TRYPANOSOMIASIS Flashcards
TRYPANOSOMIASIS is caused by
Trypanosoma spp
They are flagellates that live in blood and tissues of their human hosts
Belonging to the phylum: Sarcomastigophora
Class: Mastigophora
AETIOLOGICAL AGENTS
Trypanosoma brucei has three subspecies:
1. Trypanosoma brucei (an animal pathogen)
2. Trypanosoma brucei gambiense
3. Trypanosoma brucei rhodesiense
The last two species cause African trypanosomiasis or sleeping sickness in man
Trypanosoma cruzi causes South American trypanosomiasis or Chagas disease
African Trypanosomiasis
Transmitted by the tsetse fly (Glossina spp.), found across Africa (14°N and 29°S of the equator).
Human African trypanosomiasis (HAT) caused by two subspecies of the extracellular protozoan parasite
HAT: diseases with distinct clinical and epidemiological patterns
1. T. b. gambiense: chronic form in Central and West Africa and represents >95% of all cases
2. T. b. rhodesiense: a more acute disease form in East and Southern Africa
Epidemiology
HAT common in:
Rural areas (suitable habitats for the tsetse fly vector and frequent human– tsetse contact)
Periurban areas (especially where riverine)
People can be infected while farming, fishing, hunting, collecting water or wood (exposes them to insect bite)
All age groups and both sexes are at risk (prevalence is higher in adults, and sex distribution varies in relation to gender-specific at-risk activities)
Reservoir: T. brucei gambiense (human)
T. brucei rhodesiense (domestic and wild animals )
HABITAT: connective tissue spaces of various organs, reticular tissue of the lymph nodes and spleen, intercellular spaces in the brain, lymph channels throughout the body, blood and cerebrospinal fluid
MORPHOLOGY: T. b. gambiense exists as trypomastigote form in the blood of the vertebrate host.
It is said to be polymorphic, occurring in three forms: a long slender form having a flagellum, a short stumpy form without a flagellum and an intermediate form
Vectors
Thirty-one tsetse species and subspecies are classified as forest, riverine, or savannah, according to morphological differences and habitat preference
Transmission of T. b. gambiense is linked to species favoring riverine vegetation (Glossina fuscipes, Glossina palpalis)
T. b. rhodesiense is typically transmitted in wood land savanna habitats (G. fuscipes, G. morsitans, G. pallidipes)
Vector Biology
The vector for HAT is the tsetse fly
Inhabits rural areas
Bites during daytime hours
Both males and females are capable of carrying and transmitting the disease
Clinical features of HAT
These depend on the T. brucei subspecies, host response, and disease stage
Generally, both forms of the disease lead to death if untreated
T. brucei rhodesiense disease is typically acute, progressing to second stage disease within a few weeks, and death within 6 months
T. brucei gambiense disease follows a chronic progressive course
Life Cycle of Trypanosoma brucei gambiense
- When an infected tsetse fly bites a person (or animal), it injects a form of the protozoa that can cause infection (called trypomastigotes) into the skin. The protozoa move to the lymphatic system and bloodstream.
- Inside the person, they change forms and travel to organs and tissues throughout the body, including lymph and spinal fluid.
- The protozoa multiply in the bloodstream and other body fluids.
- They circulate in the bloodstream.
- A fly ingests the protozoa when it bites an infected person.
- Inside the fly, the protozoa change forms and multiply.
7–8. The protozoa travel to the fly’s salivary glands, multiply, and change into trypomastigotes—the form that is injected when the fly bites a person
Stages of T.brucei
Typically 2 stages: haemolymphatic stage followed by meningoencephalitic stage (trypanosomes cross the blood–brain barrier and invade the CNS)
3–4-cm dermal reaction at the site of the tsetse bite (inoculation chancre) appears within 2–3 days (rarely seen in those with T brucei gambiense disease)
Discuss the first stage of T.brucei
Systemic features: Fever, Debility, Headache, Facial oedema, Anaemia (mainly haemolytic), Lymph node enlargement (mainly posterior cervical)
Skin: Rash, Chancre, Pruritis
Gastro-intestinal features: Hepatic dysfunction and hepatomegaly Splenomegaly
Heart: Early tachycardia, Myocarditis, Congestive cardiac failure, Pericarditis
Endocrine dysfunction: Menstrual disorders, sterility and abortion, Premature still births, Loss of skin hair, Loss of libido and impotence, Gynaeacomastia, Testicular atrophy and orchitis
Eye: Iritis, Iridocyclitis, Keratitis, Conjunctivitis, Choroidal atrophy
Discuss the second stage of T.brucei
Psychiatric and mental disturbances: Lassitude and indifference, Anxiety and irritability, Mania and agitation, Violent and suicidal behaviour, Uncontrolled sexual impulses, Hallucinations and delirium
Sleep disturbances: Daytime somnolence, Nocturnal insomnia, Uncontrollable urges to sleep
Motor disturbances: Pyramidal signs, Extrapyramidal (abnormal movements and tremors), Muscle fasciculation, Slurred speech, Cerebellar ataxia, Neuritis and polyneuritis
Sensory disturbances: Pruritis, Paraesthaesia, hyperaesthesia, anaesthesia
Abnormal reflexes: Palmo-mental reflex
Visual involvement: Double vision, Optic neuritis, Optic atrophy, Papilloedema
Principle features
Laboratory diagnosis of HAT
Depends on the demonstration of the trypomastigote forms of the parasite
In blood, lymph node aspirates, sternal bone marrow, cerebrospinal fluid or fluid aspirated from the trypanosomal chancre
By direct microscopic examination of unstained and stained films
Serologic techniques may be employed for mass field surveys
Treatment of HAT
Suramin or Pentamidine isethionate (in primary stage infections that do not involve the CNS)
Melarsoprol (in late secondary CNS stages of trypanosomiasis)
American Trypanosomiasis
Caused by Trypanosoma cruzi
It occurs in Central and South America, causing Chagas disease
