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Davis AT Collection. Davis PT Collection. Murtagh Collection. About Search. Enable Autosuggest. Previous Chapter. Next Chapter. Cunningham E. Riordan-Eva P, Augsburger J. Paul Riordan-Eva, and James J. Accessed June 27, Download citation file: RIS Zotero. Reference Manager. Autosuggest Results. Expand All Sections.

Jump to a Section 7. Figure 7—1. Furthermore, SchB specifically reduced the size of the abnormally large rods. Together, our study has successfully unveiled a possible visual benefit of SchB on a retinal-degeneration model. When this line was raised, only the heterozygous carriers and their wild-type WT siblings would survive to adulthood. These heterozygous carriers were crossed to obtain homozygous mutant embryos i. The medium was changed every day. During the process, unhealthy embryos were discarded.

Zebrafish genotyping was conducted based on a previously reported protocol [ 23 ]. The resulting PCR product was base pairs bp long. During the amplification, a restriction site for BsaXI was created in the PCR product of the mutated pde6c w59 allele but not in that of the WT allele. On the gel, a WT allele would migrate as a single bp band, whereas the pde6c w59 allele would be restricted by BsaXI, and would migrate as a bp band and a bp band. SchB was extracted and purified from Fructus Schisandrae as previously reported [ 35 ]. During an experiment, the stock solution was diluted to the desired working concentration with E3 medium.

These solutions were used to treat zebrafish embryos from 3 to 6 dpf. During the course of treatment, the media was changed every day.

Eye - Wikipedia

An enzymatic assay [ 36 ] was used to measure the specific activity of G6pd. This enzyme catalyzes the first rate-limiting step of the pentose phosphate pathway. In the assay, the rate of NAPDH formation was measured in a known amount of protein extract to determine the specific G6pd activity. The proteins were extracted from larvae by grinding them in a buffer containing 0. The resulting lysate was centrifuged to obtain the supernatant. Furthermore, the amount of protein in the supernatant was separately determined by the standard Bradford assay.

Using these values, the specific G6pd activity was calculated by dividing the amount of NADPH produced per min with the measured protein amount. In this study, a custom-made OKR apparatus was constructed based on the basic specifications reported in a previous study [ 37 ]. During the OKR measurement, the rotation speed of the drum was set at eight revolutions per minute. In response to stripe rotation, normal larval eyes move in saccades [ 37 ]. This movement was independently evaluated by two individuals under a stereomicroscope to ensure accurate larval classification.

The VMR assay was based on a published design [ 30 , 31 ]. Inside the system, animals were isolated from environmental light and stimulated by white light emitted by a light-controlling unit from the bottom of the plate. The larval movement was recorded by an infra-red camera at a rate of 30 frames per second under nm infrared illumination, which the animals could not perceive.

Before the actual experiment, the well plate with the larvae was dark-adapted in the ZebraBox system for 3. The actual test consisted of three consecutive trials of light onset Light-On and light offset Light-Off periods, with each period lasting for 30 minutes S1 Fig. The light change On or Off was abrupt and instantaneous. The total irradiance from nm to nm was measured by an EPP Spectrometer StellarNet Inc, Tampa, FL at nine evenly distributed locations across the surface of the light-controlling unit that would be covered by the well plate. The following parameters were used to collect activity data: detection sensitivity per pixel per image—grey level 6; burst threshold—4 pixels; bin size—1 second.

The detection sensitivity registered pixels with a grey level below a preset level. These registered pixels detected the individual larvae in each frame. If these pixels were detected in a different location in successive frames, they were declared as active pixels. These active pixels represented the part of the larvae that moved in successive frames. The burst threshold selected movements that were larger than a predefined number of active pixels between successive frames to separate small movements from major movements.

Larval movement was summarized as the fraction of frames that a larva displayed movement in each second as defined by the bin size. This fraction was defined as the Burst Duration, and was individually computed for all larvae. VMR assays were started at around the same time at 2 p. The media were changed every day.

The larval genotype was confirmed by PCR after all behavioural experiments. Enucleation was performed on 5-dpf larvae. First, they were anaesthetized with 0. Then, their eyes were removed by a fine tungsten-wire loop etched as described [ 39 ]. Finally, they were transferred back to the original treatment medium overnight and subjected to the VMR assay at 6 dpf. The dissection removed the adhering sclera and retinal pigment epithelium RPE , which was critical for antibody penetration. To dissect retinas, a larva was held dorsal side up on a Petri dish using Dumont 55 forceps.

Then, the RPE-attached retina was detached from the sclera by dissecting through the lateral side of the eye with a fine hook created by bending a tungsten needle, etched as described previously [ 39 , 40 ] see S2B Fig. For the lateral-side dissection, the hook was inserted into the anterior chamber by puncturing the cornea. The tip of the hook would slide beneath the scleral region just outside the pupil S2A Fig , black circular arrow. Then, the RPE-attached retina could be easily detached from the sclera by a gentle push from the medial side of the eye S2A Fig , white arrow.

Retinas were washed in a microcentrifuge tube once with 0. They were then incubated in 0. After RPE detachment, the tissues were washed twice with 0. The dissected retinas were kept in a microcentrifuge tube for immunostaining S2C Fig. During all incubation steps, the microcentrifuge tubes were gently shaken on a rotary platform. The z-stack confocal images were trimmed in ZEN black edition version 8. This region contained the more mature PRs, which were substantially degenerated in the pde6c w59 mutant [ 22 ].

For zpr1-stained and 4cstained retinas, the analyzed areas were and The following procedure was used to conduct 3D analysis.


ROIs were excluded if their morphology was distorted by proximity to the optic nerve region. Finally, the selected ROIs were used to measure several morphological parameters, including volume, sphericity, Feret diameter, ratios between the radii of a fitted 3D ellipsoid, and ratio of the volume of the fitted 3D ellipsoid to the measured volume. Statistical analyses were performed in R version 3.

G6pd activity was analyzed by Welch two-sample t- test. Extracted data were plotted to show average activity and corresponding standard error under the same light stimulus in every second. To compare activity profiles, the locomotor activity from different conditions was segregated into two time periods: before light change —0 s and after light change 1—30 s. The period 31—60 s after light change was sometimes also analyzed. For each comparison, five thousand permutations were performed to estimate the null distribution for p- value calculation. Finally, the resulting p -values were corrected for multiple-hypothesis testing by controlling the false discovery rate.

For immunostaining results, the PR count data were analyzed by Welch two-sample t- test for two-group comparison or Kruskal-Wallis rank sum test for three-group comparison. The PR morphological data were analyzed by linear mixed-effects modeling, with individual retinas modeled as a random effect. To study SchB effect in the zebrafish system, a treatment concentration had to be determined. The effective concentrations of SchB have been defined in several other biological systems before [ 10 — 18 ].

These conditions served as guidelines for optimizing a SchB concentration for treating zebrafish larvae. A dilution series of SchB 15, 7. The larvae were treated starting at 3 dpf, a stage when the first visual response appeared [ 48 , 49 ], and the normal Pde6c protein would be functional to transduce light signal.

Botfly Larvae Removal from Puppies/Kittens EYEs to Save her SIGHT

Starting the treatment at this stage would minimize any unwanted drug effects on early retinogenesis of the treated larvae. Larvae were then observed daily until 8 dpf. The gross morphology of zebrafish larvae under different treatment schemes from 3 to 8 dpf. In each treatment group, the lateral view of a representative larva at 3, 6 and 8 dpf is shown. Larvae exposed to higher SchB concentrations, including 7. Normal WT embryos were exposed to 1.

The treatment took place from 3 to 8 dpf. The survival of larvae in each condition was counted every day. The DMSO percentage in the controls was 0. These were the corresponding DMSO amounts used as the drug carrier in treatment groups with 1. Hence, the use of these specific amounts of DMSO should not affect the survival of the larvae. Indeed, they did not. In each experimental group, 60 embryos were used. Then, the survival was counted every day from 3 to 8 dpf.

The 3-dpf count was obtained immediately after the addition of chemicals. The 3. On the contrary, those treated with 1. Thus, 1. To determine whether 1. Ten WT larvae were exposed to either 1. This treatment time was chosen for our ultimate characterization of prophylactic property of SchB on the pde6c w59 PRs, which began to degenerate at 4 dpf [ 22 ]. G6pd specific activity was substantially enhanced in the SchB-treated group compared with that in the DMSO-treated controls 0. These results suggest that the known pharmacological effect of SchB could be induced by exposing the embryos to 1.

The SchB treatment was then tested on the pde6c w59 mutants. In particular, their potential change in visual performance was evaluated by VMR, a primitive startle response displayed by the larvae within seconds after light onset and offset [ 30 ]. Hence, this VMR assay was used to evaluate the light sensation of the pde6c w59 mutants under different conditions. First, the VMR assay was used to evaluate the difference between the untreated pde6c w59 mutants and the WT controls.

In this experiment, the mutant larvae were identified by their lack of optokinetic response OKR at 5 dpf, a response that became robust at this stage [ 37 , 49 ]. This is also the earliest stage to identify a large number of mutants by a non-invasive approach. Specifically, 34 OKR-negative larvae and 34 WT controls were individually arranged in the wells of a well plate. Then, their VMR was measured from 5 to 8 dpf Fig 2. The VMR was significantly different between these larvae. From 6 to 8 dpf, smaller activity peaks were also prominent after the main peak.

At all stages, the activity rapidly returned to baseline in approximately 15—20 s. When subjected to the light offset Light-Off , the WT activity was substantially increased in the first 5—10 s Fig 2E—2H , black traces. By 15 s, it was reduced to an intermediate level and sustained for an extended period of time. This sustained activity would gradually return to baseline before the end of the Light-Off period at 30 mins i. Compared with the WT controls, the pde6c w59 larvae displayed a significantly attenuated VMR at all stages Fig 2 ; red traces.

Each stimulus would last for 30 mins. During the experiment, the larval movement was recorded by computer as movement duration per second. Then, the activity of the same type of larvae was averaged across the three Light-On or Light-Off trials and plotted in the figures. The solid traces in each plot show the mean activities from 60 s before light change to 60 s after light change, whereas the ribbons surrounding these activity traces indicate the corresponding standard error of the mean.

At the top of the plots, the white and black bars indicate light and dark phases respectively. These plots show that the pde6c w59 larvae displayed a substantially attenuated VMR compared with the WT larvae. The problem was likely caused by the retinal degeneration in the pde6c w59 mutants, which affected their capability to sense light change in the environment.

The raw data for Fig 2 are available in S1 File. Mutant larvae were exposed to the SchB treatment i. At this stage, the mutants could not be reliably identified by any non-invasive approach. They were rather identified at 5 dpf by their lack of OKR as discussed before. The identification was possible because the SchB treatment did not induce an OKR in the pde6c w59 mutants, as demonstrated by the following independent experiment: The embryos obtained from a heterozygous cross were randomly divided into two groups.

Their OKR was then measured at 5 dpf. The results suggest this was not the case. In the SchB-treated group, out of larvae The pde6c genotype of these larvae was also confirmed by PCR of randomly sampled individuals from the experimental groups. The true positive rate i. In the VMR experiment, these OKR-negative larvae were identified at 5 dpf and individually arranged in the wells of a well plate that contained the corresponding treatment medium.

After acclimatizing overnight, their VMR was analyzed at 6 dpf Fig 3. This VMR enhancement induced by SchB was not a general excitation of the larvae but rather an effect specifically associated with light onset. At the end of the VMR experiments, all larvae were also genotyped to confirm their identity. In each plot, the solid traces show the mean activities from 60 s before light change to 60 s after light change, whereas the ribbons surrounding these activity traces indicate the corresponding standard error of the mean.

The same plots without the error ribbons are shown in S3 Fig to emphasize just the average traces. At the top of these plots, the white and black bars indicate light and dark phases. Together, these observations suggest that SchB enhanced the response of pde6c w59 larvae to light onset through their eyes. The raw data for Fig 3 are available in S2 File. The analysis indicates that the Light-On VMR of the enucleated pde6c w59 larvae with SchB treatment was significantly attenuated compared with those with intact eyes Fig 3A , green vs.

It was also noted that the activity of the enucleated SchB-treated pde6c w59 larvae gradually increased and reached a similar level as those with intact eyes from approximately 40 s onwards. Together, the eye-enucleation test suggests that SchB enhanced the first 30 s of Light-On VMR of the pde6c w59 larvae through their eyes. The L3 of Trichostrongylus species burrow underneath the mucosa of the duodenum and the first 6 or 7 m of the jejunum. When these tunnels rupture to release the young adult worms, there is oedema and haemorrhage and a loss of plasma proteins. The Cooperia species have a similar pathogenesis.

The L4 and fifth stages of Nematodirus severely damage the villi of especially the ileum — and this leads to villous atrophy and erosion of the mucosa. The larvae of Strongyloides cause erythematous lesions where they penetrate the skin and petechiae in the lungs, and the adults produce a catarrhal enteritis of the duodenum and anterior jejunum.

The hookworm larvae cause skin lesions on penetrations and anaemia; hypoalbuminaemia and occasionally diarrhoea are caused by the adults. Initial infection causes swelling at the site of skin penetration and within 24 hours the formation of small isolated scabs. Repeated infections cause severe swelling that may persist for several days. The large mouths of the adults that cut the intestinal villi at their bases, cause intestinal lesions.

Exposed, haemorrhaging ulcers remain when the worms move to a new feeding site. Anaemia develops gradually and haemoglobin levels drop to as low as 0. The anaemia is of the progressive aplastic type — with no regenerative changes occurring in circulating red cells. The tapeworms are considered to be nonpathogenic, and even in heavy infections there is little damage to the intestine. They do, however, cause unthriftiness by competing with the host for available nutrients, and may cause the deaths of young lambs and malnourished pregnant sheep.

In acute cases of trichostrongylosis the carcass is emaciated and there is atrophy of the fatty tissues. The intestines show catarrhal inflammation with numerous small petechiae in the first few metres of the small intestine. The intestinal walls are thickened and the mesenteric lymph nodes are enlarged. Adult parasites are found beneath the greyish white film that covers the mucosa, but their presence can only be determined by examining a scraping of the mucosa against the light. Changes such as fluid accumulations in the serous cavities, ruminal atony and food retention in the rumen and abomasum, dry ingesta, and distension of the small intestine by fluid may also occur.

Carcasses from chronic cases are markedly emaciated, and there is muscular and myocardial atrophy. Mucous membranes are generally pale and the intestinal walls may be thickened. In nematodirosis the carcass has a dehydrated appearance, and there is loss of the intestinal villi and necrosis of the lamina propria. It is seldom seen in cattle — because they are rarely infected. In strongyloidosis the carcass is emaciated and wet, and most of the skeletal muscles are atrophied.

There are serous effusions in the body cavities and widespread serous atrophy of fat. Intestines are red and the mucosa is lacking in severe infections. The worms can sometimes be seen clumped together and they resemble pieces of cotton wool. Bunostomum causes emaciation, and bleeding ulcers occur in the mucosa of the small intestines of sheep. In cattle, a typical anaemic carcass with pale mucous membranes and watery blood, is seen. Lesions are present in the mucosa, but free blood in the lumen is seldom seen.

The haemopoietic tissues may show signs of compensation — i. Young animals show skin lesions due to larval penetration. Gaigeria causes the same lesions as Bunostomum species. Cooperia is more of a problem in cattle — in which necrotic enteritis with parasites penetrating the mucosa, haemorrhages in the first 3 m of the small intestine, and catarrhal exudate in the posterior half of the small intestine, are seen on necropsy. The carcass of a Calicophoron -infected animal is emaciated, dehydrated and there is severe fibrino-catarrhal inflammation of the small intestine, and occasionally the abomasum.

Large numbers of small, immature flukes can be found on the mucosa. Ulceration and haemorrhage of the small intestinal mucosa is also evident. The clinical signs caused by any one of the Trichostrongylus species appear in acute and chronic forms. The acute disease develops when approximately infective larvae are ingested. Pain caused by the parasite causes anorexia, closure of the pyloric sphincter, and retention of food in the abomasum and rumen.

Sheep become listless, signs of submandibular oedema develop, and there is a yellow foetid diarrhoea. Sheep die 16 to 17 days after infection. Death is due to the combined effects of starvation, liver impairment, circulatory failure, and pulmonary oedema. Acute disease is rarely seen. The chronic disease is more commonly seen and develops when about larvae are ingested. Anorexia gets progressively worse, with concomitant loss of body mass.

Anaemia is caused by a lack of available protein to form haemoglobin. The overall result is emaciation, atrophy of muscles, hydrothorax, hydropericardium and ascites. The clinical signs may be aggravated by poor grazing — especially during winter. Dorper sheep seem to be more susceptible to trichostrongylosis and develop a slight transient bottle jaw.

Uveal Tract & Sclera

Faeces become putty-like — but not fluid — and animals become weak and listless. Mucous membranes become pale. Merino sheep show slightly pale mucous membranes and putty-like faeces. On lush green pastures, the sheep may have a dark diarrhoea. The clinical signs in Nematodirus infection are depression, listlessness, anorexia, fluid faeces and death 10 to 14 days after infection.

The clinical signs are caused by the L4 rather than by the adults. Animals with a severe infestation of Cooperia species — i. Like most helminths infecting percutaneously, Strongyloides larvae cause marked urticaria at the site of infection. In goats, adult worms cause anorexia, diarrhoea or constipation, sunken eyes with a purulent discharge, a frothy mucous discharge from the nose, muscle atrophy, and paresis just before death. Bunostomum causes itching of the skin — particularly that of the limbs often accompanied by foot-stamping — and wet eczema.

Rapid mass loss occurs, with emaciation, anaemia, submandibular oedema and constipation followed by diarrhoea, with the faeces being foetid and tarry.

Ocular Parasitic Infections – An Overview

Animals lie down for a few days before they die. A massive dose 4 larvae can kill adult sheep or young calves without any ante mortal clinical signs. However, more commonly, as few as to adults can produce severe anaemia — causing a fall in the haematocrit levels as well as hypoalbuminaemia. Gaigeria is a voracious bloodsucker in sheep, and severe anaemia that develops over a period of about 13 weeks is seen together with emaciation, weakness, and loss of weight and appetite.

It is usually fatal in under-nourished animals. Unthriftiness and intermittent diarrhoea are the only clinical signs seen in Toxocara infections — and then only in calves less than 6 months old. Calicophoron immatures cause anorexia, foetid diarrhoea, mass loss and occasionally bottle jaw.

In severe cases death occurs 5 to 9 days after the onset of diarrhoea. Sheep are very susceptible, show severe clinical signs, and quickly die of amphistomosis — whereas cattle rapidly develop a good immunity. Both Moniezia benedeni and M. They do not cause significant clinical effects — even with large worm burdens. However, clinical signs may include unthriftiness, diarrhoea, respiratory signs and even convulsions — but then only with massive burdens. Thysaniezia giardi and Avitellina are considered to be apathogenic.

Several of the eggs can be identified to genus level, but the eggs of the trichostrongylids and hookworms are difficult to distinguish from one another. Differential diagnoses for intestinal helminthoses includes such conditions as poisoning with certain plants or metals, malnutrition, and — in the case of the hookworms Bunostomum and Gaigeria — causes of anaemia like fasciolosis or haemonchosis.

The anthelmintic selected must be suitable for the endoparasites on the farm. Although no resistance has been detected so far in intestinal nematodes, good basic practice should be implemented as in the discussion under the control of abomasal worms in small stock. Although considered apathogenic, in practice heavy burdens of Moniezia have been shown to cause mortalities in calves, lambs, and pregnant ewes on dry lands. This can be prevented by strategic dosing of ewes on old lands and of young ruminants when they begin to graze. There is anecdotal evidence of niclosamide resistance in the field, and in such cases suitable alternatives like praziquantel can be used.

Few helminths utilise the large intestine, but those that do are often severely pathogenic. Nematodes that occur here are Oesophagostomum species, Chabertia ovina, and the Trichuris species. Trematodes and cestodes are not, as a rule, found in the large intestine of ruminants. Adult Oesophagostomum are also known as nodular worm and occur in the caecum and colon, while immature stages are found in nodules in the wall of the small and large intestines. They are present in ruminants in the tropical and subtropical regions of the world. The life cycle of Oesophagostomum columbianum of sheep and goats, and Oesophagostomum radiatum of cattle, is direct.

The developmental period of the former is 35 to 39 days for the first infection, increasing to 46 to 47 days to many months for subsequent infections. The developmental period of Oesophagostomum radiatum is 32 to 34 days. Wet, warm weather, overgrazed camps or unhygienic kraals and pens will predispose calves and they can be expected to show clinical signs.

A third species, Oesophagostomum venulosum , seems to be of lesser importance in sheep and goats. Chabertia ovina is the largemouthed bowel worm of sheep, goats and rarely cattle, and also occurs in some antelope species. Their habitat is the colon and they are found wherever sheep are kept and the climate is suitable. The life cycle is direct and the developmental perio d is 49 days or more.

The whipworms Trichuris species are named for their long, thin anterior end and a short, thicker posterior. They are found in the caecum and colon. The eggs are lemon-shaped and have a plug at each end. Oesophagostomum columbianum is present in the summer rainfall areas, where rainfall is in excess of mm per annum. It is absent in the semi-arid, non-seasonal and winter rainfall areas. Oesophagostomum radiatum does not occur in the arid, non-seasonal and winter rainfall areas. In semi-arid areas, it is found in modest numbers in calves in May. In the summer rainfall areas, calves are infested throughout the year, with burdens rising to a peak in August and declining in spring.

Irrigated pastures are an unsuitable habitat for this parasite. Chabertia ovina is confined to winter- and non-seasonal rainfall areas, and is present throughout the year in moderate numbers. Trichuris species occur throughout the world — wherever ruminants, domesticated animals and wildlife are present. Ruminants are the main hosts of Oesophagostomum species, although there are about nine other species that occur in domestic pigs, warthogs and bushpigs.

These species are not transmissible to ruminants. Chabertia is only known in sheep, and Trichuris species are present in ruminants, carnivores, suids, and even in humans. Wild antelope are often the reservoir host for the nodular worms and whipworms of domesticated ruminants. The life cycle of all the worms of the large intestine is direct, and infection takes place per os. The free-living stages of Oesophagostomum species are susceptible to desiccation and require hot, moist conditions for optimal development to the infective stages.

The species are present in the summer rainfall areas where rainfall exceeds mm per annum. They are absent in the semi-arid, non-seasonal and winter rainfall areas. Sheep quickly expel the worms on improved pastures, and the parasite is absent on irrigated pastures. Trichuris also has a direct life cycle, but in this case the eggs contain the infective L1 and can survive for years in dry pellets. The socio-economic impact of the helminths of the large intestine of ruminants is severe — not only in direct losses through death of the animals, but also through the erosive disease caused by Trichuris species in sheep and O.

Treatment is expensive and few farmers are able to afford it, which further adds to the impact that these worms have. Anorexia is the most important finding with ovine and caprine oesophagostomosis. It is caused by the intestinal discomfort starting with the larval migration to the intestinal lumen — and persists until death or recovery.

A mild mucoid to projectile foetid diarrhoea sets in, and this may lead to intussusception. Death caused by starvation, dehydration and exhaustion may occur from days 18 to Calves pass blood from as early day This becomes more severe from the 19th and 20th day as the worms moult M4. Like lambs and kids, calves die of dehydration and exhaustion, or recover from the 10th week onwards.

Chabertia browse on the mucosa causing haemorrhage from the 4th week onwards — and faeces become blood-flecked. Larval stages of Trichuris cause haemorrhage and local oedema when they penetrate the intestinal wall. These injuries are considered to predispose to the development of secondary bacterial infections. Unless they are present in large numbers, adult worms are not pathogenic. Extensive nodule formation and thickening of the mucosa of the colon occurs — together with peritonitis and adhesions Figure There may be a diphtheritic jejunitis, typhlitis and colitis — with numerous perforations and adhesions.

At a later stage the nodules may calcify. Once the worms have reached patency, only nodules and a thickened intestinal wall with adhesions may be visible. The lesions caused by O. The mucosa of the caecum and colon of sheep infected with Chabertia contain haemorrhages and inflammatory areas which are produced by the adult worms. The adults cause extensive damage because they frequently move to new sites to feed. Only in heavy infections do the immature stages cause tissue damage — and then throughout the entire intestine from the pylorus to the ileocaecal valve.

It is caused by larvae that have not yet reached patency and is characterised by pain, a rise in temperature, diarrhoea and rapid dehydration. In the chronic disease food and water consumption decreases and then improves again. Diarrhoea starts from the 10th day onwards, and persists until death.

The faeces vary in consistency — from putty-like to mucopurulent, green and foul smelling. Intussusception may occur. This form of oesophagostomosis used to be quite common, but, due to intensive treatment aimed mainly at Haemonchus contortus , it has become scarce. In calves, pain, anorexia, loss in mass, hypoproteinaemia, anaemia and diarrhoea are seen. Submandibular oedema and progressive cachexia occur after 7 weeks. Chabertiosis manifests with weight loss, diarrhoea and faeces that may be flecked with blood.

Adult Trichuris worms are not pathogenic — unless present in large numbers when they may cause abdominal pains, mucoid diarrhoea, anaemia, loss of body mass, and, rarely, death. Faecal nematode egg counts are of little value for a diagnosis of oesophagostomosis. Clinical signs — and the presence of nodules in the wall of the small intestine and colon — are diagnostic at necropsy of sheep; nodules are seldom seen in cattle.

To make a diagnosis of chabertiosis, consider the clinical signs, the season and the area. Lesions in the intestines and the presence of small numbers of the worms are diagnostic. The eggs of Trichuris are diagnostic. As mentioned above, large numbers of the worms — and thus their eggs — must be present before a diagnosis can be made, as the worms are usually apathogenic.

Causes of diarrhoea such as coccidiosis and nutritional causes should be taken into account for Oesophagostomum and Trichuris species. For Chabertia , consider causes of anaemia like haemonchosis, trichostrongylosis, fasciolosis, coccidiosis and nutritional issues. Also consider causes of diarrhoea like other helminth infections, nutritional deficiencies, poisonings, and coccidiosis.

On commercial farms, where sheep are regularly drenched, oesophagostomosis should not be a problem. The drenching interval for Haemonchus is such that Oesophagostomum is exposed to the anthelmintic twice during its pre-patent period. Sheep also develop a local immunity against the larvae — mainly in the large intestine — and adult worms are expelled in subsequent infections. Figure 25 Nodules in the large intestinal wall caused by O. Cattle in the field develop a strong immunity after 8 to 12 months of age.

The immunity may cause a great reduction in the number of re-infesting larvae developing to adults during the normal pre-patent period. The immunity will persist if adult worms are removed by anthelmintics. Living Chabertia stimulate high levels of reaginic antibody, which is probably linked to cell-mediated immunity. It is almost impossible to control Trichuris in the environment and only in intensive situations where floors can be cleaned daily, is environmental control possible.

No anthelmintic resistance is known for any of the worms in the large intestine. Select a suitable anthelmintic using the process discussed under the control of abomasal worms in small stock. Apart from the trematodes that migrate through the liver on their way to their predilection sites, the larvae of Taenia hydatigena, Echinococcus granulosus, and Echinococcus multilocularis also cause significant damage. Various Schistosoma species may be found in the blood vessels of the liver. The pentastome genus Linguatula bores tunnels of about 1 mm in diameter in the parenchyma.

Nematode larvae, mostly ascarids, may occasionally be found. Ruminants are also the intermediate hosts for some tapeworms — of which Taenia hydatigena and Echinococcus granulosus are possibly the most commonly encountered in Africa. The pentastome genera Linguatula and Armillifer are also occasionally found, but their prevalence seems to be higher in wild animals. Eggs of Taenia are eaten with the food and the hexacanth larvae oncospheres hatch in the small intestine. These burrow through the wall of the intestine, and, depending on the species, are transported by the blood to the liver, lungs, heart, or striated muscles.

In the case of T. Here they develop to cysticerci up to 8 cm in diameter — the socalled Cysticercus tenuicollis Figures 27 and The life cycle of E. Oncospheres are carried to the liver by the blood or to the lungs by the lymph — the two commonest sites for development — where they form hydatid cysts Figure The eggs of the pentastomes are also ingested and the primary larvae hatch in the small intestine. In the case of Linguatula , the larvae moult several times to form infective nymphs that keep migrating through the body, and these are often found free in the liver or heart. Cysticercosis is common throughout the world wherever sheep and goats occur, and wherever the cestode Taenia hydatigena is present.

Pentastomes are widely spread but do not occur in large numbers, and are therefore seldom encountered. The definitive hosts of Taenia hydatigena are domestic dogs and other canids and the intermediate hosts are primarily sheep and goats — although cattle and camels are infected on occasion. The definitive hosts of Echinococcus granulosus are domestic dogs and cats and a variety of wild carnivores, e.

The list of intermediate hosts comprises ruminants — including camels, suids, horses, and rodents. Humans are accidental, but entirely suitable, intermediate hosts. The pentastome genera Linguatula and Armillifer use ruminants as an intermediate host. As a final host, Linguatula parasitises the nasal sinuses and respiratory passages of carnivores, while Armillifer is a parasite of the lungs of snakes. In all cases, the acquisition of larval cestodes occurring in the liver is through ingestion of eggs by the intermediate host. Eggs are dispersed in the environment by various agents — notably insects and rain.

Adult worms develop after ingestion of the metacestodes by the final host, and in the case of the pentastomes, the infective nymph. The socio-economic influence of cysticercosis is considerable. Few animals die as a result of acute infection, but chronic infection leads to condemnation of the liver. The cysticerci on the outside of the liver are often just trimmed away and fed to dogs, which further compounds the problem.

Cystic echinococcosis has a severe influence on those populations — human or animal — where it occurs, and cost is only one of them. Cost can be categorised as the cost due to the disease in humans e. Humans are occasionally infected with pentastomes — but to what extent, is unknown. In sheep and goats the hexacanth larvae occasionally cause a severe hepatitis during the four weeks they migrate through and grow in the liver.

This resembles acute fasciolosis, and death occurs due to haemorrhage into the abdominal cavity. Once they have attained a certain size, they leave that organ and attach to the peritoneum — usually close to the liver. After another four weeks they have become large, flabby structures — Cysticercus tenuicollis — which are filled with fluid through which the protoscoleces can easily be seen Figure Hydatids in the liver and lungs are well tolerated and most infections are discovered at necropsy.

Where the oncospheres have been carried in the blood to other organs, a variety of clinical signs may present, depending on the organ in which the oncospheres lodged. Pentastomes are also well tolerated, and even with heavy infections there is little haemorrhage into the abdominal cavity. In most cases infection with cestode or pentastome larvae goes unnoticed and is detected only at meat inspection or necropsy. Infrequently, however, large numbers of developing cysticerci migrate in the liver, causing hepatitis cysticercosa.

This is a condition that is similar to acute fasciolosis and is often fatal refer to pathogenesis and pathology. Once the cysticerci have developed, there are no clinical signs. Cystic echinococcosis refers to an infection with hydatid cysts, and is a common occurrence in Africa. As a clinical entity, it is rarely suspected — but is frequently diagnosed at necropsy. Pentastomes often encapsulate in the liver or peritoneum of ruminant intermediate hosts, but no clinical signs have been ascribed to them.

Acute hepatitis cysticercosa in sheep is characterised by an enlarged liver in the parenchyma in which numerous migration tracts are seen. The surface of particularly the ventral lobe is covered with a fibrinous exudate. Subcapsular haemorrhages are common, and these may rupture so that blood is found in the abdominal cavity. Acute hepatitis cysticercosa is seldom seen in cattle.

Depending on the number of oncospheres invading, there may or may not be significant damage. In the former case, it will resemble chronic fasciolosis and the large cysticerci can be seen on the peritoneum or close to the gall bladder. In the case of cystic hydatidosis, the lesions are associated with pressure — which in the different organs i.

Chronic cysticercosis is usually only diagnosed at the abattoir or at necropsy, as is infection with pentastomes. Figure 28 T. Cystic echinococcosis in humans can be diagnosed by various imaging techniques, e. X-ray, ultrasound, CT scan or magnetic resonance, or by serological methods — of which a whole battery is available. In animals the diagnosis of cystic echinococcosis is seldom called for, and is usually only diagnosed at the abattoir or at necropsy. The diagnosis of infection in dogs is difficult because of the small size of the tapeworm and few proglottids are shed.

In some countries a purgative like arecoline hydrochloride is administered — which results in the expulsion of the entire tapeworm. Differential diagnoses for acute deaths from acute hepatitis cysticercosa would include acute fasciolosis. Cysticercosis and cystic hydatidosis are both relatively easy to control, but the lack of knowledge in many parts of Africa still makes for large numbers of infected animals and humans. Firstly, dogs should never be fed uncooked offal — this may contain the cysticerci or hydatid cysts.

Secondly, humans should wash their hands thoroughly before eating or drinking, especially if they have been playing with dogs or gardening. Thirdly, where possible, dogs should be dewormed using praziquantel and the faeces disposed of so that the tapeworm eggs cannot contaminate the pastures where ruminants graze. Fourthly, where dogs are found positive for Echinococcus , contamination of vegetables and water is possible, and therefore everything, including the water, should be boiled before consumption.

It is not possible to control the pentastomes, since the final hosts are either wild carnivores or snakes. Although many helminths pass through the liver during their development in their respective hosts, few adult parasites occur here. The major trematode genera are Fasciola, Fascioloides, and Dicrocoelium. Eurytrema occurs mainly in the pancreatic duct, and more rarely in the bile ducts. The only adult cestode found here is Stilesia hepatica.

Apart from the trematodes that migrate through the liver on their way to their predilection sites, the larvae of Taenia hydatigena, Echinococcus granulosus and Echinococcus multilocularis also cause significant damage. Nematode larvae — mostly ascarids — may occasionally be found. The trematodes have indirect life cycles involving either a terrestrial or an aquatic snail — and in some genera an arthropod intermediate host. The Fasciola life cycle starts with an egg that contains a miracidium Figure 30 and which must fall in a wet or damp area in order to release the miracidium Figure The miracidium must enter a suitable snail within three hours of hatching from the egg.

In the snail, development proceeds through the sporocyst and redial stages to cercariae that are the final stage of development in the intermediate host. The motile cercariae are shed, and attach to any solid object in the water like vegetation, dead leaves and even twigs and dead insects — where they encyst to the metacercariae. The latter are infective for the final host.

Once ingested by the final host, the metacercariae excyst in the small intestine, pass through the intestinal wall, cross the abdominal cavity, and then penetrate the liver. The young flukes tunnel through the parenchyma and enter the small bile ducts after 6 to 8 weeks. They migrate to the larger bile ducts where they develop to adults Figure The prepatent period of F. Figure 32 Haemorrhage due to rupture of the liver caused by F. Figure 33 Chronic fasciolosis with thickened bile ducts and peri-portal fibrosis.

The life cycle of Dicrocoelium is different in that a second intermediate host is utilised. The egg — which contains a miracidium — must be eaten by a terrestrial snail in order to hatch. Two generations of sporocysts develop, which then produce cercariae, but there are no rediae. The cercariae are extruded in masses cemented together with mucus. The slime balls of cercariae are ingested by an ant of the genus Formica D.

This presumably increases the possibility that infected ants will be eaten by the final host. The metacercariae excyst in the small intestine and the young flukes migrate up the main bile duct into the smaller ones, where they attain sexual maturity. The pre-patent period is 10 to 12 weeks. The life cycle of Eurytrema is similar, in that a terrestrial snail is the first intermediate host and a tree cricket or grasshopper the second. The metacercariae hatch in the small intestine and enter the pancreatic duct; occasionally the main bile duct is entered and the flukes are found in the smaller bile ducts in the liver.

Stilesia hepatica are shed with the faeces, and a soil mite — probably of the family Oribateidae — is used as an intermediate host. A cysticercoid develops in the mite and the mite must be eaten by the final host for the life cycle to continue. In the final host, the cysticercoid evaginates its scolex and moves to the opening of the common bile duct, through which it enters to lodge in the very small bile ducts.

In Africa, the major helminths infecting the liver are the trematodes Fasciola hepatica , Fasciola gigantica and Dicrocoelium hospes. In Europe and North America Fascioloides magna is fairly common, while Dicrocoelium dendriticum is widespread. The genus Eurytrema occurs in Brazil and Asia.

The small cestode Stilesia hepatica occurs worldwide; it is also common in ruminants in Africa, except cattle. A prerequisite, which ultimately determines the distribution of the trematodes, is the presence of suitable snail intermediate hosts for the trematodes, and a suitable arthropod for Stilesia. The snails can be terrestrial Eurytrema, Dicrocoelium or aquatic Fasciola, Fascioloides , and, in some cases, a second intermediate host — usually an arthropod — is required.

Stilesia requires one of the soil mites, probably of the family Oribateidae. The main hosts of trematodes and the cestode are ruminants. Sheep, goats, cattle and a variety of wild ruminants are affected, but often not to the same degree. Dicrocoelium is present in rabbits and in ruminants, and Stilesia is rare in cattle. In all cases the transmission of helminths parasitising the liver is through ingestion of metacercariae the trematodes or cysticercoids Stilesia that occur either on vegetation or in an intermediate host.

The epidemiology of the snails is also important for the transmission of the parasites. Some snails are aquatic, others are semi-aquatic, and suitable habitats must be present. The aquatic snail Lymnaea truncatula prefers wet mud to free water, and temporary habitats like hoof marks and rain ponds that develop after heavy rain or excessive irrigation, are colonised. During winter, the snails hibernate and the development of the fluke larvae is halted. Development resumes when temperatures rise and metacercariae are available during spring.

There is some evidence that the prevalence of fasciolosis in warm countries is higher after several months of drought — possibly because animals congregate around watering places, so increasing the chances of snails becoming infected. Rainfall should exceed the transpiration rate of the vegetation in order for the eggs to develop, the miracidia to find the snails, and the cercariae to disperse after having left the snails. The socio-economic influence of trematode infection of the liver — and, in particular, fasciolosis — can be considerable.

Many animals die as a result of infection, and in developing countries this has a major impact on the cash flow and economics of a region. During the acute phase of infection, the immature flukes burrow through the parenchyma and their rapid growth during this period causes substantial damage — especially just before they enter the bile ducts. Depending on the number of flukes present, this causes severe haemorrhage and often the death of the animal.

Similarly, the fibrosis in the parenchyma and thickened bile ducts seen in chronic cases lead to condemnation of the liver, which is a further economic loss. Humans are occasionally infected with liver fluke, but it seems to be under-reported in the literature.

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Recent estimates, based on serodiagnosis, indicate that as many as 17 million people in the world suffer from fasciolosis. In humans, clinical manifestations appear early in the infection, long before parasitologic diagnosis is possible, and the symptoms and clinical signs are as severe as they are in ruminants. The pathogenesis of fasciolosis depends on the host species, the stage of the infection, and the number of infecting flukes. In field situations, animals acquire infections over an extended period, so that flukes of all developmental stages are in the liver. This results in clinical signs of both acute and chronic disease.

The passage of the young Fasciola species through the intestinal wall into the peritoneal cavity causes little damage, and the changes that do occur are mostly localized and transient. Once in the liver the young flukes burrow through the parenchyma creating tracks or tunnels, and this is the acute stage. Blood vessels and small bile ducts are damaged — resulting in haemorrhage, thrombosis and disruption of the flow of bile. During their migration, the young flukes feed on hepatic cells and blood, and also secrete proteolytic enzymes.

They grow rapidly, causing even more damage, especially during the period just before they enter the bile ducts. Haemorrhage may become severe in the late acute stage, and may cause the death of the host either through haemorrhage into the abdominal cavity or beneath the capsule of the liver Figure 32 and If the host survives, hepatic fibrosis and hyperplastic cholangitis develop.

The chronic stage develops slowly and is the result of the presence of the fluke in the bile ducts, where they become sexually mature. Chronic fasciolosis is a combination of cholangitis, biliary obstruction, destruction of hepatic tissue, and the release of a haemolytic substance by the fluke. The tracts in the parenchyma heal and connective tissue forms in and between tracts.

Foci of coagulative necrosis form parallel and adjacent to the healing tracts — which, in turn, also eventually heal by fibrosis Figure