Chorioretinitis
Toxoplasmosis, Ocular
Panuveitis
Uveitis, Posterior
Onchocerca
Pupil Disorders
Fundus Oculi
Uveitis
Toxoplasmosis, Congenital
Anterior Chamber
Toxoplasma
Endophthalmitis
Fluorescein Angiography
Vitreous Body
Protozoan Infections
Uvea
De novo lesions in presumed ocular histoplasmosis-like syndrome. (1/118)
Two patients with multifocal choroiditis similar or identical to POHS are presented. Colour photographs and fluorescein angiography document the occurrence of de novo lesions in the originally involved eye. The cases also demonstrate the development of new choroidal lesions within the originally involved eye, the early evolution of the "basic choroidal lesion", and the need for fluorescein angiography for visualizing the underlying choroidal lesion. (+info)New animal model for human ocular toxocariasis: ophthalmoscopic observation. (2/118)
BACKGROUND/AIMS: Although human ocular toxocariasis causes severe vision defect, little is known about its aetiology, diagnosis, and treatment. To develop a new animal model for human ocular toxocariasis, ophthalmological findings of fundi in Mongolian gerbils, Meriones unguiculatus, and BALB/c mice were investigated following infection with Toxocara canis. METHODS: Using an ophthalmoscope, which was specifically developed to observe the fundi of small animals, ocular changes of fundi of 20 gerbils and 11 mice were monitored after oral infection with embryonated eggs of T canis. RESULTS: Vitreous, choroidal, and retinal haemorrhages were consistently observed in Mongolian gerbils, but rarely in mice. Severe exudative lesions and vasculitis were often present in gerbils but not in mice. Migrating larvae were also frequently observed in gerbils. CONCLUSION: Mongolian gerbils are more appropriate animal model for human ocular toxocariasis than previously used experimental animal such as mice, guinea pigs, rabbits, and monkeys because of its high susceptibility of ocular infection. (+info)Detection of specific immunoglobulin E during maternal, fetal, and congenital toxoplasmosis. (3/118)
Toxoplasma immunoglobulin E (IgE) antibodies in 664 serum samples were evaluated by using an immunocapture method with a suspension of tachyzoites prepared in the laboratory in order to evaluate its usefulness in the diagnosis of acute Toxoplasma gondii infection during pregnancy, congenital infection, and progressive toxoplasmosis. IgE antibodies were never detected in sera from seronegative women, from patients with chronic toxoplasma infection, or from infants without congenital toxoplasmosis. In contrast, they were detected in 86.6% of patients with toxoplasmic seroconversion, and compared with IgA and IgM, the short kinetics of IgE was useful to date the infection precisely. For the diagnosis of congenital toxoplasmosis, specific IgE detected was less frequently than IgM or IgA (25 versus 67.3%), but its detection during follow-up of children may be interesting, reflecting an immunological rebound. Finally, IgE was detected early and persisted longer in progressive toxoplasmosis with cervical adenopathies, so it was also a good marker of the evolution of toxoplasma infection. (+info)Toxoplasma gondii infection induces gene expression and secretion of interleukin 1 (IL-1), IL-6, granulocyte-macrophage colony-stimulating factor, and intercellular adhesion molecule 1 by human retinal pigment epithelial cells. (4/118)
We have used human retinal pigment epithelial (HRPE) cultures to investigate the primary cellular responses of retinal resident cells to intracellular Toxoplasma gondii replication. At 4 days postinoculation, when all of the cells were infected, the secretion of interleukin 1beta (IL-1beta), IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), and intercellular adhesion molecule 1 (ICAM-1) was augmented by 23-, 10-, 8-, and 5-fold, respectively, over the control. Northern and reverse transcriptase PCR analyses showed significant upregulation of steady-state levels of mRNA for IL-1beta, IL-6, GM-CSF, and ICAM-1. The secretion of these molecules by HRPE cells may play a critical immunoregulatory role in the pathophysiological processes associated with T. gondii-induced retinochoroiditis. (+info)Childhood blindness and visual loss: an assessment at two institutions including a "new" cause. (5/118)
PURPOSE: This study was initiated to investigate the causes of childhood blindness and visual impairment in the United States. We also sought a particular etiology--congenital lymphocytic choriomeningitis virus (LCMV)--which has been considered exceedingly rare, in a fixed target population of children, the severely mentally retarded. METHODS: We undertook a library-based study of the world literature to shed light on the causes of childhood blindness internationally and to put our data in context. We prospectively examined all consented children (159) at 2 institutions in the United States to determine their ocular status and the etiology of any visual loss present. One of the institutions is a school for the visually impaired (hereafter referred to as Location V), in which most of the students have normal mentation. The other is a home for severely mentally retarded, nonambulatory children (hereafter referred to as Location M). This institution was selected specifically to provide a sample of visual loss associated with severe retardation because the handful of cases of LCMV in the literature have been associated with severe central nervous system insults. Histories were obtained from records on site, and all children received a complete cyclopleged ophthalmic examination at their institution performed by the author. Patients at Location M with chorioretinal scars consistent with intrauterine infection (a possible sign of LCMV) had separate consents for blood drawing. Sera was obtained and sent for standard TORCHS titers, toxoplasmosis titers (Jack S. Remington, MD, Palo Alto, Calif), and ELISA testing for LCMV (Centers for Disease Control and Prevention, Atlanta, Ga). RESULTS: The diagnoses at Location V were varied and included retinopathy of prematurity (19.4%), optic atrophy (19.4%), retinitis pigmentosa (14.5%), optic nerve hypoplasia (12.9%), cataracts (8.1%), foveal hypoplasia (8.1%), persistent hyperplastic primary vitreous (4.8%), and microphthalmos (3.2%). The most common diagnosis at Location M was bilateral optic atrophy, which was found in 65% of the patients examined who had visual loss. Of these, the insults were most often congenital (42.6%), with birth trauma, prematurity, and genetics each responsible for about 15% of the optic atrophy. The second most common diagnosis was cortical visual impairment (24%), followed by chorioretinal scars (5%), which are strongly suggestive of intrauterine infection. Of 95 patients examined at Location M, 4 had chorioretinal scars. Two of these had dramatically elevated titers for LCMV, as did one of their mothers. One of the other 2 children died before serum could be drawn, and the fourth had negative titers for both TORCHS and LCMV. CONCLUSIONS: At both locations studied, visual loss was most often due to congenital insults, whether genetic or simply prenatal. The visual loss at Location V was twice as likely as that at Location M to be caused by a genetic disorder. The genetic disorders at Location V were more often isolated eye diseases, while those among the severely retarded at Location M were more generalized genetic disorders. Our study identified optic atrophy as a common diagnosis among the severely mentally retarded with vision loss, a finding that is supported by previous studies in other countries. In our population of severely retarded children, the target etiology of lymphocytic choriomeningitis virus was responsible for half the visual loss secondary to chorioretinitis from intrauterine infection. This is more common than would be predicted by the few cases previously described in the literature, and strongly suggests that LCMV may be a more common cause of visual loss than previously appreciated. We believe that serology for LCMV should be part of the workup for congenital chorioretinitis, especially if the TORCHS titers are negative, and that perhaps the mnemonic should be revised to "TORCHS + L." Childhood blindness and visual impairment are tragic and co (+info)Population based assessment of uveitis in an urban population in southern India. (6/118)
AIM: To assess the prevalence of active and inactive uveitis unrelated to previous surgery or trauma in an urban population in southern India. METHODS: As part of the Andhra Pradesh Eye Disease Study, 2522 subjects (85.4% of those eligible), a sample representative of the population of Hyderabad city in southern India, underwent interview and detailed dilated eye examination. Presence of sequelae of uveitis without current active inflammation was defined as inactive uveitis. RESULTS: Unequivocal evidence of active or inactive uveitis unrelated to previous surgery or trauma was present in 21 subjects, an age-sex adjusted prevalence of 0.73% (95% confidence interval (CI) 0.44-1.14%). Active uveitis was present in eight subjects, an age-sex adjusted prevalence of 0.37% (95% CI 0. 19-0.70), of which 0.06% was anterior, 0.25% intermediate, and 0.06% posterior. The 0.36% (95% CI 0.17-0.68%) prevalence of inactive uveitis included macular chorioretinitis scars (0.26%), anterior (0. 07%) and previous vasculitis involving the whole eye (0.03%). The prevalence of visual impairment due to uveitis of less than 6/18 in at least one eye was 0.27%, less than 6/60 in at least one eye was 0. 16%, and less than 6/60 in both eyes was 0.03%. CONCLUSION: These population based cross sectional data give an estimate of the prevalence of various types of uveitis in this urban population in India. Active or past uveitis that might need treatment at some stage was present in one of every 140 people in this population. (+info)Rapid progressive subacute sclerosing panencephalitis in a 2-year-old child with congenital athyreosis. (7/118)
We present the unique case of a 2-year-old girl with congenital athyreosis who acquired primary measles virus infection at the age of 18 months, coincidentally with an Epstein-Barr virus infection. First neurologic symptoms of subacute sclerosing panencephalitis appeared 5 months later, and the girl died within 6 months after a rapid progressive illness. Factors possibly predisposing to this extraordinary disease course-primary measles virus infection at an early age and lack of evidence for immunodeficiency-are discussed. (+info)Effect of Fas and Fas ligand deficiency in resistance of C57BL/6 mice to HSV-1 keratitis and chorioretinitis. (8/118)
PURPOSE: To investigate the effect of Fas and Fas ligand (FasL) deficiency on the development of herpes stromal keratitis and on the von Szily model of herpes retinitis in C57BL/6 mice, which are ordinarily resistant to development of both of these herpetic diseases. METHODS: Anterior chamber inoculation of the right eye of each mouse with various titers of HSV-1 (KOS strain) was performed. Both eyes of each mouse were enucleated on postinoculation day 15 and processed for histopathologic examination. HSV-1 was inoculated into one cornea of other mice, and the severity of stromal keratitis was scored. RESULTS: Contralateral destructive chorioretinitis developed in susceptible Balb/cByj mice (19/23); ipsilateral chorioretinitis did not occur (0/23). Stromal keratitis developed in susceptible C.AL-20 mice (15/16). None of the C57BL/6 (0/10 for keratitis or 0/20 for retinitis) developed inflammation. Neither did B6.SMN.C3H.gld (FasL deficient; 0/12 or 0/28) or B6.MRL.lpr (Fas deficient; 0/11 or 0/34) mice (keratitis or contralateral chorioretinitis). Minimal scattering of inflammatory cells in the contralateral retina but not destructive chorioretinitis was observed in two C57BL/6, three B6.SMN.C3H.gld, and five B6.MRL.lpr mice. Few inflammatory cells were also found in the ipsilateral vitreous and vitreoretinal interface (but not destructive chorioretinitis) of all C57BL/6, two gld, and three lpr mice. CONCLUSIONS: Immune dysregulation secondary to deficiency in Fas or FasL system does not influence the resistance of the C57BL/6 mice to develop herpes simplex keratitis or destructive herpes simplex chorioretinitis. (+info)Chorioretinitis is a medical term that refers to the inflammation of the choroid and the retina, which are both important structures in the eye. The choroid is a layer of blood vessels that supplies oxygen and nutrients to the retina, while the retina is a light-sensitive tissue that converts light into electrical signals that are sent to the brain and interpreted as visual images.
Chorioretinitis can be caused by various infectious and non-infectious conditions, such as bacterial, viral, fungal, or parasitic infections, autoimmune diseases, or cancer. The symptoms of chorioretinitis may include decreased vision, floaters, blurry vision, sensitivity to light, and eye pain. Treatment for chorioretinitis depends on the underlying cause and may include antibiotics, antiviral medications, corticosteroids, or other immunosuppressive therapies. It is important to seek medical attention promptly if you experience any symptoms of chorioretinitis, as timely diagnosis and treatment can help prevent permanent vision loss.
Ocular toxoplasmosis is an inflammatory eye disease caused by the parasitic infection of Toxoplasma gondii in the eye's retina. It can lead to lesions and scarring in the retina, resulting in vision loss or impairment. The severity of ocular toxoplasmosis depends on the location and extent of the infection in the eye. In some cases, it may cause only mild symptoms, while in others, it can result in severe damage to the eye. Ocular toxoplasmosis is usually treated with medications that target the Toxoplasma gondii parasite, such as pyrimethamine and sulfadiazine, often combined with corticosteroids to reduce inflammation.
Panuveitis is a medical term that refers to inflammation that affects the entire uveal tract, including the iris, ciliary body, and choroid. The uveal tract is the middle layer of the eye between the inner retina and the outer fibrous tunic (sclera). Panuveitis can also affect other parts of the eye, such as the vitreous, retina, and optic nerve.
The symptoms of panuveitis may include redness, pain, light sensitivity, blurred vision, floaters, and decreased visual acuity. The condition can be caused by various factors, including infections, autoimmune diseases, trauma, or unknown causes (idiopathic). Treatment typically involves the use of corticosteroids to reduce inflammation, as well as addressing any underlying cause if identified. If left untreated, panuveitis can lead to complications such as cataracts, glaucoma, and retinal damage, which can result in permanent vision loss.
Posterior uveitis is a type of uveitis that specifically affects the back portion of the uvea, which includes the choroid (a layer of blood vessels that provides nutrients to the outer layers of the retina), the retina (the light-sensitive tissue at the back of the eye), and the optic nerve (which carries visual information from the eye to the brain).
Posterior uveitis can cause symptoms such as blurred vision, floaters, sensitivity to light, and decreased vision. It may also lead to complications such as retinal scarring, cataracts, glaucoma, and retinal detachment if left untreated. The condition can be caused by a variety of factors, including infections, autoimmune diseases, and trauma. Treatment typically involves the use of corticosteroids or other immunosuppressive medications to reduce inflammation and prevent complications.
Onchocerca is a genus of filarial nematode worms that are the causative agents of onchocerciasis, also known as river blindness. The most common species to infect humans is Onchocerca volvulus. These parasites are transmitted through the bite of infected blackflies (Simulium spp.) that breed in fast-flowing rivers and streams.
The adult female worms live in nodules beneath the skin, while the microfilariae, which are released by the females, migrate throughout various tissues, including the eyes, where they can cause inflammation and scarring, potentially leading to blindness if left untreated. The infection is primarily found in Africa, with some foci in Central and South America. Onchocerciasis is considered a neglected tropical disease by the World Health Organization (WHO).
A pupil disorder refers to any abnormality or condition affecting the size, shape, or reactivity of the pupils, the circular black openings in the center of the eyes through which light enters. The pupil's primary function is to regulate the amount of light that reaches the retina, adjusting its size accordingly.
There are several types of pupil disorders, including:
1. Anisocoria: A condition characterized by unequal pupil sizes in either one or both eyes. This may be caused by various factors, such as nerve damage, trauma, inflammation, or medication side effects.
2. Horner's syndrome: A neurological disorder affecting the autonomic nervous system, resulting in a smaller pupil (miosis), partial eyelid droop (ptosis), and decreased sweating (anhidrosis) on the same side of the face. It is caused by damage to the sympathetic nerve pathway.
3. Adie's tonic pupil: A condition characterized by a dilated, poorly reactive pupil due to damage to the ciliary ganglion or short ciliary nerves. This disorder usually affects one eye and may be associated with decreased deep tendon reflexes in the affected limbs.
4. Argyll Robertson pupil: A condition where the pupils are small, irregularly shaped, and do not react to light but constrict when focusing on nearby objects (accommodation). This disorder is often associated with neurosyphilis or other brainstem disorders.
5. Pupillary dilation: Abnormally dilated pupils can be a sign of various conditions, such as drug use (e.g., atropine, cocaine), brainstem injury, Adie's tonic pupil, or oculomotor nerve palsy.
6. Pupillary constriction: Abnormally constricted pupils can be a sign of various conditions, such as Horner's syndrome, Argyll Robertson pupil, drug use (e.g., opioids, pilocarpine), or oculomotor nerve palsy.
7. Light-near dissociation: A condition where the pupils do not react to light but constrict when focusing on nearby objects. This can be seen in Argyll Robertson pupil and Adie's tonic pupil.
Prompt evaluation by an ophthalmologist or neurologist is necessary for accurate diagnosis and management of these conditions.
"Fundus Oculi" is a medical term that refers to the back part of the interior of the eye, including the optic disc, macula, fovea, retinal vasculature, and peripheral retina. It is the area where light is focused and then transmitted to the brain via the optic nerve, forming visual images. Examinations of the fundus oculi are crucial for detecting various eye conditions such as diabetic retinopathy, macular degeneration, glaucoma, and other retinal diseases. The examination is typically performed using an ophthalmoscope or a specialized camera called a retinal camera.
Uveitis is the inflammation of the uvea, the middle layer of the eye between the retina and the white of the eye (sclera). The uvea consists of the iris, ciliary body, and choroid. Uveitis can cause redness, pain, and vision loss. It can be caused by various systemic diseases, infections, or trauma. Depending on the part of the uvea that's affected, uveitis can be classified as anterior (iritis), intermediate (cyclitis), posterior (choroiditis), or pan-uveitis (affecting all layers). Treatment typically includes corticosteroids and other immunosuppressive drugs to control inflammation.
Congenital toxoplasmosis is a medical condition that results from the transmission of the Toxoplasma gondii parasite from an infected pregnant woman to her developing fetus through the placenta. The severity of the infection can vary widely, depending on the stage of pregnancy at which the mother becomes infected.
Infection during early pregnancy is associated with a higher risk of severe symptoms in the newborn, including:
* Intracranial calcifications
* Hydrocephalus (fluid buildup in the brain)
* Microcephaly (abnormally small head)
* Chorioretinitis (inflammation of the eye's retina and choroid layer)
* Seizures
* Developmental delays
* Hearing loss
Infection later in pregnancy may result in less severe symptoms or be asymptomatic at birth, but can still lead to developmental delays, learning disabilities, and vision problems as the child grows.
Diagnosis of congenital toxoplasmosis typically involves a combination of tests, such as blood tests to detect antibodies against Toxoplasma gondii, imaging studies (e.g., ultrasound, CT, or MRI) to assess any structural abnormalities in the brain and other organs, and ophthalmologic examinations to evaluate potential eye damage.
Treatment for congenital toxoplasmosis usually involves a combination of antiparasitic medications (such as spiramycin, pyrimethamine, and sulfadiazine) and corticosteroids to reduce inflammation. Early treatment can help minimize the severity of symptoms and improve outcomes for affected children.
The anterior chamber is the front portion of the eye, located between the cornea (the clear front "window" of the eye) and the iris (the colored part of the eye). It is filled with a clear fluid called aqueous humor that provides nutrients to the structures inside the eye and helps maintain its shape. The anterior chamber plays an important role in maintaining the overall health and function of the eye.
"Toxoplasma" is a genus of protozoan parasites, and the most well-known species is "Toxoplasma gondii." This particular species is capable of infecting virtually all warm-blooded animals, including humans. It's known for its complex life cycle that involves felines (cats) as the definitive host.
Infection in humans, called toxoplasmosis, often occurs through ingestion of contaminated food or water, or through contact with cat feces that contain T. gondii oocysts. While many people infected with Toxoplasma show no symptoms, it can cause serious health problems in immunocompromised individuals and developing fetuses if a woman becomes infected during pregnancy.
It's important to note that while I strive to provide accurate information, this definition should not be used for self-diagnosis or treatment. Always consult with a healthcare professional for medical advice.
Endophthalmitis is a serious inflammatory eye condition that occurs when an infection develops inside the eyeball, specifically within the vitreous humor (the clear, gel-like substance that fills the space between the lens and the retina). This condition can be caused by bacteria, fungi, or other microorganisms that enter the eye through various means, such as trauma, surgery, or spread from another infected part of the body.
Endophthalmitis is often characterized by symptoms like sudden onset of pain, redness, decreased vision, and increased sensitivity to light (photophobia). If left untreated, it can lead to severe complications, including blindness. Treatment typically involves administering antibiotics or antifungal medications, either systemically or directly into the eye, and sometimes even requiring surgical intervention to remove infected tissues and relieve intraocular pressure.
Toxoplasmosis is a disease caused by the parasitic protozoan Toxoplasma gondii. It can infect humans, birds, and most warm-blooded animals, including marine mammals. In humans, it is usually contracted through eating undercooked, contaminated meat or ingesting oocysts (a form of the parasite) from cat feces, often through contact with litter boxes or gardening in soil that has been contaminated with cat feces.
The infection can also be passed to the fetus if a woman becomes infected during or just before pregnancy. Most healthy individuals who become infected with Toxoplasma gondii experience few symptoms and are not aware they have the disease. However, for those with weakened immune systems, such as people with HIV/AIDS, organ transplant recipients, and pregnant women, toxoplasmosis can cause severe complications, including damage to the brain, eyes, and other organs.
Symptoms of toxoplasmosis in individuals with weakened immune systems may include swollen lymph nodes, fever, fatigue, muscle aches, and headache. In pregnant women, infection can lead to miscarriage, stillbirth, or severe developmental problems in the baby. Treatment typically involves antiparasitic medications such as pyrimethamine and sulfadiazine.
Fluorescein angiography is a medical diagnostic procedure used in ophthalmology to examine the blood flow in the retina and choroid, which are the inner layers of the eye. This test involves injecting a fluorescent dye, Fluorescein, into a patient's arm vein. As the dye reaches the blood vessels in the eye, a specialized camera takes rapid sequences of photographs to capture the dye's circulation through the retina and choroid.
The images produced by fluorescein angiography can help doctors identify any damage to the blood vessels, leakage, or abnormal growth of new blood vessels. This information is crucial in diagnosing and managing various eye conditions such as age-related macular degeneration, diabetic retinopathy, retinal vein occlusions, and inflammatory eye diseases.
It's important to note that while fluorescein angiography is a valuable diagnostic tool, it does carry some risks, including temporary side effects like nausea, vomiting, or allergic reactions to the dye. In rare cases, severe adverse reactions can occur, so patients should discuss these potential risks with their healthcare provider before undergoing the procedure.
The vitreous body, also known simply as the vitreous, is the clear, gel-like substance that fills the space between the lens and the retina in the eye. It is composed mainly of water, but also contains collagen fibers, hyaluronic acid, and other proteins. The vitreous helps to maintain the shape of the eye and provides a transparent medium for light to pass through to reach the retina. With age, the vitreous can become more liquefied and may eventually separate from the retina, leading to symptoms such as floaters or flashes of light.
Protozoan infections are diseases caused by microscopic, single-celled organisms known as protozoa. These parasites can enter the human body through contaminated food, water, or contact with an infected person or animal. Once inside the body, they can multiply and cause a range of symptoms depending on the type of protozoan and where it infects in the body. Some common protozoan infections include malaria, giardiasis, amoebiasis, and toxoplasmosis. Symptoms can vary widely but may include diarrhea, abdominal pain, fever, fatigue, and skin rashes. Treatment typically involves the use of antiprotozoal medications to kill the parasites and alleviate symptoms.
The Uvea, also known as the uveal tract or vascular tunic, is the middle layer of the eye between the sclera (the white, protective outer coat) and the retina (the light-sensitive inner layer). It consists of three main parts: the iris (the colored part of the eye), the ciliary body (structures that control the lens shape and produce aqueous humor), and the choroid (a layer of blood vessels that provides oxygen and nutrients to the retina). Inflammation of the uvea is called uveitis.
Protozoan infections in animals refer to diseases caused by the invasion and colonization of one or more protozoan species in an animal host's body. Protozoa are single-celled eukaryotic organisms that can exist as parasites and can be transmitted through various modes, such as direct contact with infected animals, contaminated food or water, vectors like insects, and fecal-oral route.
Examples of protozoan infections in animals include:
1. Coccidiosis: It is a common intestinal disease caused by several species of the genus Eimeria that affects various animals, including poultry, cattle, sheep, goats, and pets like cats and dogs. The parasites infect the epithelial cells lining the intestines, causing diarrhea, weight loss, dehydration, and sometimes death in severe cases.
2. Toxoplasmosis: It is a zoonotic disease caused by the protozoan Toxoplasma gondii that can infect various warm-blooded animals, including humans, livestock, and pets like cats. The parasite forms cysts in various tissues, such as muscles, brain, and eyes, causing mild to severe symptoms depending on the host's immune status.
3. Babesiosis: It is a tick-borne disease caused by several species of Babesia protozoa that affect various animals, including cattle, horses, dogs, and humans. The parasites infect red blood cells, causing anemia, fever, weakness, and sometimes death in severe cases.
4. Leishmaniasis: It is a vector-borne disease caused by several species of Leishmania protozoa that affect various animals, including dogs, cats, and humans. The parasites are transmitted through the bite of infected sandflies and can cause skin lesions, anemia, fever, weight loss, and sometimes death in severe cases.
5. Cryptosporidiosis: It is a waterborne disease caused by the protozoan Cryptosporidium parvum that affects various animals, including humans, livestock, and pets like dogs and cats. The parasites infect the epithelial cells lining the intestines, causing diarrhea, abdominal pain, and dehydration.
Prevention and control of these diseases rely on various measures, such as vaccination, chemoprophylaxis, vector control, and environmental management. Public awareness and education are also essential to prevent the transmission and spread of these diseases.
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