DIAGNOSIS Medical Assignment Help

The definitive diagnosis depends on demonstrating trypomastigotes in the peripheral blood, lymph node aspirates or CSF. If the organism is not easily demonstrated, concentration techniques should be utilized. IgM levels in the serum and CSF are markedly elevated.

TREATMENT

Therapy is usually effective if commenced before eNS symptoms develop. Suramin, a polysulphated compound, is given intravenously;
initially 0.1 g is given as a test dose to exclude an idiosyncratic reaction, followed by 1.0 g i.v, on the first, third, seventh, fourteenth and twenty-first days. If proteinuria or haematuria develop, therapy should be discontinued. Pentamidine 3-4 mg kg-t intramuscularly on alternate days for 10 injections is an effective alternative. Rapid intravenous injection of pentamidine results in hypotension. Although suramin and pentamidine have been found to be effective and should be used initially to control the fever, they do not cross the blood-brain barrier. It is believed that relapse or failure to respond to therapy will occur when CNS involvement occurs early in the disease. After eNS involvement Drugs that penetrate the blood-brain barrier are recommended as part of the initial treatment of trypanosomiasis.
Melarsoprol, a trivalent arsenic, is used most widely for this purpose. Three to four consecutive injections of 2.0-3.6 mg kg-t body weight (up to a maximum of 250 mg per injection) are given intravenously. The course is usually repeated after an interval of 2 weeks. Major side-effects include an acute encephalitis-like condition and skin rashes. Iarisch-Herxheimer-rype reactions can be reduced by clearing the parasites from the blood with suramin initially. Oral nitrofurazone 10 mg kg-t in divided doses three times daily for 10 days has also been found to be useful in cerebral trypanosomiasis. Peripheral neuropathy and haemolytic anaemia may be troublesome side-effects in patients with glucose-6-phosphate dehydrogenase deficiency. Difluoromethylornithine is also used for Gambian sleeping sickness.

PREVENTION AND CONTROL

Elimination of the vector-the tsetse fly-by insecticides or by making environmental conditions unsuitable for its inhabitation would effectively eradicate trypanosomiasis. Both these approaches require formidable mobilization of manpower and money. Insect repellents and protective, light-coloured clothing should be used when visiting endemic areas. A single intramuscular prophylactic injection of pentamidine 4 mg kg-l body weight (up to a maximum dose of 300 mg) gives effective protection against Gambian sleeping sickness, but is less effective against Rhodesian sleeping sickness.
African trypanosomiasis in children In children the early manifestations and eNS symptoms overlap. Lymphadenopathy and neurological abnormalities may occur together. Seizures and choreiform movements are not uncommon. Treatment is as for the adult form. American trypanosomiasis (Chagas’ disease) This is a zoonotic disease caused by T. cruzi that is transmitted by various reduviid insects. The principal vectors are Triatoma infestans and Rhodnius prolixus (Latin America) and Panstrongylus megistus (Venezuela). Once infected, these insects remain infective for at least 2 years. Domestic and wild animals are important reservoirs. Humans are infected usually at night when the insect feeds and infected faeces are rubbed into a skin abrasion or mucosal surface such as the conjunctiva. Less commonly the infection may spread via blood transfusions or transplacentally. Chagas’ disease is confined to South and Central America. Occasional cases have also been reported from southern Texas.

CLINICAL FEATURES

The incubation period varies from 1 to 2 weeks. Two clinically distinct presentations are recognized. Acute Chagas’ disease Acute Chagas’ disease predominantly affects children. In 50% of cases an erythematous, indurated papule (chagoma) develops at the site of bite, and is associated with regional lymphadenopathy. This resolves spontaneously.If the portal of entry is the conjunctiva, unilateral periorbital and palpe bral oedema (Rornana’s sign),conjunctivitis and preauricular lymphadenopathy develop. Systemic findings such as fever, a transient morbilliform or urticarial rash, a peculiar gelatinous oedema of the face and trunk, tender lymphadenopathy and hepatosplenomegaly may be present. Death may occur in a small proportion of patients owing to myocarditis or meningo-encephalitis. More commonly the patient recovers completely in a few weeks.

Chronic Chagas’ disease

Chronic Chagas’ disease occurs after a latent period of many years. It is due to an autoimmune reaction mediated by cytotoxic T cells and antibodies against the endocardium, vascular tissue and striated muscle, together with myenteric plexus damage by amastigotes. The heart is invariably involved. The patient may complain of chest pain, dyspnoea or syncope. Cardiac abnormalities and arrhythmias are usual. Signs of right-sided cardiac failure may be present. Thromboembolic phenomena may occur. With gastrointestinal involvement, megaoesophagus, leading to dysphagia and aspiration pneumonia, and megacolon, giving constipation and progressive abdominal distension, may occur. Dilatation of the biliary tree and of the bronchi have also been documented.

DIAGNOSIS

In acute Chagas’ disease trypomastigotes may be demonstrated in peripheral blood. If parasites are not demonstrated in the blood, xenodiagnosis may be used: a parasite- free laboratory-reared vector feeds on a patient or the patient’s blood suspected to have the disease and 2-3 weeks later the intestinal contents of the vector are examined for parasites. In chronic Chagas’ disease complement fixation (Machado-Guerreiro reaction), indirect fluorescent antibody or haemagglutination tests may be used. Radiological assessment of gastrointestinal abnormalities is helpful.

TREATMENT

Nifurtimox, a nitrofurazone derivative, has been found to be useful in acute disease. The dose is 20 mg kg-l daily for children below the age of 2 years and 8-10 mg kg-l daily for 3-4 months in older children and adults. Sideeffects are few and include transient leucopenia, vomiting, sleeplessness and paraesthesiae. Benzimidazole is a useful alternative drug. Over 80% of patients with the acute form of the disease and slightly more with the chronic form are cured of the infection.

PREVENTION AND CONTROL

No vaccine or chemoprophylactic agent is available. Prevention therefore involves the regular spraying of houses with benzene hexachloride in order to decrease the vector population.

TOXOPLASMOSIS

Toxoplasmosis is caused by Toxoplasma gondii, an intracellular protozoon, which requires for completion of its life-cycle a definitive host, e.g. a cat, sheep or pig, and an intermediate host, e.g. a human. Infection of humans occurs either congenitally or by ingestion of foodstuffs contaminated by infected cat faeces or lamb or pork contaminated with T. gondii cysts. Toxoplasmosis is rare in the UK.

CLINICAL FEATURES

Five major clinical forms of toxoplasmosis are recognized:
1 Asymptomatic lymphadenopathy is the commonest mode of presentation.
2 Lymphadenopathy usually involves the cervical lymph nodes and is associated with a febrile illness. This may be clinically indistinguishable from infectious mononucleosis but the Paul-Bunnell test is negative.
3 Neujological abnormalities include neck stiffness and headache, associated with sore throat and maculopapular rashes. The CSF is under pressure and the level of protein is elevated.
4 An acute febrile illness occurs, with a maculopapular rash, hepatosplenomegaly and reactive lymphocytes in the peripheral blood. Uveitis, chorioretinitis, myocarditis and hepatitis may occur.
5 Congenital toxoplasmosis exhibits symptoms and signs are indicative of CNS involvement. The characteristic ‘syndrome of Savin’, which comprises internal hydrocephalus, chorioretinitis, convulsions and cerebral calcification, may be seen. Tremors, nystagmus, microophthalmia and pneumonitis are also present. The prognosis is usually poor, the survivors generally exhibiting mental retardation, epilepsy and spastic paraplegia. In the immunocompromised host, features present in the acute febrile and neurological forms are prominent.

DIAGNOSIS

Serological tests are the mainstay of diagnosis of acquired infection. The Sabin-Feldman dye test, a measure of IgG antibodies, has been widely used. Antibodies can also be detected by indirect fluorescence or indirect haemagglutination. Raised antibody levels are common in the general population and only a rising antibody titre is highly suggestive of toxoplasmosis. The IgM-immunofluorescent antibody (IgM-IFA) test is particularly useful for detecting acute infection since titres rise early and fall rapidly. T. gondii can be isolated by injecting the peritoneum of mice with tissue extracts, e.g. bone marrow, body fluids or CSF when available, and examining the peritoneal fluid 6-10 days later for the organism.

TREATMENT

Most patients require no therapy as the disease is mild. Pyrimethamine (25-50 mg three times daily) and sulphadiazine (4-5 g daily) are used in combination for severe disease since they are synergistic. Therapy should be continued for at least 1 month. Since pyrimethamine is teratogenic, spiramycin is a useful alternative during pregnancy. Steroids are probably useful in ocular toxoplasmosis.

PREVENTION

Domestic cats that kill mice and birds are the chief source of infection and care should be taken in handling their faeces. Pneumocystis carinii infection  Although genetic analysis has shown this organism to be homologous with fungi, its morphological characteristics are more similar to protozoa. The organism exists as a trophozoite, which is probably motile and reproduces by binary fission. After the trophozoite invades the lung parenchyma, its wall thickens and forms a cyst. On maturation, further division takes place to yield eight merozoites which, after cyst wall rupture, develop into trophozoites.

CLINICAL FEATURES

Infection is probably common in infancy but most infections in otherwise healthy infants remain undetected. Outbreaks in infant nurseries have been reported but are now less common. Infection in adults is associated with a major defect in cell-mediated immune mechanisms. Thus, infection with P. carinii is one of the most common opportunistic infections in AIDS.

BABESIOSIS

This is a tick-borne disease, found chiefly in North America and Europe, and is occasionally transmitted to humans, especially those who are immunosuppressed. The causative organism is the plasmodium-like Babesiamicroti. The incubation period averages 10 days. In patients  with normal splenic function, the symptoms are mild and usually comprise fever, nausea, myalgia, chills, vomiting and abdominal pain. Hepatosplenomegaly and mild to moderate haemolytic anaemia may also be present. In splenectomized individuals, systemic symptoms are more prnounced and haemolysis is associated with haemoglobinuria, jaundice and renal failure. Examination of a peripheral blood smear may reveal the characteristic plasmodium-like organisms.

TREATMENT

The treatment of choice is a combination of quinine 650 mg and clindamycin 600 mg orally three times daily for 7 days. This reduces the fever and parasitaemia but is not curative.

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