1. AMOEBIASIS, GIARDIASIS AND TOXOPLASMOSIS

2. Giardiasis
Giardiasis: Infection with Giardia lamblia is found worldwide and is common in the tropics. It particularly affects children and immunosuppressed individuals. In cystic form, it remains viable in water for up to 3 months and infection usually occurs by ingesting contaminated water. Its flagellar trophozoite form attaches to the duodenal and jejunal mucosa, causing inflammation.

3. Clinical features and investigations
Incubation period is 1–3 weeks. There is diarrhea, abdominal pain, weakness, anorexia, nausea and vomiting. On examination, there may be abdominal distension and tenderness. Chronic giardiasis causes malabsorption syndrome. Diagnosis: A. Stool examination: Stools obtained at 2–3-day intervals should be examined for cysts. B. Duodenal or jejunal aspiration by endoscopy gives a higher diagnostic yield. C. String test’ may be used, in which one end of a piece of string is passed into the duodenum by swallowing and retrieved after an overnight fast; expressed fluid is then examined for the presence of G. lamblia trophozoites. D. A number of stool antigen detection tests are available. E. Jejunal biopsy specimens may show G. lamblia on the epithelial surface.

4. Management
Treatment is with a single dose of tinidazole 2 g, metronidazole 400 mg 3 times daily for 10 days, or nitazoxanide 500 mg orally twice daily for 3 days.

5. Amoebiasis
Transmission: Amoebiasis is caused by Entamoeba histolytica, which is spread between humans by its cysts, through water or uncooked foods contaminated by human faeces. Infection may also be acquired through anal/oral sexual practices It is one of the leading parasitic causes of morbidity and mortality in the tropics and is occasionally acquired in other countries.

6. Pathology
The ingested cysts of E. histolytica change to trophozoits in the colon. 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. Amoebic ulcers may cause severe haemorrhage but rarely perforate the bowel wall.

7. Amoebic trophozoites can emerge from the vegetative cyst from the bowel and be carried to the liver in a portal venule and cause liver abscess. The liquid contents at first have a characteristic pinkish colour, which may later change to chocolate-brown (like Anchovy sauce). Cutaneous amoebiasis, though rare, causes progressive genital, perianal or peri-abdominal surgical wound ulceration

9. Clinical features
Intestinal amoebiasis (amoebic dysentery): The incubation period of amoebiasis ranges from 2 week to many years A. Most amoebic infections are asymptomatic. B. A chronic course may occur with abdominal pains, especially right lower quadrant (which may simulate acute appendicitis)and two or more unformed stools a day. Offensive diarrhoea alternating with constipation, and blood or mucus in the stool, is common. C. An acute 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.

10. Amoebic liver abscess
A single abscess is usually found in the right hepatic lobe. There may not be associated diarrhea (not necessary). A. Early symptoms may be local discomfort only and malaise. B. Later, a swinging temperature and sweating may develop, usually without marked systemic symptoms or associated cardiovascular signs. C. An enlarged, tender liver, cough and pain in the right shoulder are characteristic. D. Symptoms may remain vague and signs minimal. E. A large abscess may penetrate the diaphragm and rupture into the lung, from where its contents may be coughed up through a hepaticobronchial fistula. Rupture into the pleural or peritoneal cavity, or rupture of a left lobe abscess in the pericardial sac, is less common but more serious

11. Investigations of intestinal amebiasis
A. 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. The finding of trophozoites rather than the cysts indicate the presence of active disease. B. Several stools may need to be examined in chronic amoebiasis before cysts are found. The patients who are cyst passers in the absence of trophozoits are usually asymptomatic but they are dangerous because they transmit the disease to others through these cysts. In endemic areas, one-third of the population are symptomless passers of amoebic cysts This is unlike the case in giardiasis in which the presences of either cysts or trophozoits indicate the presence of active disease. C. Sigmoidoscopy may reveal typical flask-shaped ulcers, which should be scraped and examined immediately for E. histolytica.

12. Diagnosis of amoebic abscess
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. Positive serology for amoebiasis is also helpful.

13. Management
Intestinal and early hepatic amoebiasis responds quickly to oral metronidazole 800 mg 3 times daily for 5–10 day or other long-acting nitroimidazoles like tinidazole I doses of 2 g daily for 3 days. Nitazoxanide 500 mg twice daily for 3 days is an alternative drug. Either diloxanide furoate or paromomycin, in doses of 500 mg orally 3 times daily for 10 days after treatment should be given to eliminate luminal cysts 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. .

14. Prevention
Personal precautions against contracting amoebiasis consist of not eating fresh, uncooked vegetables or drinking unclean water.

15. Summary: مهم جدا
Giardiasis causes small bowel type of diarrhea and stool is not containing blood or pus and it does not infect large bowel. Chronic giardiasis may lead to malabsorption syndrome but does not cause liver abscess. While amoebiasis infect large bowel (colon) and stool may contain blood or pus due to colonic ulcers and the disease may spread to liver and cause liver abscess but this doesn't cause malabsorption (not affect small bowel). Both giardiasis and amoebiasis can be treated with metronidazole or tinidazole.

16. Toxoplasmosis
Cause and lifecycle: Toxoplasma gondii is an intracellular parasite. The sexual phase of the parasite’s life cycle occurs in the small intestinal epithelium of the domestic cat. Oöcysts are shed in cat faeces and are spread to intermediate hosts (pigs, sheep and also humans) through widespread contamination of soil. Oöcysts may survive in moist conditions for weeks or months. Once they are ingested, the parasite transforms into rapidly dividing tachyzoites through cycles of asexual multiplication.This leads to the formation of microscopic tissue cysts containing bradyzoites, which persist for the lifetime of the host. Cats become infected or re-infected by ingesting tissue cysts in prey such as rodents and birds.

17. Transmission: Human acquisition of infection occurs via: 1
Transmission: Human acquisition of infection occurs via: 1. Oöcyst (from domestic cats) contaminated soil, salads and vegetables. 2. Or by the ingestion or tasting of raw or undercooked meats containing tissue cysts (Sheep, pigs and rabbits are the most common meat sources). Outbreaks of toxoplasmosis have been linked to the consumption of unfiltered water.

18. In developed countries, toxoplasmosis is the most common protozoal infection; around 22% of adults in the UK are seropositive. Most primary infections are subclinical, In India or Brazil; approximately 40–60% of pregnant females are seropositive for T. gondii. In HIV-1 infection (immunocompromized i. e. low immunity), toxoplasmosis is an important opportunistic infection with considerable morbidity and mortality. Generalised toxoplasmosis has been described after accidental laboratory infection with highly virulent strains.

19. Clinical features
A. In most immunocompetent(normal immunity) individuals, including children and pregnant women, the infection goes unnoticed(symptomless). B. In approximately 10% of patients, it causes a self-limiting illness, most common in adults aged 25–35 years. The most common presenting feature is painless lymphadenopathy, either local or generalised. In particular, the cervical nodes are involved, but mediastinal, mesenteric or retroperitoneal groups may be affected in the absence of symptoms in most cases.The spleen is seldom palpable. C. Some complain of malaise, fever, fatigue, muscle pain sore throat and headache. Complete resolution usually occurs within a few months. D. Very rarely, patients may develop encephalitis, myocarditis, polymyositis, pneumonitis or hepatitis. E. Retinochoroiditis is nearly always the result of congenital infection but has also been reported in acquired disease.

20. Congenital toxoplasmosis: In general acute toxoplasmosis in pregnant women, is mostly subclinical (symptomless) but in approximately 60% transmission rate to the fetus occurring, which rises with increasing gestation. When the fetus is infected, a congenital disease occurs in approximately 40% of them (it means it is not necessary all of the infected fetuses develop congenital abnormalities), and is more likely and more severe with infection early in gestation (see Box 13.28, p. 314). Many fetal infections are subclinical at birth but long-term sequelae include retinochoroiditis, microcephaly and hydrocephalus. Note: مهم جدا Seropositive females infected 6 months before conception have no risk of fetal transmission

21. Investigations
1. In immunocompromised patients, in whom the diagnosis often requires direct detection of parasites, 2. Serology is often used in immunocompetent individuals. Serology: The Sabin–Feldman dye test (indirect fluorescent antibody test), which detects IgG antibody, is most commonly used. Recent infection is indicated by a fourfold or greater increase in titre when paired sera are tested inparallel. 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. The detection of significant levels of Toxoplasmaspecific IgM antibody may be useful in confirming acute infection. A falsepositive result or persistence of IgM antibodies for years after infection makes interpretation difficult; however, negative IgM antibodies virtually rule out acute infection.

22. During pregnancy, it is important to differentiate between recent and past infection; the presence of high-avidity IgG antibodies excludes infection acquired in the preceding 3–4 months. 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

23. 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 .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). The cost/benefit of routine Toxoplasma screening and treatment in pregnancy is being debated in many countries .There is insufficient evidence to determine the effects on mother or baby of current anti-parasitic treatment forwomen who seroconvert in pregnancy.

24. Summary: مهم
Toxoplasmosis which can be transmitted through contamination of our diet by oocysts from domestic cats or ingestion or raw or undercooked meat from animals (like sheep) those containing tissue cysts. In most cases of infected adults with normal immunity (immune component) the disease is very mild and asymptomatic and needs no treatment (self-limiting). In certain circumstances like in immune compromised individuals as in case of AIDS, the disease becomes disseminated and serious. This is also happen in case of infected fetus, when the baby may develop multiple congenital anomalies including retinochoroiditis. Diagnosis needs serological tests but some time identification of toxoplasma gondi is necessary in cases of dissemination in immune compromised patients. Lymphnode biopsy with tissue staining for toxoplasma may also be used. Common drugs used for treatment of toxoplasmosis are: spiramycin(but it does not cross the placenta barrier), sulfadiazine and pyrimethamine (cross placental barrier)

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