Other editions. Enlarge cover. Error rating book. Refresh and try again. Open Preview See a Problem? Details if other :. Thanks for telling us about the problem. Return to Book Page. This second edition provides a comprehensive review of the facts and trends in veterinarian and human parasitology.
Encyclopedic Reference of Parasitology: Diseases, Treatment, Therapy by Heinz Mehlhorn
Several internationally renowned specialists have been added to the authors of the first edition, and the whole is now organised in an encyclopedic arrangement of comprehensive keywords, thus speeding up the search for information. Get A Copy. Hardcover , pages. Floch, Martin H. Journal of Clinical Gastroenterology34 1 , January Add Item s to:. An Existing Folder. A New Folder. The item s has been successfully added to " ".
Thanks for registering! Be sure to verify your new user account in the next 24 hours, by checking your email and clicking the "verify" link. This article has been saved into your User Account, in the Favorites area, under the new folder " ". End Note. Peer reviewers approved by Dr Colin Mak. Editor who approved publication: Professor Young Lyoo. The domestic and wild canids are the definitive host of the parasite. They shed oocysts after ingestion of tissue cysts from infected intermediate hosts ovine, equine, bovine, canine, and many other species , containing bradyzoites, or oocyst-contaminated water and food.
The presence of dogs in farms is considered a risk factor for production animals. A wide range of diagnostic methods are currently available, but the most used is serology, ie, indirect fluorescent antibody test specific to the antibody detection in blood serum samples. No vaccine is available, but control strategies should be focused on the vertical and horizontal transmission of the parasite, ie, avoid feeding dogs with raw or undercooked meat, and taking care with water for human and animal consumption.
No medicines to control the transplacental transmission are available yet. Keywords: neosporosis, Neospora caninum , pathogenesis, management, dogs. Neospora caninum is an obligate intracellular parasite protozoan that causes neosporosis in a wide range of warm-blooded animals, including domestic and wild animals.
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Neosporosis is a worldwide emergent disease, 1 — 3 and is usually associated with reproductive ie, neonatal mortality in animals, particularly in dogs and cattle and neurological ie, neuromuscular degeneration disorders and presents progressive evolution, being more severe in young animals. Sheep can also develop reproductive and neonatal disease, but the economic importance of N.
The new parasite was firstly classified N. These authors isolated and described the disease caused by a protozoan infecting a puppy with clinical signs similar to those reported by Bjerkas et al. The absence of information concerning the epidemiology of the parasite has limited the introduction of objective and effective measures to prevent and control the infection significantly over time. Three infective stages characterize the N. Tissue cysts have a huge cyst wall that protects the bradyzoites from the hostile extracellular environment formed during the host immune response.
This form is observed mainly in muscle and the central nervous system CNS.
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Each tissue cyst may have 20— bradyzoites. Tachyzoites can be found free in organic fluids and in a parasitophorous vacuole PV placed at the cytoplasm of the host cell, but are particularly vulnerable to the harmful effects of extracellular maintenance and rapidly lose their capacity for invasion. Table 1 Structural and morphological characteristics of Neospora caninum stages. A wide range of intermediate hosts has been reported Table 2. Table 2 Definitive and intermediate hosts in neosporosis Abbreviations: W, wild area; non-W, nonwild area; M, marine area.
Many aspects of the N. Vertical transmission happens during terminal stages of gestation transplacental transmission with fetal infection or postnatally, by the transmission of tachyzoites via milk transmammary transmission.
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After ingestion, sporulated oocysts or tissue cysts excyst and release sporozoites and bradyzoites, respectively, into the duodenum lumen. In the intestinal epithelium, sporozoites and bradyzoites transform into tachyzoites, undergo a phase of multiplication, possibly in the mesenteric lymph nodes, 11 reach the bloodstream, and disseminate to gravid uterus, 11 and many cell types, ie, CNS cells, vascular endothelial cells, myocytes, hepatocytes, renal cells, alveolar macrophages, and placental trophoblasts, 14 , 43 invade the cells and start the multiplication, causing severe lesions on the affected tissues.
If the host immune response is active, the extracellular environment turns hostile to the parasite; tachyzoites differentiate to bradyzoites and form tissue cysts asexual stage in intermediate hosts chronic stage of the infection. The recrudescence of the disease for any suppressive factor promotes alterations in host immunity, causing immunomodulation or immunosuppression, the conversion of bradyzoites to tachyzoites, and the rupture of the tissue cysts.
This process releases bradyzoites, which reactivate the infection. In definitive hosts, tachyzoites transform in merozoites, ie, macrogametes and microgametes, into the intestinal epithelium, undergo merogony sexual stage , and form a zygote. Zygotes, or nonsporulated oocysts, are released at the intestinal lumen, and shed up to 1 million to the environment with the host feces 20 , 25 2—30 days after ingestion.
The nonsporulated oocysts become sporulated and orally infectious outside the host in proper environmental conditions oxygen concentration, humidity, and temperature in 1—5 days. No breed predisposition or differential sex susceptibility to neosporosis in dogs is known, 33 but age can be a risk factor. Adult dogs shed fewer oocysts than puppies following primary exposure, and puppies may also develop reexcretion after new challenge. Some important factors to be considered when reporting N.
Wouda et al 32 suggested that once dogs and cattle live in the same farm, the chances of the infection in cattle increase. Neither Liu et al 63 nor Paiz et al 71 observed the pasturing system to be a significant risk factor for goats. In herbivorous creatures, N. Low levels of horizontal transmission in cattle were also observed by Hietala and Thurmond 47 and Davison et al, 46 but the importance of this route should not be underestimated, mainly due to the maintenance of the parasite in regional herds.
In South America, seroprevalence in dairy cattle has ranged from In small ruminants, prevalence ranges according to region and species. In goats, prevalence has ranged from 0. In addition, the presence of dogs and bad conditions of hygiene are important risk factors that contribute to the infection in these species.
The pathogenesis of neosporosis depends on the balance between the capacity of the tachyzoite to penetrate and multiply inside the cells and the host to impede the parasite proliferation. The cell-invasion process has two different steps — the adhesion to the host-cell surface and penetration to the cell 86 — which may take no more than 5 minutes. In this way, a more specific ligation to the host-cell surface occurs and finally the invasion. For that, adequate receptors at the host-cell surface are required to provide enough signals for the invasion of the parasite into the cell cytoplasm.
In order to initiate host-cell invasion, tachyzoites reorient themselves perpendicularly to the host cell-surface membrane and enter the cytoplasm by advancing anterior end first, until they are located in the cytoplasm, enclosed by the PV. Invasion is an active process requiring metabolic energy solely on the part of the parasite, but not on the part of the host cell. In contrast to other genera, N. Once inside, the parasite induces metabolic alterations in the host, which favor its maintenance. The parasite attracts the host Golgi apparatus to its PV, surrounding it, but induces less fragmentation into ministacks than T.
These processes are highly conserved in both parasites. The parasite must invade the host cell to avoid the host immune response. This response and the humoral immune response work together on containing the infection. In general, neosporosis is asymptomatic in adult and older dogs. The clinical signs are usually general and the same as observed in toxoplasmosis, but neurological and muscular abnormalities predominate, 33 as forelimbs paralysis. In younger puppies, it is normal to observe clinical signs starting at 3—9 weeks old.
Forelimb atrophy and gradual muscular rigidity are the most important clinical signs that differentiate neosporosis from those other disorders causing paralysis; even so, hind limbs are more severely affected than forelimbs.
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The paralysis progresses to rigid contracture of the muscle from the affected limbs. This arthrogryposis results in a scar formation on these muscles, due to injury at the lower motor neuron and myositis. Articular deformation and joint curvature genu recurvatum can occur in some puppies, 30 followed by cervical weakness, dysphagia, megaesophagus, and death. It is more probable that dogs over 6 months old can develop the disease by the reactivation of a latent chronic infection.
However, females may have immunosuppression and reactivate the infection during gestation. In this way, bradyzoites switch back to tachyzoites, cross the placenta, and infect the fetus. In buffaloes, naturally occurring disease is rare, but abortion has been reported in animals that have contact with dogs Neosporosis should be considered when hyperesthesia, muscle swelling, or atrophy is observed at the clinical exam. Dogs of any age can die by CNS or muscular inflammation. Focal lesions have been reported in the brain and spinal cord of a 6-year-old dog with severe mononuclear cell infiltration large numbers of T lymphocytes and B lymphocytes, and small numbers of macrophages of the nerve roots of the cauda equina and of the lumbar nerve roots.
Necrotizing cerebellitis and hepatitis were also observed. Epidemiological history and clinical findings can help the diagnosis of suspected neosporosis, as well as the control and prevention of the disease. The findings observed on complete blood count and serum biochemistry panel are also suggestive, but should not be used to confirm the infection. Normal complete blood count with mild nonregenerative anemia, mild eosinophilia, or monocytosis can be observed; nucleated cells are predominantly nondegenerated to mildly degenerated neutrophils.
Myositis can cause high alanine aminotransferase values, and hyperglobulinemia can also be observed. Protein concentration can also be increased. Image diagnosis can also help with the extent of the lesions, ie, radiography diffuse interstitial pattern in dogs with pneumonia , magnetic resonance imaging, and ultrasonography cerebellar atrophy in dogs with cerebellar signs , 20 but with limited contribution.
No pathognomonic findings have been reported for neosporosis. The available methodologies allow clinicians and researchers to amplify knowledge about classical and molecular epidemiology and pathogenesis of the disease, evaluate the efficacy of available and future drugs used to treat the clinical signs, and adopt measures to avoid dissemination of the parasite. The limit of detection, sensitivity, specificity, and positive and negative predictive values of each test are a crucial part of standardization, and very important to offer an accurate tool for the diagnostic routine.
Light microscopy is the cheapest and quickest method that can be used by clinicians, but has limited sensitivity and requires experience in characterizing the infective stages of the parasite, which can be misinterpreted as another apicomplexan. Both isolation techniques are laborious, require specific technical personnel to handle the animals or cell lines to control other types of infection in a closed system, and require specific infrastructure to maintain the animals and cells under ethical conditions, which all increase the costs. One drawback of both methods is limit of detection.
Depending on the sample, the parasite isolation in samples with low parasite load or avirulent or less virulent strains may be difficult. Even if possible, it may still take a minimum of 20—30 days to get results. Fecal flotation, with sugar or zinc sulfate solutions, is the best technique to isolate N. Another limitation is that dogs presenting clinical signs do not shed oocysts, resulting in negative findings. The cost is not high, but the clinical value for a clinician is limited. Histopathology and immunohistochemistry are highly recommended in reproductive problems, ie, abortion and fetal lesions, and have been used with molecular techniques.
Their sensitivity and specificity will depend on a good target, antibodies, microscope, and an experienced technician to provide an accurate evaluation and conclusion. The cost is usually higher than the methodologies reported earlier, but the results are much more conclusive concerning the extent and severity of the lesions.
Molecular methods are considered to have the best sensitivity and specificity, but are too relative. The sensitivity and specificity of these tests are linked to the standardization of the technique, type of sample, stage of the infection, targeted region, and all reagents used. A well-standardized methodology can detect down to just one copy of DNA present in the analytes, but methodologies with problems can fail to detect the parasite or misdiagnose N. Corroborating this, van Maanen et al 93 observed low agreement between the majority scores of immunohistochemistry and PCR methods single or nested in bovine fetal tissues on an interlaboratory comparison in Europe, with false-positive PCR results indicating contamination problems in some instances.
The authors strongly linked this problem to the DNA-extraction methods, which could have been optimized and improved the performance of the test. In this way, quality control is an important point in choosing tests or labs to run the samples. Quality control may increase the price of a test, but it also improves the accuracy of the results. The wide range of molecular targets allows a wide range for application of molecular techniques, ie, DNA, parasite-load measurement, parasite detection in very low concentrations, exploration of the population evolution of the parasite, analysis of the likelihood of the detected parasites with those from the same and other areas, and characterization of the isolates.
In this way, different methodologies have been developed, ie, quantitative real-time PCR, random fragment-length polymorphism PCR, and the use of multilocus microsatellite typing of ten microsatellites for molecular genotyping, which allowed Campero et al 92 to identify the isolate NC-Argentina LP1 as a unique genetic pattern, different from all reported isolates.
Differently from direct methods, indirect methods include serological tests by immunoblotting and detection of the indirect response of the host specific antibodies to the parasite challenge. The limitation of serology is related to the physiopathology of the disease. Usually, antibody levels take 2—3 weeks of infection to be detectable. Antibody research is highly recommended for screening infection in a population, mainly in a herd, and in individual patients to analyze the response of the immune system.
The presence of N. IFAT was the first serological test used. Usually, costs for a test or retest are low, but can increase in a periodic control in a herd or large population. Alvarez-Garcia et al compared ten commercial indirect or competitive available ELISA tests for bovine neosporosis and obtained excellent sensitivities In this way, laboratorial findings are of fundamental importance and make a contribution to the diagnosis of the infection and disease, but should be linked to clinical signs to have enough conclusive information for the treatment of each animal and epidemiological information to adopt adequate measures for prevention and control of the infection.
Treatment of neosporosis is usually difficult and temporarily, partially, or completely ineffective. The treatment of dogs with neurological signs is too long, and has a poor prognosis.
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