TOXOPLASMOSIS: A SIGNIFICANT PROTOZOAN FOOD-BORNE INFECTION OF ZOONOTIC IMPORTANCE

TOXOPLASMOSIS: A SIGNIFICANT PROTOZOAN FOOD-BORNE INFECTION OF ZOONOTIC IMPORTANCE

Deeksha Maletha¹ and Tanaya²

¹College of Veterinary Science and Animal Husbandry, Birsa Agricultural University, Kanke, Ranchi

²College of Veterinary and Animal Sciences, G B Pant University of Agriculture and Technology, Pant Nagar

Corresponding author email: maletha.deeksha94@gmail.com

INTRODUCTION

Zoonotic diseases exert a significant threat to public health, social stability and the world economy. According to an estimate by the World Health Organization (WHO) approximately one billion infection and millions of human fatalities occur across the globe annually due to zoonotic diseases. About 60% of the emerging infectious diseases reported worldwide stems from zoonotic sources. The dissemination of zoonotic infections of parasitic origin are common and widespread. Toxoplasmosis is an important and widely prevalent food-borne protozoan zoonotic illness caused by Toxoplasma gondii, imposing a significant threat to human as well as livestock health. Transmission of toxoplasmosis is often recognized as zoonotic transmission, with primary route being through ingestion of contaminated food or water, particularly undercooked or raw meat, and unwashed vegetables and fruits that have come into contact with the parasite’s oocysts.

It is a parasitic disease of paramount importance for people with compromised immune systems, such as HIV, as it may induce life-threatening disorders in these individuals. Distribution of toxoplasmosis varies with age, social culture, eating habits, environmental factors, geographical distribution and climatic factors, with higher prevalence reported at lower altitude and in hot and humid environments as compared to cold weather. About one-third of the global population is reported to be chronically infected with T. gondii infection, with approximately 24% of all deaths attributable to foodborne pathogens stemming from T. gondii infection alone. Toxoplasmosis is also being claimed as “silent threat” in most of the Asian countries.

ETIOLOGY AND HISTORY

Toxoplasma gondii is an obligate, intracellular, single-celled opportunistic protozoan parasite from the Phylum Apicomplexa, Class Conoidasida, Subclass Coccidiasina, Order Eucoccidiorida, Suborder Eimeriorina in the Family Sarcocystidae. T. gondii is the only member in the genus Toxoplasma. It is ubiquitous in distribution. All warm-blooded animals including humans and wild animals such as tigers acts as intermediate hosts while cats exclusively act as definitive hosts. The parasite is very unique as firstly unlike other coccidian parasites which are mostly host specific, it can infect any nucleated cell in any warm-blooded animal. Secondly, only cats act as definitive host because they are deficient in delta-6-saturase enzyme in their intestine. Delta-6-desaturase is required for linoleic acid metabolism. Birds may also acquire infection from the environment or from the infected rodents.

The parasite was first discovered by Charles Nicolle and Louis Manceaux in 1908 in a desert rodent Ctenodactylus gundi at the Institute of Pasteur in Tunis. They initially named the parasite “Toxoplasma” due to its crescent shape, resembling that of a bow or an arc (“toxon” in Greek) and a spot or stain (“plasma” in Greek) when observed under a microscope. The species term, gondii, was named in honour of Andre Gondi, a French physician. This intracellular parasite has a complex life cycle, reproducing asexually in nucleated cells in the intermediate hosts and sexually in enterocytes in definitive hosts. Felids (cat and lynx) are the only definitive hosts of T. gondii, and all the warm-blooded animals typically mammals including humans, as well as birds and other animals acts as intermediate hosts in the propagation of life cycle of T. gondii. T. gondii has three infectious stages: tachyzoites, bradyzoites and sporozoites, respectively, that are responsible for its further propagation and dissemination in definitive and intermediate hosts as well as zoonotic transmission.

EPIDEMIOLOGY

1. gondiiis worldwide in distribution and has the widest host range as compared to any other parasite.The disease is widely prevalent in India, with southern part having higher seroprevalence as compared to North India, attributable to variation in climatic zone. Incidence is higher in females as compared to males and increases with age. In Northern India, the high seroprevalence of toxoplasmosis has been found to be associated with ocular toxoplasmosis, followed by neurological, HIV-AIDS induced, post-transplant and congenital toxoplasmosis. Veterinarians, para-veterinarians, zoo workers, farmers, pet keepers are at increased risk of infection.

TRANSMISSION OF TOXOPLASMOSIS TO ANIMALS AND HUMANS

The members of the Felidae family including cats, lynx and wild felids excrete millions of oocysts of T. gondii in their faeces and thus pollute the environment. Oocysts are evident in the faeces 3 days after infection and may be released for up to 3 weeks, which measures about 12 μm in diameter and contains eight infective sporozoites. Depending upon the aeration and temperature, within 1–5 days these oocysts sporulate (become infectious) and remains viable for several month in the environment. The oocysts undergo meiosis in the environment and leads to the formation of sporozoites that are infectious to the intermediate hosts. The asexual stage takes place in the intermediate hosts where rapid intracellular growth of the parasite as tachyzoite takes place. The tachyzoites spreads throughout the body leading to the formation of cysts primarily in the neural and muscular tissues, where they persist for long time.

The intermediate hosts become infected by ingesting the oocysts from contaminated soil, water, food, or by consuming tissue cysts present in raw or undercooked meat from infected animals, and by transplacental transfer of tachyzoites from mother to foetus.  Toxoplasma gondii undertakes its sexual life cycle in the definitive host, i.e. cat. It begins following ingestion of tissue cysts containing bradyzoite stage of T. gondii (originated in the infected victim animals, such as birds or rodents) by cat. Cat can also get infected by consuming oocysts shed in the faeces of another infected cat. When the bradyzoites are inside the digestive system of a cat, the bradyzoites gets freed from the tissue cysts and attack the intestinal cells. Inside cat’s intestinal cells, bradyzoites undergoes sexual reproduction, resulting in the formation of macrogamonts (female) and microgametes (male), which later on undergoes fertilization and forms zygotes, respectively. Cats shed oocysts in its faeces, which following sporulation gets infectious. The oocysts remain resistant in the environment and persists for weeks to months. Asexual life cycle ensues following ingestion of oocysts polluted water, food and soil by birds, humans or any other types of mammals. Further, these oocysts undergo rapid asexual binary fission producing multiple daughter cell which later on differentiates into tachyzoites and attacks host cells producing acute infection in host. Further, these tachyzoites gets distinguished into bradyzoites, forming tissue cysts, primarily in the brain, muscles and other organs. Bradyzoites remains latent within the tissue cysts, allowing the parasite to hold on during entire lifespan of the intermediate host. Some tachyzoites forms tissue cysts in the muscle, brain, and other organs, which basically are the latent stages of the T. gondii enveloped in a protective cyst wall leading to the emergence of chronic infection. Tissue cysts remain viable for many years in the host, possibly for the life of the host, thus serves as an important source of infection for scavengers, both carnivores, and omnivores. If an intermediate host is consumed by a definitive host (cat), tissue cysts gets digested, releases bradyzoites (slowly replicating stage) which invades intestinal cells of the cat and undergoes sexual reproduction.

The zoonotic transmission of toxoplasmosis from animals to humans occurs through the ingestion of contaminated food or water, particularly undercooked or raw meat, as well as unwashed fruits and vegetables that have come into contact with oocysts of the parasite (eggs). Vertical transmission of infection may also occur in pregnant females, which can often threaten to abortion and in rare cases congenital toxoplasmosis may cause cerebral, neurological, cardiac or ocular abnormalities.

CLINICAL FINDINGS OF TOXOPLASMOSIS IN ANIMALS AND HUMANS

Tachyzoite stage is responsible for tissue damage in toxoplasmosis, therefore clinical signs depend on the tissue affected, number of tachyzoites released, and the ability of the host immune system to contain replication and transmission. Because adult immunocompetent animals’ control tachyzoite transmission efficiently, therefore toxoplasmosis is usually a subclinical illness in them. However, in susceptible species, as well as in young and immunocompromised animals tachyzoites are transmitted systemically and cause interstitial pneumonia, myocarditis, hepatic necrosis, meningo-encephalomyelitis, chorioretinitis, lymphadenopathy, and myositis. The corresponding clinical signs include fever, diarrhoea, cough, dyspnoea, icterus, seizures, and death. Immunocompromised adult animals (e.g., feline immunodeficiency virus infected cat) develops acute generalized toxoplasmosis, expressed as neurologic and respiratory disorders. Toxoplasmosis is also an important cause of abortion and stillbirth in sheep, goats, cervids, and sometimes pigs.

In immunocompetent individuals, toxoplasmosis is usually a subclinical infection and acute infection results in transient flu-like symptoms like fever, fatigue, muscle pain, headache, sore throat alongwith enlarged lymph nodes. However, in immunocompromised persons, the common signs include pneumonia, encephalitis and retinochoroiditis. Congenital transmission may lead to severe problems including abortion, hydrocephalus, neurological disorders, severe impairments in vision, hearing, mental disabilities, retinochoroiditis and developmental retards in newborns, respectively.

1. gondiiis a member of the TORCH group which includes Toxoplasmosis, Treponema pallidum, Rubella, Cytomegalovirus, Herpesvirus, hepatitis viruses, Human Immunodeficiency Virus, and other infections, such as Varicella, Parvovirus B19, and Enteroviruses. TORCH infections are major contributors to prenatal, perinatal, and postnatal morbidity and mortality and early diagnosis is very important to reduce the incidence.

DIAGNOSIS

1. gondiiinfection can be diagnosed on the basis of history, clinical signs and symptoms, suspected route of infections and post mortem diagnosis using histopathological examinations of tissue sections for the presence of tachyzoites and bradyzoites, alongwith immunohistochemical examinations. Toxoplasmosis can be detected using blood tests, polymerase chain reaction serological tests like ELISA, immunofluorescent assay, Sabin-Feldman Dye Test and amniotic fluid examination in case of congenital toxoplasmosis.

TREATMENT

In case of acute toxoplasmosis, the anti-coccidial drugs should be administered as soon as possible. For primary infection, in cases of acute infectious stage the specific treatment, comprising of sulfadiazine @ 15–25 mg/kg, p.o., every 12 hours and pyrimethamine @ 0.44 mg/kg, p. o., every 12 hours should be administered daily for up to 4 weeks, respectively. Trimethoprim-sulfamethoxazole @ 15 mg/kg, p.o., every 12 hours for 4 weeks is also widely recommended in dogs and cats. For dogs and cats, clindamycin @ 10–12.5 mg/kg, p. o., every 12 hours in cases of dogs and @ 25–50 mg/kg, p. o., every 12 hours in cats for 3–4 weeks is the treatment of choice. Other drugs, including diaminodiphenylsulfone, atovaquone, and spiramycin, can also be administered to treat toxoplasmosis in difficult cases. For control of acute toxoplasmosis in cats and to reduce the shedding of oocysts by cats, toltrazuril, ponazuril, and diclazuril are commonly administered.

PREVENTION AND CONTROL

As oral ingestion of oocysts contaminated feed, water and meat is the primary mode of transmission of toxoplasmosis in animals and humans so to prevent infection, the effective preventive measure ensures washing hands thoroughly with soap and water post contact with potentially contaminated environments, including meat, soil, fruits and vegetables etc. polluted with oocysts, respectively. The consumption of raw/undercooked meat, unpasteurized milk and untreated water should be stopped. Meat of any animal should be cooked to 67°C (152.6°F) before consumption, and tasting meat while cooking or while seasoning should be avoided. Pregnant women should avoid contact with cat litter, soil, and raw meat. Pet cats should be fed only cooked, dry or canned food. Before consumption of the vegetables its thorough washing should be ensured to avoid ingestion of oocysts. As toxoplasmosis is a widely prevalent food-borne zoonotic disease affecting almost one-third of the global population, so proper hygiene and associated control measures alongwith national preventive strategies should be adopted and practiced to prevent and control transmission of T. gondii.

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