Other Blood Parasites II Flashcards
Blood Parasites
- Trypanosomes
- Malaria
- Microfilariae
- Leishmaniasis
- Babesiosis
Filarial Worms (Filariasis)
> 200 species recorded but only a small number infect humans.
Most infections due to:
W. bancrofti
B malayi
These worms are up to 4cm (male) and 10cm (female) long and can live for up to 10 years in the lymphatics.
Microfilariae are only 250-300μm long and released by the female worms into the blood.
Filarial Worms - Pathology
-When infected mosquitoes bite people, mature parasite larvae enter the skin. The larvae migrate to the lymphatic vessels and develop into adult worms.
-Adult worms reside in tissues and release microfilariae into the blood-stream, continuing a cycle of transmission.
-Larval forms (microfilariae) are released into the blood with regular periodicity (important for diagnosis).
- Principle Vectors: Blood feeding flies e.g mosquitoes and deer fly
- Wide variety of symptoms e.g: Fever, Inflammation of lymphatic system, swollen skin lumps, elephantiasis, rash
Filarial Worms - Diagnosis
- Presence of microfilariae in blood samples
-Sample should be taken at the appropriate time for the particular species e.g: Wuchereria bancrofti and Brugia malayi release their microfilariae at night, Loa loa are released during the day
-Wet preps useful (motile)
-Antigen testing is now method of choice for W. bancrofti - –immunochromatographic card test (ICT)
-Concentration methods e.g. polycarbonate membrane filtration.
-PCR
MIcroscopy of Microfillae (worms)
Species identification is by thick and thin blood films
Stained with Giemsa or haematoxylin
Relatively cheap but requires skill/experience
Differentiated according to: Pattern & staining of their sheaths, Nuclei distribution and size
Treatment and Prevention : Microfillae
Large-scale treatment (preventive chemotherapy) e.g.;Diethylcarbamazine (DEC), albendazole, ivermectin
Vector Control e.g. insecticide-treated nets or indoor residual spraying
Trypanasomiasis (African Trypanasomiasis (Sleeping Sickness) - Clinical Pathology
Caused by Trypanosoma brucei gambiense (98% of cases) and T. brucei rhodesiense
Transmitted by the tetse fly
Enters the lymphatics and bloodstream
Common in Democratic Republic of Congo, Angola and southern Sudan
African Trypanasomiasis; Clinical Features
1st stage
Trypanosomes multiply in subcutaneous tissues, blood and lymph (haemo-lymphatic stage).
Lymphadenopathy and episodes of fever, headaches, joint pains and itching.
2nd stage
Parasites cross the blood-brain barrier to infect the central nervous system (neurological or meningo-encephalic stage).
More obvious signs and symptoms of the disease apparent e.g. changes of behaviour, confusion, sensory disturbances and poor coordination.
Disturbance of sleep cycle (hence the name).
- Lesion/inflammation at bite site common
- Anaemia & thrombocytopaenia can be present
- Fatal treatment
- Early diagnosis essential to avoid neurological complication
African Trypanasomiasis: Treatment &Prevention
Screening and diagnosis important.
Vector control.
Treatment depends on stage.
Safer and easier to administer in 1st stage.
Second stage depends on drugs that cross the blood-brain barrier to reach the parasite.
Examples of drugs used:
Pentamidine and suramin for the early stages
Eflornithine or Melarsoprol for late stages
America Trypanasomiasis: Chagas disease
Caused by a T. cruzi.
Transmitted by triatomine bugs in South America.
Asymptomatic infection is a problem for blood transfusion services.
Acute phase:
A high number of parasites circulate in the blood
Symptoms often absent or mild
Swelling at the site of entry
Fever, headache, muscle aches
Lymphadenopathy, mild hepatosplenomegaly
Chronic phase:
Parasites are hidden in the heart and digestive muscles
Heart disease in up to 30%. Can lead to heart failure and death
America Trypanasomiasis : Treatment & Prevention
Treated with drugs e.g. nifurtimox and benznidazole.
Focus on prevention.
Screening of blood donors important to prevent transmission by transfusion.
House improvements and good hygiene practices.
Vector control e.g. spraying houses with insecticide, bed nets.
Diagnostic testing and newborn screening.
Diagnosis of Trypansomiasis ( American and African)
Microsopy gold standard.
Examination by wet preps or fields/giemsa stain of:
Blood
Aspirates from enlarged lymph nodes
CSF
Concentration techniques may be required e.g. centrifugation and buffy coat analysis
Not possible to speciate Trypanosoma brucei gambiense T. brucei rhodesiense on stained film.
American species has larger kinetoplast and less convolution of the undulating membrane.
Other Tests:
Serological tests available e.g. enzyme immunoassays and immunofluorescence
PCR (not widely available)
American worm presentation: Large kinetoplast
African worm presentation microscopic: Kinetoplast, Undulating membrane, Nucleus
Visceral Leishmaniasis (kala-azar)- Causation and symptoms
Caused by Leishmania donovani and L. infantum.
Symptoms include: anaemia, fever, substantial weight loss, swelling of the spleen and liver (high fatality rate if untreated).
Visceral Leishmaniasis (kala-azar) - Transmission and clinical pathology
- Found in Bangladesh, India, Nepal, Sudan and Brazil.
- Transmitted through the bite of a sandfly.
- Parasite migrates to the internal organs such as liver, spleen and bone marrow.
Rarely, may be seen in monocytes or neutrophils of peripheral blood (require buffy coat preps).
Macrophage in bone marrow containing numerous organisms
Visceral Leishmaniasis (kala - azar) - Detection , treatment, prevention
Diagnosis: Bone marrow and splenic aspiration more sensitive (gold standard).
Immunological tests also available e.g. ICT.
Prevention: vector control, education and socio-economic considerations.
Treatment by pentavalent antimonials e.g. Sodium stibogluconate.
