TRYPANOSOMES AND AFRICAN SLEEPING SICKNESS Flashcards
WHAT IS TRYPANOSOMA BRUCEI AND HOW IS IT TRANSMITTED?
- A UNICELLULAR AND EXTRACELLULAR EUKARYOTIC PARASITES
- TRANSMITTED VIA TSETSE FLIES
WHICH DISEASE DOES TRYPANOSOMA BRUCEI CAUSE IN HUMANS AND WHICH IN ANIMALS? WHAT ARE THE CONSEQUENCES?
HUMANS: SLEEPING SICKNESS (FATAL DISEASE, NO VACCINE, TREATMENS CAN BE HIGHLY TOXIC)
ANIMALS, MOSTLY WILD ANIMALS AND CATTLE: NAGANA (MAJOR CONTRIBUTOR TO POVERTY, ECONOMIC IMPACT OF 4.5 BIL $ PER YEAR IN AFRICA)
HOW MANY CASES OF AFRICAN SLEEPING SICKNESS ARE THERE EACH YEAR?
CCA 1000
OTHER NAME FOR AFRICAN SLEEPING SICKNESS?
- HUMAN AFRICAN TRYPANOSOMIASIS (HAT)
WHERE DOES AFRICAN SLEEPING SICKNESS (HAT) OCCUR?
- IN THE 36 SUB SAHARAN COUNTRIES WHERE THERE ARE TSETSE (SPREAD HIGHLY RELATED TO THE PRESENCE OF THE FLY; VECTOR DEFINES THE DISEASE DISTRIBUTION)
WHICH PEOPLE ARE MOST EXPOSED TO TSETSE FLIES?
PEOPLE LIVING IN RURAL POPULATIONS DEPENDENT ON AGRICULTURE, FISHING, ANIMAL HUSBANDRY OR HUNTING
WHAT ARE THE ‘FOCI’ OF INFECTION?
the places where the key elements necessary for transmission of a disease are present: vectors and reservoirs
WHICH COUNTRY IS THE MAJOR DISEASE FOCI FOR AFRICAN SLEEPING SICKNESS?
DEMOCRATIC REPUBLIC OF THE CONGO
HOW MANY SUB SPECIES OF AFRICAN TRYPANOSOME CAUSING HAT ARE THERE? WHAT ARE THEY AND HOW PREVALENT ARE THEY?
T.B. RHODESIENSE (SEVERE, <10% OF THE CASES)
T.B.B. GAMBIENSE (VHRONIC, 90% OF THE CASES)
—-> HAVE DISTINCT GEOGRAPHIC PROFILES, T.B.G. MORE CENTRAL AND WESTER AREAS, T.B.R. MOR EASTER AREAS
ANIMAL TRYPANOSOMIASIS? NAMA+MEANING
IN CATTLE, THE DISEASE IS CALLED NAGANA, WHICH IS A ZULU WORD MEANING ‘TO BE DEPRESSED’
IMPACT OF NAGANA (ANIMAL TRYPANOSOMIASIS) ON THE ANIMALS AND THE ECONOMY?
- IN ANIMALS, CAUSES LETHARGY, MASSIVE WEIGHT LOSS AND LOSS OF PRODUCTIVITY
- MAJOR OBSTACLE FOR ECONOMIC DEVELOPMENT OF THE AFFECTED RURAL AREAS
- DOMESTIC AND WILD ANIMALS ARE AN IMPORTANT PARASITE ‘RESERVOIR’ FOR HUMAN INFECTIVE PARASITES
EPIDEMIOLOGY OF AFRICAN SLEEPING SICKNESS IN THE HISTORY?
- EPIDEMIC 1896-1906, KILLING 300,000-500,000 PEOPLE (MOSTLY UGANDA AND CONGO)
- EPIDEMIC IN 1920
- DISEASE ALMOST WIPED OUT IN THE 1960s, BUT RELAXING CONTROL MEASURES CAUSED A RESURGENCE IN THE 1970s
CONTROL STRATEGIES FOR AFRICAN SLEEPING SICKNESS?
TARGET PARASITE RESERVOIR IN THE HOST: SCREENING AND TREATMENT PROGRAMS FOR HUMANS, TREATMENT OF DOMESTIC CATTLE, ELIMINATING THE WILD ANIMAL RESERVOIR, BETTER HEALTH OF THE POPULATION
TARGET THE VECTOR: SPRAYING OF INSECTICIDES, INSECTICIDE TREATED FLY TRAPS, INSECTICIDE TREATED BED NETS
AFTER RESURGANCE IN SLEEPING SICKNESS IN 1970s, CONTROL PROGRAMS WERE RE-IMPLEMENTED, WHEN?
1990s
EXAMPLE OF VECTOR CONTROL FOR AFRICAN SLEEPING SICKNESS - NETS
- BLUE FLY TRAPS; NET THAT HAS A PIECE OF BLUE FABRIC NEXT TO IT, FLIE ATTRACTED TO THE COLOUR, FLY AROUND THE NET AND GET INTO IT
- COST IS CCA250$ PER SQUARE MILE
- MUST BE REPLACED EVERY 5 MONTHS
TSETSE FLY BITE: WHAT HAPPENS FIRST IN THE PATHOLOGY OF HAT?
- TRYPANOSOMES MULTIPLY IN THE TISSUE AROUND THE INITIAL BITE SITE
- THIS OFTEN RESULTS IN A CHARACTERISTIC LOCAL INFLAMMATION TERMED ‘TRYPANOSOME CHANCRE’
- MOR COMMON IN EUROPEANS; AFRICAN PATIENTS OFTEN EXHIBIT NO PATHOLOGY AT THIS STAGE
PATHOLOGY OF AFRICAN SLEEPING SICKNESS?
1) TRYPANOSOMES MULTIPLY AT THE SITE OF THE BITE, PATCH OF INFLAMMATION FORMS (MORE COMMON IN EUROPEAN THAN AFRICAN PATIENTS)
2) EARLY STAGE=HAEMOLYMPHATIC STAGE: FROM THE INITIAL BITE SITE, PARASITES ENTER THE BLOOD, LYMPHATIC SYSTEM AND BODY TISSUES WHICH CAUSES REGULAR BOUTS OF FEVER AND FLU LIKE SYMPTOMS + MAY CAUSE SWELLING OF THE LYMPH NODES (WINTERBOTTOM’S SIGN) —> SYMPTOMS AT THIS STAGE ARE QUITE MILD IN THE GAMBIENSE SPECIES BUT CAN BE SEVERE IN THE RHODESIENSE WITH OFTEN A FATAL OUTCOME
3) LATE STAGE=ENCEPHALITIC STAGE: TRYPANOSOMES CROSS THE ‘BLOOD-BRAIN’ BARRIER AND ENTER THE CNS LEADING TO SYMPTOMS LIKE ENCEPHALITIS, HEADACHES, SLEEPING DISORDER, ABNORMAL BEHAVIOUR (AGRESSION IRATIONALITY, LEADING TO LOSS OF CONSCIOUSNESS AND COMA
- –> OFTEN FATAL IF UNTREATED
- —> ACUTE FORM LASTS A FEW WEEKS, CHRONIC FROM LASTS MONTHS TO YEARS
UNTIL 2010, THE MOST WIDELY USED TREATMENT FOR SLEEPING SICKNESS WAS?
MELARSOPROL, AN ARSENIC DERIVATIVE, THAT KILLED 1 IN 20 PATIENTS
HOW MANY STAGES DOES AFRICAN SLEEPING SICKNESS HAVE?
3, AND THE 3RD ONE IS TRYPANOSOMES CROSSING THE BLOOD-BRAIN BARRIER TO KILL THE PATIENT
WINTERBOTTOM’S SIGN?
SWELLING IN THE LYMPH NODES ASSOCIATED WITH THE 2ND STAGE OF THE AFRICAN SLEEPING SICKNESS
PARASITAEMIA RELATED TO TRYPANOSOMES IS MUCH HIGEHER IN RODENTS OR COWNS AND HUMAN?
RODENTS
STUDIES IN 2016 REVEALED THAT WHICH ORGANS ARE MAJOR RESERVOIRS OF TRYPANOSOMES? HOW DID THAT INFLUENCE UNDERSTANDING OF THE DISEASE, HAT?
SKIN (MAKES SENSE BECAUSE THE PATHOGEN IS INTRIDUCED BY THE TSETSE FLY BITING THE SKIN) & ADIPOSE TISSUE
—> BEFORE THAT, PRESENCE OF TRYPANOSOMES IN THE SKIN WAS OVERLOOKED AND HAT WAS CONSIDERED TO BE A ‘HAEMOLYMPHATIC DISESE’
ARGUMENTS FOR AND AGAINST ADIPOSE TISSUE BEING A FUNCTIONALLY SIGNIFICANT AREA FOR TRYPANOSOMES TO INHABIT?
FOR:
- TRYPANOSOMES APPEAR TO ADAPT TO THIS NICHE BY UPREGULATING FAT METABOLIC ENZYMES
- MAY EXPLAIN THE WASTING DISEASE PATHOLOGY
AGAINST:
- LARGELY HIDDEN FROM BITING TSETSE
- AFRICAN COWS HAVE LITTLE FAT ANYWAY
SOME UNANSWERED QUESTIONS ABOUT BLOODSTREAM TRYPANOSOME HABITAT?
- ARE PARASITES IN THE FAT, SKIN AND THE BLOOD FUNCTIONALLY IDENTICAL
- ARE FAT AND SKIN PARASITES ‘PROTECTED’ FROM DRUG TREATMENT
- CAN PARASITES FROM THE FAT, SKIN AND BLOOD REPOPULATE EACH OTHER
- ARE PARASITES FROM THE FAT, SKIN AND BLOOD EQUALLY TRANSMISSIBLE
- ARE PARASITES FROM THE FAT, SKIN AND BLOOD EQUALLY PATHOGENIC (WHICH POPULATION KILLS PEOPLE???)