1. Toxoplasma gondii (toxoplasmosis)

2. Objectives: Upon completion this lecture ,the student will be able to :
Identify methods of transmission of Toxoplasma Gondii
Judge when infection can affect pregnancy outcomes
Recognize the clinical features of both acquired and congenital toxoplasmosis
Perform the suitable investigations for the diagnosis
Manage and Treat a case of toxoplasmosis

3. Introduction
Toxoplasmosis is caused by infection with the obligate intracellular parasite Toxoplasma gondii. Acute infection acquired after birth may be asymptomatic but frequently results in the chronic persistence of cysts in the host's tissues. In both acute and chronic toxoplasmosis, the parasite is responsible for clinically evident disease, including lymphadenopathy, encephalitis, myocarditis, and pneumonitis. .

4. Congenital toxoplasmosis is an infection of newborns that results from the transplacental passage of parasites from an infected mother to the fetus. These infants usually are asymptomatic at birth but later manifest a wide range of signs and symptoms, including chorioretinitis, strabismus, epilepsy, and psychomotor retardation

6. Epidemiology
T. gondii infects a wide range of mammals and birds. Its seroprevalence depends on the locale and the age of the population. Generally, hot arid climatic conditions are associated with a low prevalence of infection. In the United States and most European countries, the seroprevalence increases with age and exposure. For example, in the United States, 5–30% of individuals 10–19 years old and 10–67% of those >50 years old have serologic evidence of exposure.

7. Transmission Oral Transmission Transmission Via Blood or Organs
Transplacental Transmission

8. Clinical features
In most immunocompetent individuals, including children and pregnant women, the infection goes unnoticed.
10% of patients it causes a self-limiting illness, most common in adults aged years. The most common presenting feature is painless lymphadenopathy, local or generalised..
Most patients have no systemic symptoms, but some complain of malaise, fever, fatigue, muscle pain, sore throat and headache.

9. Complete resolution usually occurs within a few months, although some patients do not recover completely for a year or more.
Very infrequently, patients may develop encephalitis, myocarditis, polymyositis, pneumonitis or hepatitis. Retinochoroiditis is nearly always the result of congenital infection but has also been reported in acquired disease

10. Congenital toxoplasmosis
Acute toxoplasmosis, mostly subclinical, affects 0.3-1% of pregnant women, with an approximately 60% transmission rate to the fetus which increases with increasing gestation.
Seropositive females infected 6 months before conception have no risk of fetal transmission.

11. Congenital disease affects approximately 40% of infected fetuses, and is more likely and more severe with infection early in gestation.
Many fetal infections are subclinical at birth but long-term sequelae include retinochoroiditis, microcephaly and hydrocephalus.

12. Investigations
In immunocompromised patients:direct detection of parasites.
immunocompetent individuals :serology The Sabin-Feldman dye test (indirect fluorescent antibody test), which detects IgG antibody.
Recent infection is indicated by a fourfold or greater increase in titre when paired sera are tested in parallel. Peak titres of 1/1000 or more are reached within 1-2 months of the onset of infection, and the dye test then becomes an unreliable indicator of recent infection.

13. The detection of significant levels of Toxoplasma-specific IgM antibody may be useful in confirming acute infection. False positives or persistence of IgM antibodies for years after infection make interpretation difficult; however, negative IgM antibodies virtually rule out acute infection.
During pregnancy it is critical to differentiate between recent and past infection; the presence of high-avidity IgG antibodies excludes infection acquired in the preceding 3-4 months.

14. If necessary, the presence of Toxoplasma organisms in a lymph node biopsy can be sought by staining sections histochemically with T. gondii antiserum, or by the use of PCR to detect Toxoplasma-specific DNA.

15. Management
In immunocompetent subjects uncomplicated toxoplasmosis is self-limiting and responds poorly to antimicrobial therapy. Treatment with pyrimethamine, sulfadiazine and folinic acid is therefore usually reserved for rare cases of severe or progressive disease, and for infection in immunocompromised patients

16. In a pregnant woman with an established recent infection, spiramycin (3 g daily in divided doses) should be given until term. Once fetal infection is established, treatment with sulfadiazine and pyrimethamine plus calcium folinate is recommended (spiramycin does not cross the placental barrier).

17. Amebiasis
Objectives: Upon completion this lecture ,the student will be able to :
Determine methods of transmission of Entamoeba histolytica
Recognize the clinical features of Amebic dysentery and its coplications
Perform the suitable investigations for the diagnosis
Manage a case of toxoplasmosis Amebic dysentery and amoebic liver abscess.

18. Amebiasis
Amebiasis is an infection with the intestinal protozoan Entamoeba histolytica. About 90% of infections are asymptomatic, and the remaining 10% produce a spectrum of clinical syndromes ranging from dysentery to abscesses of the liver or other organs.It is spread between humans by its cysts. It is one of the leading parasitic causes of morbidity and mortality in the tropics

19. Life Cycle and Transmission
E. histolytica is acquired by ingestion of viable cysts from fecally contaminated water, food, or hands. Food-borne exposure is most prevalent and is particularly likely when food handlers are shedding cysts or food is being grown with feces-contaminated soil, fertilizer, or water.
Besides the drinking of contaminated water, less common means of transmission include oral and anal sexual practices and—in rare instances—direct rectal inoculation through colonic irrigation devices.

20. Motile trophozoites are released from cysts in the small intestine and, in most patients, remain as harmless commensals in the large bowel. After encystation, infectious cysts are shed in the stool and can survive for several weeks in a moist environment.
In some patients, the trophozoites invade either the bowel mucosa, causing symptomatic colitis, or the bloodstream, causing distant abscesses of the liver, lungs, or brain.

21. The trophozoites may not encyst in patients with active dysentery, and motile hematophagous trophozoites are frequently present in fresh stools.
Trophozoites are rapidly killed by exposure to air or stomach acid, however, and therefore cannot transmit infection.

22. The parasite may invade the mucous membrane of the large bowel, producing lesions that are maximal in the caecum but found as far down as the anal canal. These are flask-shaped ulcers, varying greatly in size and surrounded by healthy mucosa.
A localised granuloma (amoeboma), presenting as a palpable mass in the rectum or a filling defect in the colon on radiography, is a rare complication which should be differentiated from colonic carcinoma.

23. Amoebic ulcers may cause severe haemorrhage but rarely perforate the bowel wall.
Amoebic trophozoites can emerge from the vegetative cyst from the bowel and be carried to the liver in a portal venule. They can multiply rapidly and destroy the liver parenchyma, causing an abscess The liquid contents at first have a characteristic pinkish colour which may later change to chocolate brown (like anchovy sauce).

24. Cutaneous amoebiasis, though rare, causes progressive genital, perianal or peri-abdominal surgical wound ulceration.

25. Clinical features Intestinal amoebiasis-amoebic dysentery
Most amoebic infections are asymptomatic.
The incubation period of amoebiasis ranges from 2 weeks to many years, followed by a chronic course with abdominal pains and two or more unformed stools a day.
Offensive diarrhoea alternating with constipation, and blood or mucus in the stool, are common.

26. There may be abdominal pain, especially right lower quadrant (which may simulate acute appendicitis).
A dysenteric presentation with passage of blood, simulating bacillary dysentery or ulcerative colitis, occurs particularly in older people, in the puerperium and with superadded pyogenic infection of the ulcers.

27. Amoebic liver abscess
The abscess is usually found in the right hepatic lobe. There may not be associated diarrhoea. Early symptoms may be local discomfort only and malaise; later, a swinging temperature and sweating may develop, usually without marked systemic symptoms or associated cardiovascular signs.

28. An enlarged, tender liver, cough and pain in the right shoulder are characteristic, but symptoms may remain vague and signs minimal.
A large abscess may penetrate the diaphragm and rupture into the lung, from where its contents may be coughed up. Rupture into the pleural cavity, the peritoneal cavity or pericardial sac is less common but more serious.

29. Investigations
The stool and any exudate should be examined at once under the microscope for motile trophozoites containing red blood cells. Movements cease rapidly as the stool preparation cools. Several stools may need to be examined in chronic amoebiasis before cysts are found. Sigmoidoscopy may reveal typical flask-shaped ulcers, which should be scraped and examined immediately for E. histolytica.

30. In endemic areas one-third of the population are symptomless passers of amoebic cysts.
An amoebic abscess of the liver is suspected on clinical grounds; there is often a neutrophil leucocytosis and a raised right hemidiaphragm on chest X-ray. Confirmation is by ultrasonic scanning.
Aspirated pus from an amoebic abscess has the characteristic anchovy sauce or chocolate brown appearance but only rarely contains free amoebae.

31. Serum antibodies are detectable by immunofluorescence in over 95% of patients with hepatic amoebiasis and intestinal amoeboma, but in only about 60% of dysenteric amoebiasis.
DNA detection by PCR has been shown to be useful in diagnosis of E. histolytica infections but is not generally available.

32. Management
Intestinal and early hepatic amoebiasis responds quickly to oral metronidazole (800 mg 8-hourly for 5-10 days) or other long-acting nitroimidazoles like tinidazole or ornidazole (both in doses of 2 g daily for 3 days). Either diloxanide furoate or paromomycin, in doses of 500 mg orally 8-hourly for 10 days after treatment, should be given to eliminate luminal cysts.

33. If a liver abscess is large or threatens to burst, or if the response to chemotherapy is not prompt, aspiration is required and is repeated if necessary.
Rupture of an abscess into the pleural cavity, pericardial sac or peritoneal cavity necessitates immediate aspiration or surgical drainage. Small serous effusions resolve without drainage.