Lecture 05a Tissue Coccidia

Lecture 5a Tissue Coccidia

Aims and Learning Objectives 

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It is intended that the student will be familiar with the biology of major tissue coccidia of humans and selected domesticated animals; the infections they cause; and effective control measures applied At the end the lecture, you will be: 

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able to recognise as a group the main tissue coccidia, particularly Toxoplasma gondii, but also other tissue coccidia of humans and domesticated animals in situ and ex situ familiar with the life cycle of the parasites familiar with the pathology of infections able to recommend measures for control of infections

Toxoplasmosis Causal Agent Toxoplasma gondii is a coccidian that infects most species of warm blooded animals, including humans, causing the disease toxoplasmosis. Geographic Distribution Serologic prevalence data indicate that toxoplasmosis is one of the most common of humans infections throughout the world. Infection is more common in warm climates and at lower altitudes than in cold climates and mountainous regions. High prevalence of infection in France has been related to a preference for eating raw or undercooked meat, while high prevalence in the Caribbean and Central America has been related to the frequency of stray cats in a climate favoring survival of oocysts

Toxoplasmosis - clinical features Acquired infection 

In immunocompetent persons is generally an asymptomatic infection. The clinical course is benign and self-limited; symptoms usually resolve within a few months to a year.

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In patients with HIV/AIDS, toxoplasmic encephalitis is the most common cause of intracerebral mass lesions and is thought to be caused by reactivation of chronic infection.

Toxoplasma gondii cyst in brain tissue stained with hematoxylin and eosin (100×).

Toxoplasmosis - clinical features 

Congenital toxoplasmosis results from an acute primary infection acquired by the mother during pregnancy. The incidence and severity of congenital toxoplasmosis vary with the trimester during which infection was acquired. Most infants with subclinical infection at birth will subsequently develop signs or symptoms of congenital toxoplasmosis unless the infection is treated.

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Ocular Toxoplasma infection, an important cause of retinochoroiditis in the United States, is frequently a result of congenital infection. Patients are often asymptomatic until the second or third decade of life, when lesions develop in the eye.

Toxoplasmosis Prevention       

Undercooked meat is a source of tissue cysts Tissue cyst killed by freezing/cooking meet (stray) cats spread oocysts – minimise Pregnant women should avoid cats Maintain clean litter boxes for cats Cover kiddy’s sand boxes Phoretic transmission by flies and cockroaches.

Toxoplasmosis Laboratory Diagnosis: 

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Serologic testing (commercial kit) is the routine method of diagnosis, because the techniques described below are technically complex and generally not rewarding Bronchoalveolar lavage from immunocompromised patients, or lymph node biopsy. Isolation of parasites from blood or other body fluids, by intraperitoneal inoculation into mice or tissue culture - xenodiagnosis. The mice should be tested for the presence of Toxoplasma organisms in the peritoneal fluid 6 to 10 days post inoculation

Treatment:   

Treatment is not needed for a healthy person who is not pregnant. Symptoms will usually go away within a few weeks. Treatment may be recommended for pregnant women or persons who have weakened immune systems (e.g. HIV/AIDS). Pentamidine/sulphonamide cocktails

Eimeria       

Coccidian of the epithelium of intestinal cecea of chickens and turkeys Infection by oocysts; release sporozoites and infect epithelial cells – ~2 cycles gamete production High mortality in young birds Serious disease causing bloody diahorrea, and intestinal obstruction by blood clots Infected birds are listless, unthrifty, and prone to 2o infections No effective cure once established Cocidiostats administered continuously in water and food

Eimeria pathology 

A histological section showing the asexual reproductive stages of a coccidian in the tissues of the host's small intestine.

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Note the many developing schizonts (the large dark blue structures enclosed within the rectangle) in the tissues.

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* merozoites

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Marked destruction ensues.

Babesia infections Causal Agents: 

Babesiosis is caused by coccidian parasites of the genus Babesia (also called a piroplasm)

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Ticks serve as vectors

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While more than 100 species have been reported, only a few have been identified as causing human infections

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Babesia microti (rodents) and Babesia divergens (cattle) have been identified in most human cases, but variants (considered different species) have been recently identified

Babesia Geographic Distribution: 

Worldwide, but little is known about the prevalence of Babesia in malaria-endemic countries, where misidentification as Plasmodium (malaria) probably occurs.

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In Europe, most reported cases are due to B. divergens (cattle) and often occur in splenectomized patients

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In the United States, B. microti is the agent most frequently identified (Northeast and Midwest), and can occur in non-splenectomized individuals.

Babesia microti

Ixodes dammini

Vector for Babesia bigemina

Vector for Babesia canis

Babesia bigemina in cattle   

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B. bigemina in cattle, zebu, water buffalo, deer, etc Causes tick fever, or red water fever (haematuria) Vectors are one-host ticks Boophilus annulatus in USA and Caribbean Adult ticks pass infection to larvae via eggs i.e. “transovarian transmission” Massive destruction of rbc’s Severe anaemia (older animals) 50-90% mortality in infected cattle Arsenical drugs ( = salivarian trypanosomes)

Babesia in man Clinical Features 

B. divergens spread by Boophilus annulatus B. microti spread by Ixodes dammini

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Most human infections are probably asymptomatic, as indicated by serologic surveys.

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Manifestations of disease include fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia.

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Symptoms typically occur after an incubation period of 1 to 4 weeks, and can last several weeks.

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The disease is more severe in patients who are immunosuppressed, splenectomized, and/or elderly.

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Infections caused by B. divergens tend to be more severe (frequently fatal if not appropriately treated) than those due to B. microti, where clinical recovery usually occurs.

Babesia infections Laboratory Diagnosis: 

Diagnosis can be made by microscopic examination of thick and thin blood smears stained with Giemsa stain.

Treatment: 

Clindamycin plus quinine or atovaquone plus azithromycin are the options.