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COURSE OVERVIEW

Flora Gunn PII - Parasitology Inglês 83 flashcards

Flashcards do conjunto (83)

  1. 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
  2. 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
  3. 3GIVE DETAILS OF NEMATODES + EXAMPLESDEVELOP FROM EGG, THE LARVAE, TO ADULT STAGE
    TOXOCARA CANIS (DOGS - DIRECT LC)
    HAEMONCHUS CONTORTUS (SHEEP - DIRECT LC)
  4. 4GIVE DETAILS OF FLATWORMS + EXAMPLESFLUKES + TAPEWORMS
    FASCIOLA HEPATICA (LIVER FLUKE) - SHEEP/CATTLE, SNAIL VECTOR
    SCHISTOSOMA BOVIS - CATTLE, AQUATIC SNAIL
    TAENIA SOLIUM - PIG TAPEWORM
  5. 5WHAT ARE COMMON FEATURES OF NEMATODES?- CYLINDRICAL (ROUND WORMS)
    - SEPARATE SEXES
    - FEMALE PRODUCES EGGS OR L1
    - WIDE SIZE RANGE
  6. 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
  7. 7WHAT HAPPENS DURING THE MOULTING PROCESS?- SHED EXOSKELETON + GROW A NEW ONE
    - ALLOWS FOR GROWTH AND FURTHER DEVELOPMENT
  8. 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
  9. 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
  10. 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
  11. 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
  12. 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
  13. 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
  14. 14GIVE TREATMENT OPTIONS OF T.CANIS- PREVENT ENVIRONMENTAL CONTAMINATION WITH EGGS
    - START TREATMENT BEFORE PARASITE LAYS EGGS
    - TREAT BITCH + PUPPIES
  15. 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
  16. 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
  17. 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)
  18. 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
  19. 19DESCRIBE TRICHOSTRONGYLOIDEAMOST IMPORTANT GROUP OF NEMATODE PATHOGENS IN GRAZING RUMINANTS
    PPP APROX 21 DAYS
  20. 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
  21. 21WHAT IS DEVELOPMENT OF HATCHING EGGS DEPENDENT ON?TEMPERATURE + HUMIDITY
    WARMER + DAMPER = FASTER DEVELOPMENT
    SUMMER PPP = 3 WEEKS
    SPRING PPP = 1-2 MONTHS
  22. 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
  23. 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
  24. 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
  25. 25WHEN ARE THE 2 PEAKS OF OSTERTAGIOSIS OUTBREAKS?1ST - SPRING TIME (TYPE 2)
    2ND - SUMMER (TYPE 1) MUCH MORE COMMON
  26. 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
  27. 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
  28. 28WHAT ARE INCLUDED IN THE FLATWORMS FAMILY?CESTODES: TAPEWORMS
    TREMATODES: FLUKES
  29. 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)
  30. 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
  31. 31GIVE FEATURES OF GRAVID SEGMENTS- A MATURE SEGMENT CONTAINS ORGANS OF REPRODUCTION (FERTILISATION WITHIN THE SEGMENT)
    - A GRAVID SEGMENT CONTAINS EGGS ONLY
  32. 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)
  33. 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
  34. 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
  35. 35CYST NAMES DESCRIBE THE TYPE OF CYST, WHAT IS MEANT BY: CYSTICERCUS HYDATIDSINGLE SCOLEX
    MULTIPLE SCOLECES
  36. 36ALL TAENIIDAE ARE SCOLEX ARMED EXCEPT WHICH?T.SAGINATA
  37. 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)
  38. 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)
  39. 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
  40. 40GIVE THE FEATURES OF ECHINOCOCCUS GRANULOSUSFINAL HOST: DOG/WILD CANIS
    IMH: RUMINANT/PIG/MAN
    SITE: SI
  41. 41GIVE THE FEATURES OF ECHINOCOCCUS EQUINUSFINAL HOST: DOG/RED FOX
    IMG; HORSE/DONKEY
    SITE: SI
  42. 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
  43. 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
  44. 44WHAT IS THE MAIN FLUKE FOUND IN THE UK?FASCIOLA HEPATICA/LIVER FLUKE
  45. 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)
  46. 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
  47. 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
  48. 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
  49. 49WHEN DO THE SNAILS BECOME ACTIVE AND BREED?AT 15 DEGREES
    MAY TO OCTOBER
  50. 50METHODS TO CONTROL FASCIOLOSIS*REDUCTION OF SNAIL POPULATION
    - DRAINAGE (TAKE AWAY HABITAT FOR FLUKES)
    - FENCE OFF SATURATED PASTURE
    - TREAT AND QUARANTINE NEW ARRIVALS
  51. 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
  52. 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
  53. 53WHAT IS THE DICROCOELIUM DENDRITICUM FLUKE ALSO KNOWN AS?TEA LEAF FLUKE
  54. 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
  55. 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
  56. 56WHICH IMMUNE RESPONSE DO HELMINTHS INDUCE?TH2 RESPONSE (NEEDS TO BE MODULATED)
  57. 57WHAT DOES THE DEPLETION OF TREG CELLS RESULT IN?MULTI ORGAN AUTOIMMUNITY
  58. 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
  59. 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
  60. 60WHAT IS THE IDEAL ANTI-PARASITIC VACCINE?RECOMBINANT VACCINE (IDENTIFY SINGLE ANTIGEN)
  61. 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
  62. 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
  63. 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
  64. 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)
  65. 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
  66. 66HOW DOES DRUG RESISTANCE DEVELOP?DRUG TREATING SELECTS FOR PARASITES WITH MUTATED RESISTANCE GENES
  67. 67WHAT CAUSES BENZIMIDAZOLE DRUG RESISTANCE?MUTATION IN ISOTOPE 1 OF THE BETA TUBULIN GENE = POINT MUTATION
    *AFFECTS DRUG BINDING - CANNOT BIND ANYMORE
  68. 68GIVE AN EXAMPLE OF A ZOONOTIC NEMATODETOXOCARA CANIS (FOUND IN GI TRACT, OCULAR DISEASE IN MAN)
  69. 69OUTCOME OF T. CANIS INFECTION: AGE DEPENDENT< 3 MONTHS - LIVER/LUNG MIGRATION +DEVELOPMENT TO ADULTS IN SI
    > 3 MONTHS - LARVAE MIGRATE TO TISSUES
  70. 70WHAT IS ANISAKIS SIMPLEX?ZOONOTIC INFECTION OF DOLPHINS AND WHALES
    - FISH INGEST INFECTED EGGS
    SUSHI AND IMPROPERLY COOKED FISH CAUSE TRANSMISSION TO HUMANS
  71. 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
  72. 72WHAT ARE 2 EXAMPLES OF PROTOZOAN PARASITES THAT ARE ZOONOTIC?TOXOPLASMA GONDII
    CRYPTOSPORIDIUM - C.PARVUM
  73. 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
  74. 74WHAT IS THE ONLY EUKARYOTIC CELL THAT CAN EVADE OTHER CELLS + PROLIFERATE?THEILERIA - ACTS LIKE A CANCER CELL
    ANIMALS DROWN IN THEIR OWN FLUID
  75. 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
  76. 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
  77. 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
  78. 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
  79. 79DESCRIBE LEISHMANIATRANSMITTED BY PHLEBOTOMINE SANDFLIES
    HUMAN, DOGS + WILD RODENTS ARE INFECTED WHEN FLIES TAKE A BLOOD MEAL
  80. 80WHAT ARE TRYPANOSOMES?BLOOD PARASITE THAT CAN INVADE ORGANS AND SKIN - IF IN BRAIN, CAN KILL
    *ABLE TO RESIST LYSIS BY APOL 1
  81. 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
  82. 82GIVE DETAILS OF TOXOPLASMA GONDIICAUSE ABORTION AND PERINATAL MORTALITY IN SHEEP
    INFECTION LATE IN PREGNANCY = CHOCOLATE BROWN MUMMIFIED FOETUS
  83. 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 sobre COURSE OVERVIEW , criado por Flora Gunn em 12-04-2018.
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Flora Gunn
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