis. The evidence indicates, however, that an anti-T. canis vaccine to eliminate the parasite in dogs is feasible.

Toxocara vitulorum in beef calves kept on effluent-irrigated pastures in Zimbabwe.

Faeces from 20 calves aged 13 +/- 5 days were examined for Toxocara vitulorum eggs fortnightly for a period of 20 weeks. The age of calves when eggs were first detected varied from 24 to 110 days (mean 41 +/- 20 days). The mean egg count varied from 257 to 19,821 g-1 of faeces with a highest count of 68,400. The patency period of T. vitulorum lasted from 14 to 112 days (mean 65 +/- 30 days). None of the calves showed clinical signs of illness.

The effect of radiation on the viability and migratory ability of second-stage larvae of Toxocara canis in mice.

Larval counts were made on mice 2 days after oral inoculation with X-ray (0-320 Krad) or of gamma ray (0-6 Mrad) irradiated eggs containing second-stage Toxocara canis larvae. The majority of the larvae irradiated with 0-40 Krad were recovered from the liver and lungs, while most of the larvae irradiated with 80 or 160 Krad remained in the digestive tract, mainly in the stomach and the proximal half of the small intestine. Only a small number of the 320 Krad irradiated larvae was recovered from the mice. No significant difference was observed in the viability of irradiated larvae incubated in vitro up to 13 days after irradiation. However, a substantial percentage of the 160 and 320 Krad-irradiated larvae hatched during that period. Very few larvae were recovered from the digestive tract of mice inoculated with eggs irradiated with 0.5 Mrad, and only one and four larvae were recovered from the liver and lungs of a mouse. No visceral larval migration was observed in mice inoculated with 1 Mrad-irradiated eggs. The minimum lethal radiation dose for second-stage T. canis larvae in eggs is proposed to be 1 Mrad.

Experimental infection of Japanese quail with Toxocara canis larvae through earthworms.

The migration and distribution of Toxocara canis larvae in the tissues of earthworms exposed to 5 x 10(5) infective eggs in soil, as well as the reinfectivity of the larvae in Japanese quail fed with three earthworms, were studied. The average number of larvae recovered from an earthworm gradually declined from 9 +/- 3.21 to 4.5 +/- 2.00 at 4-16 days. No larvae were recovered at Day 20. When compared between three portions of the earthworms' body, the middle part showed the greatest recovery in comparison with the anterior and posterior parts. At necropsy, the average larval burden of quail at 15 days post-infection was 6 +/- 3.60 in the liver and no larvae were recovered from other tissues. The role of the earthworm in relation to paratenism is discussed.

A field evaluation of treatment with febantel for the control of Toxocara canis in pups.

The faecal egg count depression (FECD) of febantel (Rintal vet. 100 mg tablets, Bayer AG, Veterinär-Bereich, Leverkusen), against Toxocara canis was tested in suckling pups treated at 2 weeks of age. The dose rate was 30 mg kg-1 body weight given orally, once every 12 h, three times. The effect of a further treatment of 6- and 12-week-old pups on excreted eggs was also evaluated. The FECD of 6-week-old pups was 100%. However, some of the 12- and 17-week-old pups had low eggs per gram (epg) values indicating that shorter intervals between the treatments should have been used in order to minimize the risk of spreading T. canis eggs. The control pups of the first treatment group were untreated litter mates. They were treated when 4 weeks old and then followed a similar regimen to the experimental animals. At 6 weeks of age, their FECD was 100%, but low epg values were observed among 12- and 17-week-old pups, similar to the test group.

Evaluation of a beef-based chewable formulation of pyrantel pamoate against induced and natural infections of hookworms and ascarids in dogs.

Pyrantel pamoate, formulated in a beef-based chewable tablet, was evaluated for efficacy in dogs against induced and natural infections of Toxocara canis, Toxascaris leonina, Ancylostoma caninum and Uncinaria stenocephala. Dose titration trials were conducted in Canada, the UK and Germany in dogs treated with pyrantel (as pamoate salt) at 0, 2.5, 5 or 10 mg kg-1 body weight. These studies showed that a dose rate of 2.5 mg kg-1, the efficacy of pyrantel against adult T. canis, T. leonina, U. stenocephala and A. caninum was 76.1, 85.6, 100 and 87.9%, respectively. Efficacy at 5 mg kg-1 against the same parasites was 94.2, 92.0, 93.5 and 93.8%, respectively, and at 10 mg kg-1 efficacy was 91.2, 97.6, 98.7 and 91.3%, respectively. No adverse effects due to treatment were seen in any of these trials.

Infection of Japanese quail with Toxocara canis larvae and establishment of patent infection in pups.

Migration and distribution of Toxocara canis larvae in the tissues of Japanese quail, infected orally with 5 X 10(3) infective eggs, and the establishment of patent infection from the quails to the definitive host, were studied. Larval yield at necropsy from various tissues and organs of quail varied from 4.72 to 7.54% of the infective eggs inoculated within the period 1-60 days post-infection (PI). The total number of larvae recovered on different days showed a gradual increase. The percent inoculum recovered at necropsy was highest on Day 60. Most of the larvae were found in the liver throughout the period and only a few migrated to other tissues, such as lung, heart, muscle and brain. The establishment of patent infections in the definitive host was studied by feeding the 15-day infected livers of Japanese quail (400 larvae) to Toxocara-free pups. Eggs first appeared in the faeces 38 days post-infection, the mean worm burden at necropsy was 87 and the percentage of infection established was 21.75%. Thus the role of Japanese quail as a paratenic host of T. canis is established.

Acquired immunity to Toxocara canis infection in mice.

Acquired immunity develops against Toxocara canis infection in mice, and NIH mice are more immunoresponsive than CD1 mice. Twice infected NIH female mice showed 27% reduction in the total larval recoveries compared with non-sensitized controls. Twice-infected NIH male, and CD1 (both sexes) mice showed a negligible reduction in the total recoveries, though a significant (P less than 0.05) number of larvae were retained in the liver compared with the non-sensitized controls. All twice-infected mice showed a significant reduction in the number of larvae recovered from the brain compared with once-infected mice. Vaccination using ultraviolet irradiated embryonated eggs gave the best protection against reinfection. Excretory/secretory antigen afforded less protection, whilst whole adult worm vaccine and whole L2 culture vaccine gave no protection. Vaccinated mice had a higher 'free:penetrating ratio' of larvae in their intestine than similarly challenged but non-vaccinated mice. When the ileum was examined histologically 9 h post-infection, an inflammatory reaction was seen around the penetrating larvae in the sensitized and vaccinated mice but not in untreated controls, suggesting a role played by the intestine in the resistance against T. canis infection in mice.

Patent Toxocara canis infection in ascarid-naive dogs.

The effect of feeding different numbers of Toxocara canis eggs on patent intestinal infections was studied in 45 ascarid-naive 62--64-day-old pups and 6 adult dogs. Twenty-four of 25 pups fed 10 to 1,000 eggs developed patent intestinal infections, whereas none of the 20 pups fed 10,000 eggs developed patent intestinal infection. Three of 6 presumably ascarid-naive dogs, 7, 10, and 52 months old fed 100 eggs each, developed intestinal infections.

Disseminated granulomatous disease in a cat caused by larvae of Toxocara canis.

The gross and histological findings of a case of disseminated granulomatous disease caused by larval nematode infection in a cat are presented. The larvae were identified as those of Toxocara canis and the lesions associated with infection of cats with various ascaridoid larvae are discussed.

Intestinal changes in puppies infected with Toxocara canis.

Small intestinal histopathology and absorption were examined in Beagle puppies infected with either a moderate or a low burden of Toxocara canis. Infection with T. canis significantly reduced absorption of xylose, but only slightly delayed absorption of para-aminobenzoic acid. Fat assimilation was reduced and faecal proteolytic activity was increased. A significant reduction in villous height occurred and was inversely related to the extent of the infection. Villous goblet cell numbers, particularly those in the luminal third of the villus, were lowest and crypt goblet cell numbers were highest in the most heavily infected of the puppies. Villous goblet cell numbers increased rapidly after treatment of the puppies with piperazine or after the spontaneous elimination of the T. canis infection while crypt goblet cell numbers were less affected by elimination of the parasites. Intra-epithelial lymphocyte numbers were lowest in 33- to 37-day-old puppies infected with greater than 127 T. canis and highest in 44- to 46-day-old puppies losing their infection. Infection with T. canis had no apparent effect on mast cell numbers or pyroninophilic cell numbers in the lamina propria.

Toxocara vitulorum in the milk of buffalo (Bubalus bubalis) cows.

The duration of excretion of Toxocara vitulorum larvae in the milk of buffalo cows determines the optimum time for treating calves. Studies on 10 cows showed that a few larvae occur in the colostrum of some cows before the calf has suckled, but most are present from the day after calving and for a further five days. From day 9 onwards, very few larvae were found in the milk. The total number of larvae found was comparable with the number of adult parasites collected from the calves of cows with similar histories. The larvae were 1254 +/- 60 microns long and 36 +/- 6.7 microns in diameter at the ventriculus, figures which are substantially different from some published results.