Beruflich Dokumente
Kultur Dokumente
07 February 2008
TRYPANOSOMA
occur in blood of mammals as mature elongated
trypomastigotes
multiplying epimastigotes precedes the foremation of
infective trypomastigotes in the intermediate host in all
species of trypanosomes that infect humans
Expressed as:
o African spleeing sickness
o Chaga’s Disease
o Asymptomatic trypanosomiasis
MORPHOLOGY
A. TYPICAL ORGANISM
T.b. gambiense and T. b. rhodesiense
vary in shape of the body and length of flagellum(
15-30μm)
i. Stumpy short form
Infective to the insect host and possess a full
battery of enzymes for energy metabolism
ii. Elongated form
Requires host metabolic assistance and is
specialized for rapid multiplication in the richly
nutritious vertebrate bloodstream
Seen in blood as in lymph node aspirates
iii. Blood form of T. cruzi
present during the early acute stage and at
intervals thereafter in smaller numbers
typical trypomastigotes, mean size 20 μm
frequently curved in a C shape when fixed and
stained
iv. Tissue forms
common in heart muscle, liver, brain
develop from amstigotes that multiply to form an
intracellular colony after invasion of the host cell
or phagocytosis of the parasite
Trypanosome rangeli
infects humans w/o causing disease
B. CULTURE
T. cruzi & T. rangeli
cultivated (3-6 weeks) in the epimastigote form in
fluid or diphasic media
C. VARIATION
T. brucei complex
undergo development of a series of genetically
controlled glycoprotein antigenic coats (variant
surface glycoproteins)
VSGs – means of escaping the host’s antibody
response by producing different antigenic membranes
each trypanosome – thought to possess 1000 VSG
gene – mosaic gene formation
PATHOGENESIS • Tobie’s
• Wenyon’s semisolid
T. b. gambiense and T b. rhodesiense • Growth at 22-24 °C
introduced through the bite of the tsetse fly • Subcultured every 1-2 weeks
indurationa and swelling progress to trypanosomal ANIMAL INOCULATION
chancre • detected by inoculating blood intraperitoneally in mice
spread to lymph nodes, bloodstream, and to CNS • T. b rhodesiense often detectable
(terminals stage)
• T b. gambiense sometimes detectable
sleeping sickness syndrome: lassitude, inability to SEROLOGY
eat, tissue wasting, unconsciousness and death • confirmatory test
o positive IHA, IFA, CF (Machado’s) tests
T b rhodesiense T b gambiense • ELISA
Appears in CSF in 1 month Several months
• Useful in blood blank screening
Rapidly fatal produces Chronic and leads to
somnolence and coma only progressive diffuse • African forms cause IFA rxns after 12 days of infxn
during the final weeks of meningoencephalitis, w/ XENODIAGNOSIS
terminal infection death from sleeping • Method of choice in Chaga’s Dse
syndrome usually ff 1-2 yrs • For trained workers only!
• Impractical for African forms
T. cruzi
introduced when infected bug feces are rubbed into DIFFERENTIAL DIAGNOSIS
the conjunctiva, the bite site or a break in the skin
subcutaneous inflammatory nodule or chagoma • Presence of specific IgM- pathognomonic for the
Chaga’s disease encephalitic stage of African trypanosomiasis
• Differentiation of 2 specie based on total parasite DNA
Insterstitial myocarditis – most serious
element digestant electrophoresed on agarose gels which are
then stained w/ ethidium bromide
Romañas sign – unilateral swelling of the eyelids, a
characteristic at onset. T. cruzi T. rangeli
fever, acute lymphadenitis, dissemination to blood and
tissues Blood forms
Size 20μm Over 30 μm
detected 1-2 weeks as trypomastigotes in blood
Shape Often c-shaped in Rarely c-shaped
multiplies mostly w/in reticuloendothelial cells fixed preparations
Posterior Terminal, large Distinctly
• African forms multiply extracellularly as Kinetoplast subterminal, small
trypomastigotes in blood & lymphoid tissues
• Parasitimia Developmental Amastigote to Not found (only
stages in tissues epimastigote trypomastigotes)
punctuates multiplication
w/ later destruction by the host of blood forms, Triatomine bugs
accompanied by bouts of intermittent fever gradually In salivary gland Always absent Usually present
decreasing in intensity or proboscis
T.b rhodesiense –common In hindgut or Present Present
feces
T. cruzi – intermittent & scant
• Toxin relase explains systemic and local reactions.
• Brazilian Chaga’s Disease
IMMUNITY
causes megaesophagus and megacolon
***all three trypanosomes are transmissible through the • Strain-specific CF and protecting antibodies detected
placenta, and congenital infections occur in hyperendemic in human plasma
areas***
TREATMENT
DIAGNOSIS
• Nifurtimox (Bayer 2505) – shorten acute phase
SPECIMENS • Gamma-interferon –temporary relief
• blood • Suramin Sodium/ pentamidine isethionate – for
• CSF African trypanosomiasis
• Lymph node or primary lesion aspirates • Melarsoprol / Suramin/ Tryparsamide– late dse w/
• Specimes obtaine by iliac crest, sternal bone marrow CNS involve
or spleen punctured • Eflornithine – (DFbIO) for blood and CNS phases of
MICROSCOPIC EXAM T. gambiense and hemolytic stages of T. rhobdesiense
• Thick films – by Giemsa’s stain
• Most reliable
o Smears of blood by T b rhodesiense
o Lymph gland puncture for Tb gambiense
o CSF – tb rhodiense & advanced Tb
gambiense
CULTURE
Microbiology – TRYPANOSOMA by Jawetts (reading assignment) Page 3 of 3
EPIDEMIOLOGY
To follow nlng yung iba.. peace ;)
• Tb gambiense
transmitted by the streamside tsetse
Glossina palpalis
West to central Africa
Produce chronic infxn w/ progressive CNS
involvement
Human reservoir
• T. rhodiense
Transmitted by woodland –savanna Glossina
morsitans, Glossina pallidipes and Glossina
fuscipes
Eastern and southeastern savannas of Africa,
w/ foci West of Lake Victoria
Bushbuck & other antelopes – serves as
reservoir
• American trypanosomiasis
Important in Central & south America
extends widely to Maryland & southern
California
• Certain triatomine bugs become as domiciliated as
bedbugs & infextion may be brought in by rats,
opossums or armadillos w/c may spread the
infection to domestic animals such as dogs and cats
• Largely among poor economic circumstances