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Malaria is caused Plasmodium falciparum
, P. vivax
, P. ovale
. More than 1 million children under the age of 5 years
die each year in Africa alone. In the UK there are more than 2000
reported cases and up to 10 deaths every year. Immigrants returning
to their home country are at high risk as they have lost their
natural immunity and may not take prophylaxis.
Malaria is transmitted by the bite of a female anopheles mosquito
that injects sporozoa. The parasites develop in hepatocytes then
invade red blood cells and multiply rapidly. They provoke the
release of cytokines, which are responsible for many of the signs
and symptoms of malaria. Infected red blood cells develop knoblike
projections that make them adhere to the capillary wall. This
may occur in the brain, causing cerebral malaria.
The life cycle is completed when the sexual stages (gametocytes)
are taken up by another mosquito and develop in the mosquito
gut into sporozoites, which migrate to the insect salivary glands
ready for another bite. P. vivax and P. ovale develop dormant
stages (hypnozoites) that cause relapses.
- Fever or 'flu-like symptoms, although there may be no 'typical'
- Residence or travel history.
- Rapid progression is possible in P. falciparum infection in the
young or travellers.
- Complications of P. falciparum may include cerebral malaria,
circulatory shock, acute haemolysis and renal failure, hepatitis and
- Other species are associated with milder, more chronic disease.
- Urgent blood film examination - usually three.
- Antigen detection tests are useful where laboratories have less
- Nucleic acid amplification tests (NAATs) are used to detect drug
Prevention and control
- Artesunate combination therapy or quinine is recommended for
management of P. falciparum malaria.
- Intensive care support may be required.
- Chloroquine and primaquine are used for other malaria species.
- Insecticide-treated bed-nets.
- Insecticide room spraying.
- Covering of exposed skin between dusk and dawn.
- Prophylaxis should be taken according to expert, up-to-date
- Despite extensive research no vaccine is yet available.
This is a protozoan disease transmitted by sandflies, which inject
infective promastigotes that adapt to survival in cells of the reticuloendothelial
system as amastigotes.
Two disease forms exist: visceral disease (Leishmania donovani
or L. chagasi
) and cutaneous disease (L. major
, L. tropica
and L. aethiopica
in the Old World and L. braziliensis
in the Americas).
Diagnosis and Treatment
- Visceral disease: Fever and wasting are important symptoms.
The bone marrow, liver and spleen are infiltrated by parasites so
the patient becomes anaemic, leucopenic and thrombocytopenic.
Reactive hypergammaglobulinaemia makes patients susceptible to
secondary bacterial infections. Untreated patients will deteriorate
and die within 2 years.
- Cutaneous disease: Chronic, circular skin lesions occur at the
site of the bite, with satellite lesions. Some infections with L. braziliensis
may cause destruction of structures around the mouth and
- Microscopy of skin biopsy, bone marrow sample, blood sample
or splenic aspirate and culture.
- NAAT is used for primary diagnosis and speciation.
- Serological diagnosis by direct agglutination and dipstick tests
for field use.
- Visceral and cutaneous leishmaniasis can be treated with
parenteral liposomal amphotericin B. Alternatives include antimony
compounds, paromomycin and oral miltefosine.
African trypanosomiasis, caused by Trypanosoma brucei gambiense
and T. brucei
rhodesiense, is transmitted by the tsetse fly.
Humans are the only host of T. brucei
gambiense, but antelope or
cattle act as the reservoir for T. brucei
rhodesiense. Parasites in the
blood are inhibited by immune responses, but antigenic variation
allows the organisms to multiply again. Generalized lymphadenopathy
may be present and the skin may appear oedematous.
The patient exhibits a hypergammaglobulinaemia and is susceptible
to secondary bacterial infection. When parasites invade the
brain they cause chronic, progressive encephalitis and the patient
lapses into coma. Death is often the result of secondary bacterial
Diagnosis and Treatment
Parasites are demonstrated in blood, CSF or lymph-node aspirate.
Serological tests are available. Lumbar puncture should only be
performed after circulating parasites have been eliminated with
Primary treatment T. brucei
gambiense is treated with pentamidine;
rhodesiense with suramin.
Secondary treatment of cerebral infection T. brucei
treated with melarsoprol or eflornithine +/- nifurtimox; T. brucei
rhodesiense with melarsoprol.
South American trypanosomiasis
, which causes Chagas disease, is transmitted by
the bite of reduviid bugs. There are three phases of the disease:
acute infection characterized by cutaneous oedema, intermittent
fever, shock and a significant mortality in children; latent infection;
and late manifestations, such as achalasia, megacolon,
cardiac dysrhythmias, cardiomyopathy and neuropathy.
Parasites are demonstrated by microscopy, or culture in artificial
media or laboratory bugs (xenodiagnosis). Serological tests are
Nifurtimox and benznidazole are useful in the acute phase but
efficacy declines as infection progresses. Treatment of complications
is mainly palliative (e.g. cardiac pacemakers for heart block
secondary to cardiomyopathy, surgery for megacolon).