Flashcards
COURSE OVERVIEW
Cards in this deck (83)
- 1WHAT ARE THE HOSTS AND SYMPTOMS OF LEISHMANIAHOSTS: MNA, DOG, WILD ANIMALS
IMH: SANDFLY
SYMPTOMS: SKIN ULSCERS, HAIR LOSS + ECZEMA
*INCREASE IN UK CASES DUE TO PET TRAVEL - 2WHAT FALLS INTO THE CATEGORY OF HELMINTHS? (METAZOAN PARASITES)ROUNDWORMS (NEAMTODES)
PLATYHELMINTHS (FLATWORMS)
TREMATODES (FLUKES)
CESTODES (TAPEWORMS)
*ALSO INCLUDE ECTOPARASITES E.G. FLEAS AND TICKS - 3GIVE DETAILS OF NEMATODES + EXAMPLESDEVELOP FROM EGG, THE LARVAE, TO ADULT STAGE
TOXOCARA CANIS (DOGS - DIRECT LC)
HAEMONCHUS CONTORTUS (SHEEP - DIRECT LC) - 4GIVE DETAILS OF FLATWORMS + EXAMPLESFLUKES + TAPEWORMS
FASCIOLA HEPATICA (LIVER FLUKE) - SHEEP/CATTLE, SNAIL VECTOR
SCHISTOSOMA BOVIS - CATTLE, AQUATIC SNAIL
TAENIA SOLIUM - PIG TAPEWORM - 5WHAT ARE COMMON FEATURES OF NEMATODES?- CYLINDRICAL (ROUND WORMS)
- SEPARATE SEXES
- FEMALE PRODUCES EGGS OR L1
- WIDE SIZE RANGE - 6WHAT IS THE COMMON LIFE CYCLE OF NEMATODES?1. ADULT PARASITE PRODUCE EGGS OR L1
2. EGGS HATCH (L1)
3. L2
4. L3
5. L4
6. ADULT PARASITE
*ALL NEMATODES MUST UNDERGO MOULTING PROCESS IN ORDER TO DEVELOP FROM EGG TO ADULT - 7WHAT HAPPENS DURING THE MOULTING PROCESS?- SHED EXOSKELETON + GROW A NEW ONE
- ALLOWS FOR GROWTH AND FURTHER DEVELOPMENT - 8WHAT DOES PPP STAND FOR/MEAN?PRE PATENT PERIOD
TIME IT TAKES FROM HOST INGESTING INFECTIOUS STAGES/BEING INFECTED TO THE PARASITES MATURING AND REACHING DISPERSAL STAGE - 9GIVE FEATURES OF TOXOCARA CANIS- GUT NEMATODE
- EGGS EMBRYONATE OVER 4 WEEKS + PERSIST IN ENVIRONMENT FOR YEARS
- HIGHLY PITTED, THICK EGGSHELLS
- LARGE ADULT FORMS, SMALL INFECTIVE STAGE LARVAE
- ADULT HEAD
*EGG IS STAGE FOUND IN ENVIRONMENT, LARVAE HATCH AND ARE INFECTIOUS STAGE THAT MIGRATE THROUGH TISSUES - 10ROUTES OF INFECTION: TOXOCARA CANISORAL (DIRECT) - INGEST INFECTIVE LARVAE IN EGG - MOST COMMON
TRANSPLACENTAL + TRANSMAMMARY - LARVAE ARRESTED IN TISSUES OF DOG BECOMES RE ACTIVATED VIA PLACENTA, AND MILK PRODUCTION = INFECTION OF PUPPIES
PARATENIC HOST - TRANSPORT HOST (NOT IMH) DOGS AFFECTED IF INGEST HOST - 11GIVE THE CYCLE OF INFECTION OF TOXOCARA CANIS IN < 3 MONTH OLDSPPP 4-5 WEEKS
1. EGG MATURES IN ENVIRONMENT
2. EGG CONTAINING L3 IS INGESTED
3. L3 HATCHES IN SI
4. HEPATOTRACHEAL MIGRATION, VIA LIVER TO LUNGS
5. L3 TO SI VIA TRACHEA
6. L3-L4 ADULT IN SI
7. ADULT IN SI RELEASE EGGS - 12GIVE THE CYCLE OF TRANSPLACENTAL TOXOCARA CANIS TRANSMISSIONPPP IN PUPS 16D-3WEEKS
1. L3 IN EGG INGESTED
2. L3 HATCHES IN SI
3. L3 MIGRATES INTO TISSUES (ARRESTS)
4. L3 ACTIVATES 3 WEEKS PRE PARTUM
5. IN PUP, L3 MIGRATES TO FOETAL LUNG
6. AT BIRTH, L3 TO SI VIA TRACHEA
7. L3-L4 ADULT IN SI
8. ADULT IN SI
*ENSURES 100% INFECTION - 13GIVE DETAILS OF TRANSMAMMARY TRANSMISION OF T. CANISL3 IN MILK FOR UP TO 5 WEEKS - NO MIGRATORY PHASE
*ARRESTED LARVAL DEVELOPMENT IS RE-ACTIVATED WHEN IMMUNITY IS LOWERED DURING PREGNANCY - 14GIVE TREATMENT OPTIONS OF T.CANIS- PREVENT ENVIRONMENTAL CONTAMINATION WITH EGGS
- START TREATMENT BEFORE PARASITE LAYS EGGS
- TREAT BITCH + PUPPIES - 15GIVE FEATURES OF HOOKWORMS:1-3CM, STOUT, HOOKED HEAD
DIRECT LIFE CYCLE
L3 INFECTIVE
IMPORTANT PATHOGENS IN TROPICS - CAUSE OF SEVERE ANAEMIA
*RE-ACTIVATION OF L3 CAN PRODUCE LATENT INFECTION IN BITCH, CAN INFECT 3 CONSECUTIVE LITTERS - 16HOW DO HOOKWORMS SUCK BLOOD?- HEAD IS BURIED IN MUCOSA AND ACTIVELY INGESTS BLOOD AND OTHER TISSUES
- PRODUCE LYTIC FACTOR, ANTI-COAGULANTS AND VARIOUS PROTEASES THAT DEGRADE HAEMOGLOBIN - 17WHAT ARE THE CLINICAL SIGNS OF A.CANINUM?YOUNG ANIMALS - SEVERE ACUTE HAEMORRHAGIC ANEAMIA (BLOODY DIARRHOEA)
OLDER ANIMALS - CHRONIC HAEMORRHAGIC ANAEMIA
RESPIRATORY SIGNS DUE TO LARVAL DAMAGE
MULTIPLE INFECTION (SKIN REACTION - DERMATITIS) - 18CONTROL METHODS OF A.CANINUMCHEMOTHERAPY (3 MONTHLY) - BENZAMIDAZOLES + IVERMECTIN
HIGH DOSE FENBENDAZOLE IN PREGNANT
CLEAN DRY BEDDING - EARTH/GRASS SUPPORTS SURVIVAL OF L3
VACCINATION (USING GUT MEMBRANE ANTIGENS) - INHIBITS ENZYME HAEMOGLOBINASE = STARVE WORMS - 19DESCRIBE TRICHOSTRONGYLOIDEAMOST IMPORTANT GROUP OF NEMATODE PATHOGENS IN GRAZING RUMINANTS
PPP APROX 21 DAYS - 20DESCRIBE THE LIFE CYCLE OF OSTERTAGIA OSTERTAGI (CATTLE)*MAIN NEMATODE IN THE UK
1. ADULTS IN ABOMASUM
2. EGGS HATCH IN FAECES
3. L1
4. L2
5. L3 (INGESTED)
6. PENETRATE ABOMASAL GLAND
7. L4 (EL4 HYPOBIOSIS) ARRESTED LARVAL DEVELOPMENT - REMAIN IN TISSUES
8. IMMATURE ADULT - 21WHAT IS DEVELOPMENT OF HATCHING EGGS DEPENDENT ON?TEMPERATURE + HUMIDITY
WARMER + DAMPER = FASTER DEVELOPMENT
SUMMER PPP = 3 WEEKS
SPRING PPP = 1-2 MONTHS - 22WHAT CAUSES THE PATHOLGOY OF OSTERTAGIA OSTERTAGI?ONCE L3 IS INGESTED IT PENETRATES THE ABOMASAL GLAND AND MOULTS TO REACH L4 STAGE. THESE THEN RUPTURE OUT OF THE TISSUE CAUSING THE PATHOLOGY
- 23WHAT ARE THE TWO CLINICAL FORMS OF OSTERTAGIOSIS?TYPE 1 - GRAZING CALFS (1ST SEASON) JULY- OCTOBER *DUE TO LARVAE ACQUIRED FROM PASTURE 2-3 WEEKS PREVIOUSLY
TYPE 2 - YEARLINGS (OFTEN HOUSED) OCCURS MARCH-MAY *DUE TO MATURATION OF LARVAE ACQUIRED FROM PASTURE DURING PREVIOUS AUTUMN - 24WHAT ARE THE CLINICAL SIGNS OF TYPE 1 + 2 OSTERTAGIOSIS?1 - PROFUSE WATERY DIARRHOEA
- WEIGHT LOSS
*MORBIDITY HIGH, MORTALITY LOW (IF TREATED)
2 - INTERMITTENT DIARRHOEA
- WEIGHT LOSS (ANOREXIA + INCREASED THIRST)
*MORBIDITY LOW, MORTALITY HIGH
SHOW FEW SYMPTOMS BUT VERY PATHOGENIC - 25WHEN ARE THE 2 PEAKS OF OSTERTAGIOSIS OUTBREAKS?1ST - SPRING TIME (TYPE 2)
2ND - SUMMER (TYPE 1) MUCH MORE COMMON - 26DESCRIBE IMMUNITY TO OSTERTAGIA- SLOW TO DEVELOP (AT LEAST 1 GRAZING SEASON)
- SECOND SEASON CALFS AND ADULTS GENERALLY IMMUNE
*IMMUNE ANIMALS STILL CARRY LOW BURDENS - 27GIVE FEATURES OF HAEMONCHUS CONTORTUS (SHEEP)- VERY PATHOGENIC (POOR IMMUNITY)
- LARGEST PARASITE IN ABOMASUM
- CAUES HAEMORRHAGIC ANAEMIA, PIERCES SURFACE OF ABOMASUM CREATING PUNCTURE WOUNDS + FEEDS OFF BLOOS
- CAN BE LONG LIVED *SIGNIFICANT BLOOD LOSS - 28WHAT ARE INCLUDED IN THE FLATWORMS FAMILY?CESTODES: TAPEWORMS
TREMATODES: FLUKES - 29WHAT ARE FEATURES OF CESTODES?- SEGMENTED BODY
- HERMAPHRODITE *ONLY NEED ONE WORM INSIDE HOST FOR REPRODUCTION
- NO ALIMENTARY CANAL (DON'T HAVE A GUT, ABSORB FOOD FROM SURFACE) - 30WHAT STRUCTURE DO ADULT CESTODES PROCESS?- SCOLEX/HEAD
- ARMED, SUCKERS + ROSTELLUM (ROWS OF HOOKS TO HOLD ON + DON'T GET WASHED OUT)
- CHAIN OF SEGMENTS OR PROGLOTTIDS - 31GIVE FEATURES OF GRAVID SEGMENTS- A MATURE SEGMENT CONTAINS ORGANS OF REPRODUCTION (FERTILISATION WITHIN THE SEGMENT)
- A GRAVID SEGMENT CONTAINS EGGS ONLY - 32WHAT ARE THE FEATURES OF TAENIA EGG?- RADIALLY STRIATED EGGSHELL
- HEXACANTH (6 HOOKED)
*VERY DISTINCTIVE EGG (CAN LIVE IN ENVIRONMENT FOR NUMBER OF YEARS BEFORE IT HATCHES) - 33GIVE DETAILS OF CESTODE LIFE CYCLES:- INDIRECT
- FINAL HOST (ADULT TAPEWORM) OFTEN IN SI
- IMH, LARVAL STAGE OR METACESTODE (USUALLY ENCYSTED)
*FINAL HOST ALWAYS CONTAIN THE ADULT WORM WHICH UNDERGOES ASEXUAL REPRODUCTION - 34WHAT ARE THE LARVAL STAGES IN THE IMH?- CYST CONTAINS THE HEAD(S) OR SCOLEX OF THE FUTURE TAPEWORM
- CYST INGESTED BY FINAL HOST + HEAD LATCHED ONTO WALL OF SI
*STARTS TO BUD SEGMENTS - 35CYST NAMES DESCRIBE THE TYPE OF CYST, WHAT IS MEANT BY: CYSTICERCUS HYDATIDSINGLE SCOLEX
MULTIPLE SCOLECES - 36ALL TAENIIDAE ARE SCOLEX ARMED EXCEPT WHICH?T.SAGINATA
- 37CONTROL MEASURES OF T.SAGINATA- MEAT INSPECTIONS
> 25 CYCSTS CONDEMN CARCASS
< 25 CYCTS CHILL INFECTED CARCASSES FOR 10 DAYS AT -10 DEGREES
COOK MEAT PROPERLY (57 DEGREES) - 38GIVE FEATURES OF TAENIA SOLIUMFINAL HOST: MAN
IMH: PIG OR MAN
LIFE CYCLE SIMILAR TO T.SAGINATA (SISTER SPECIES BUT MUCH MORE DANGEROUS)
*SINGLE CYST GIVES RISE TO SINGLE WORM
CYCTS IN CNS OR EYE (VERY COMMON CAUSE OF LATE ONSET EPILEPSY DUE TO CYSTS IN THE BRAIN) - 39WHAT ARE THE FEATURES OF UK TAENIA SPECIES?TRANSMITTED BETWEEN DOGS (FINAL HOST) AND SHEEP (IMH)
*COMMON IN SHEEP FARMING AREAS
RESULT IN HUGE ECONOMIC LOSS TO SHEEP FARMING INDUSTRY - 40GIVE THE FEATURES OF ECHINOCOCCUS GRANULOSUSFINAL HOST: DOG/WILD CANIS
IMH: RUMINANT/PIG/MAN
SITE: SI - 41GIVE THE FEATURES OF ECHINOCOCCUS EQUINUSFINAL HOST: DOG/RED FOX
IMG; HORSE/DONKEY
SITE: SI - 42LIFE CYCLE OF ECHINOCOCCUS GRANULOSUSPPP 40-50 DAYS
1. GRAVID SEGMENTS SHED 1/WEEK
2. EGGS RESISTANT + INGESTED BY IMH
3. ONCOSHPERE RELEASED + PENETRATE SI WALL
4. HYDATID CYST IN LIVER/LUNG (6+ MONTHS PI)
5. CYST INGESTED BY FINAL HOST
6. ADULTS IN SI OF DOG
*TAKES 6 MONTHS TO BECOME MATURE
PATHOLOGY IS ASSOCIATED WITH CYSTIC STAGE + NOT ADULT WORMS - 43WHAT ARE THE FEATURES OF GRANULOSUS CYSTS?SHEEP NATURAL IMH
IN SHEEP - MOST CYSTS IN LUNGS
IN CATTLE/HORSES - MOST CYSTS IN LIVER
*IN CATTLE CYSTS ARE STERILE - 44WHAT IS THE MAIN FLUKE FOUND IN THE UK?FASCIOLA HEPATICA/LIVER FLUKE
- 45WHAT ARE THE FEATURES OF F.HEPATICA?FINAL HOST: MOST MAMMALS (FOUND IN BILE DUCTS OR GALL BLADDER)
IMH: GLABA TRUNCATULA, AMPHIBIOUS SMALL BROWN SNAIL
*CHARACTERISTIC LEAF SHAPE (LOOKS LIKE NO OTHER FLUKE) - 46DESCRIBE ACUTE FASCIOLOSISDETECTED: AUTUMN/EARLY WINTER *TOWARDS END OF GRAZING SEASON
OCCURS: 2-6 WEEKS POST INGESTION
CAUSED BY: MIGRATION OF JUVENILE FLUKES
RESULTS IN: LIVER DAMAGE, HAEMORRHAGE + OFTEN SUDDEN DEATH - 47DESCRIBE SUBACUTE FASCIOLOSISDETECTED: LATE AUTUMN/WINTER
OCCURS: 6-10 WEEKS POST INGESTION
CAUSED BY: JUVENILE MIGRATION + ADULT FLUKES IN BILE DUCTS
ADULTS: FEED ON BLOOD AND DAMAGE BILIARY MUCOSA + INDUCE INFLAMMATION
RESULTS IN: LIVER DAMAGE, HAEMORRHAGIC ANAEMIA, OEDEMA + ASCITES
*CAN BE FATAL BUT NOT AS OFTEN AS ACUTE - 48DESCRIBE CHRONIC FASCIOLOSISDETECTED: LATE WINTER/EARLY SPRING
OCCURS: 4/5 MONTHS POST INGESTION
CAUSED BY: ADULT FLUKES FEEDING IN BILE DUCTS
RESULTS IN: PROGRESSIVE LOSS OF CONDITION, EMATIATION, SUBMANDIBULAR OEDEMA + ASCITES - 49WHEN DO THE SNAILS BECOME ACTIVE AND BREED?AT 15 DEGREES
MAY TO OCTOBER - 50METHODS TO CONTROL FASCIOLOSIS*REDUCTION OF SNAIL POPULATION
- DRAINAGE (TAKE AWAY HABITAT FOR FLUKES)
- FENCE OFF SATURATED PASTURE
- TREAT AND QUARANTINE NEW ARRIVALS - 51WHAT ARE THE DIFFERENCES BETWEEN FASCIOLA HEPATICA AND FASCIOLA GIGANTICA?GIGANTICA IS MORE PATHOGENIC AND INTERMEDIATE HOSTS ARE AQUATIC SNAILS *BIGGER MORE PATHOGENIC VERSION
NOT FOUND IN THE UK - 52WHAT IS THE BRIEF LIFE CYCLE OF FASCIOLA GIGANTICA?1. MIRACIDIA HATCH AT BEGINNING OF WET SEASON, INFECT SNAILS AND DEVELOP BY THE END OF THE WET SEASON
2. CERCARIA SHED FROM SNAIL AT BEGINNING OF AND DURING DRY SEASON
3. METACERCARIA ENCYST ON AQUATIC PLANTS OR WATER
4. DISEASE AT END OF DRY/OR BEGINNING OF NEXT WET SEASON
*DRY SEASON = DEVELOPMENT WITHIN MAMMAL
WET SEASON = DEVELOPMENT WITHIN SNAIL - 53WHAT IS THE DICROCOELIUM DENDRITICUM FLUKE ALSO KNOWN AS?TEA LEAF FLUKE
- 54WHAT IS AN ADVANTAGEOUS FEATURE OF THE DICROCOELIUM DENDRITICUM FLUKE?HAS WIDE HOST RANGE
IMH: LAND SNAILS + ANTS
*ENSLAVER PARASITE THAT ADJUSTS THE BEHAVIOUR OF THE HOST TO MAXIMISE INFECTION (LOSES INHIBITIONS)
PARASITE WILL GO TO BRAIN OF ANT AND ENCYST - SIT AT END OF GRASS STALK AND GET EATEN - 55GIVE FEATURES OF SCHISTOSOMA BOVISIMH: AQUATIC SNAILS
MAJOR DISEASE OF MAN (SECOND BIGGEST KILLER AFTER MALARIA)
2 SEPARATE SEXES (SEXUAL DIMORPHISM)
*ATTACK SKIN OF ANIMALS WADING IN WATER
DISEASE CAUSED BY EGGS NOT THE ADULTS - 56WHICH IMMUNE RESPONSE DO HELMINTHS INDUCE?TH2 RESPONSE (NEEDS TO BE MODULATED)
- 57WHAT DOES THE DEPLETION OF TREG CELLS RESULT IN?MULTI ORGAN AUTOIMMUNITY
- 58WHY IS C.ELEGAN A MODEL ORGANISM FOR BIOLOGICAL STUDIES?- EXCELLENT GENETIC, TRANSGENIC AND GENOME TOOLS AVAILABLE
- TRANSPARENT, CAN SEE TISSUES + ORGANS
- VERY RAPID LIFE CYCLE + EASY TO GROW
- DON'T HAVE TO USE ANIMALS AS HOSTS - 59WHAT IS A POTENTIAL NEW TARGET FOR ANTI-PARASITIC DRUGS?DISRUPT ENZYME DYP-31 = COLLAGEN NOT PROCESSED AND WORM WILL FAIL TO HATCH FROM EGGS
- 60WHAT IS THE IDEAL ANTI-PARASITIC VACCINE?RECOMBINANT VACCINE (IDENTIFY SINGLE ANTIGEN)
- 61GIVE EXAMPLES OF ANTI-PARASITIC VACCINES:DICTOL VACCINE AGAINST LUNG WORK (D.VIVIPORUS)
VACCINATIONS WITH IRRADIATED L3 (2 DOSES) *ORAL VACCINE
TAPEWORM RECOMBINANT VACCINE (TAENIA OVIS)
*EFFECTIVE BUT EXPENSIVE - 62WHAT ARE THE 3 CLASSES OF BROAD SPECTRUM ANTHELMINTICS?1.BENZIMIDAZOLES (BZS) - WHITE DRENCHES
2. LEVAMISOLE + RELATED COMPOUNDS - YELLOW DRENCHES
3. MACROCYCLIC LACTONE (MLS) - CLEAR DRENCHES - 63WHAT IS THE MODE OF ACTION OF BENZIMIDAZOLES?- BIND TO BETA TUBULIN
- INHIBIT MICROTUBULE FORMATION
- ACTS ON THE GUT OF THE PARASITE, REDUCES FEEDING EFFICACY AND RESULTS IN DEATH
*SPECIFIC PATHOLOGY AS PARASITES HAVE FASTER METABOLISM THAN HOST - 64WHAT IS THE MODE OF ACTION OF LEVAMISOLE?- BIND TO NICOTINIC ACETYL CHOLINE RECEPTORS + MIMIC THE NATURAL NEUROTRANSMITTER
- CAUSE SPASTIC PARALYSIS THROUGH DEPOLARISATION OF MUSCLE (WORMS PASSED OUT WHOLE - SAFE) - 65WHAT IS THE MODE OF ACTION OF MACROCYCLIC LACTONES?- BIND TO GLUTAMATE OR GABA GATED CHLORINE CHANNELS
- CAUSE FLACCID PARALYSIS DUE TO HYPERPOLARISATION OF NERVE + MUSCLE CELL MEMBRANES
*ACTS AS AGONIST - 66HOW DOES DRUG RESISTANCE DEVELOP?DRUG TREATING SELECTS FOR PARASITES WITH MUTATED RESISTANCE GENES
- 67WHAT CAUSES BENZIMIDAZOLE DRUG RESISTANCE?MUTATION IN ISOTOPE 1 OF THE BETA TUBULIN GENE = POINT MUTATION
*AFFECTS DRUG BINDING - CANNOT BIND ANYMORE - 68GIVE AN EXAMPLE OF A ZOONOTIC NEMATODETOXOCARA CANIS (FOUND IN GI TRACT, OCULAR DISEASE IN MAN)
- 69OUTCOME OF T. CANIS INFECTION: AGE DEPENDENT< 3 MONTHS - LIVER/LUNG MIGRATION +DEVELOPMENT TO ADULTS IN SI
> 3 MONTHS - LARVAE MIGRATE TO TISSUES - 70WHAT IS ANISAKIS SIMPLEX?ZOONOTIC INFECTION OF DOLPHINS AND WHALES
- FISH INGEST INFECTED EGGS
SUSHI AND IMPROPERLY COOKED FISH CAUSE TRANSMISSION TO HUMANS - 71WHY IS TOXOPLASMA GONDII CONSIDERED THE PERFECT PARASITE?- EVASION OF HOST IMMUNE DEFENCES
- FECUND - ABLE TO REPRODUCE QUICKLY
- RESISTANT TO ENVIRONMENTAL CONDITIONS
- BROAD HOST RANGE (DOMESTIC CAT MOST SIGNIFICANT)
- LARGE GEOGRAPHICAL RANGE
- RARELY CAUSES PATHOLOGY/DISEASE - 72WHAT ARE 2 EXAMPLES OF PROTOZOAN PARASITES THAT ARE ZOONOTIC?TOXOPLASMA GONDII
CRYPTOSPORIDIUM - C.PARVUM - 73WHAT IS MEANT BY APICOMPLEXAN PARASITES?EXTENSIVELY MANIPULATE THE HOST CELL ENVIRONMENT TO ESTABLISH INFECTION, SURVIVAL AND PROLIFERATION
*APICAL COMPLEX ALLOWS THEM TO ESTABLISH + ALTER MEMBRANES - 74WHAT IS THE ONLY EUKARYOTIC CELL THAT CAN EVADE OTHER CELLS + PROLIFERATE?THEILERIA - ACTS LIKE A CANCER CELL
ANIMALS DROWN IN THEIR OWN FLUID - 75WHAT ARE THE 2 STAGES OF AFRICAN TRYPANOSOMIASIS DISEASE?1. EARLY OR HAEMOLYMPHATIC STAGE - PARASITE IN BLOOD, LYMPHATICS + PERIPHERAL ORGANS
2. LATE, CNS OR ENCEPHALITIC STAGE - PARASITES INVADE THE CENTRAL NERVOUS SYSTEM
*T.B.GAMBIENSE MOST COMMON - 76WHAT ARE THE CLINICAL SIGNS OF TYPE 1 + 2?1: CHANCRE AT SIGHT OF TSETSE BITE
ENLARGED LYMPH NODES
NON SPECIFIC CLINICAL SIGNS E.C. FEVER
2. MENTAL DISTURBANCES
PARALYSIS
ALTERED SLEEP PATTERNS
COMA - 77WHAT ARE THE TREATMENT PROTOCOLS OF AFRICAN SLEEPING SICKNESS?HAVE TO LOOK AT CSF TO KNOW WHICH STAGE DISEASE IS IN
TREAT WITH MELARSOPROL - VERY PAINFUL
CAN CURE UP UNTIL DAY 21 - AFTER THIS STAGE 1 TREATMENTS ARE INEFFECTIVE AS PARASITES HAVE CROSSED THE BBB
*MALARIA CAN CAUSE FALSE POSITIVE RESULTS AS ELICITS HUGE ANTIBODY RESPONSE - 78WHAT ARE THE FUNCTIONS OF THE BLOOD BRAIN BARRIER? (BBB)- PROTECTS THE BRAIN FROM FOREIGN SUBSTANCES
- PROTECTS THE BRAIN FROM REST OF BODY
- MAINTAINS A CONSTANT MICROENVIRONMENT FOR OPTIMAL BRAIN FUNCTION - 79DESCRIBE LEISHMANIATRANSMITTED BY PHLEBOTOMINE SANDFLIES
HUMAN, DOGS + WILD RODENTS ARE INFECTED WHEN FLIES TAKE A BLOOD MEAL - 80WHAT ARE TRYPANOSOMES?BLOOD PARASITE THAT CAN INVADE ORGANS AND SKIN - IF IN BRAIN, CAN KILL
*ABLE TO RESIST LYSIS BY APOL 1 - 81GIVE DETAILS OF EIMERIA IN POULTRYINFLAMMATORY REACTION TO THE CELLULAR DESTRUCTION THAT IS OCCURRING IN GUT EPITHELIUM AS MEROZOITES ARE RELEASED
*GUT WONT WORK PROPERLY AS EPITHELIUM IS DESTROYED - 82GIVE DETAILS OF TOXOPLASMA GONDIICAUSE ABORTION AND PERINATAL MORTALITY IN SHEEP
INFECTION LATE IN PREGNANCY = CHOCOLATE BROWN MUMMIFIED FOETUS - 83GIVE DETAILS OF TICK BORNE DISEASET.ANNULATA (EUROPE) + T.PARVA (AFRICA)
DEATH USUALLY DUE TO PULMONARY OEDEMA (DROWN IN OWN FLUID)
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- PII - Parasitology Flashcards on COURSE OVERVIEW , created by Flora Gunn on 12/04/2018.
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