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Flashcards

Malaria

tate0295 Medical Parasitology MSc Inglês 144 flashcards

Malaria

Flashcards do conjunto (144)

  1. 1Malaria is mainly in the tropicsThe extrinsic nature of the parasites moving from the stomach to the salivary glands is temperature dependent
  2. 2Malaria is not endemic in Western EuropeDue to development, even with warming climate
  3. 3R0The basic reproductive number; the average number of NEW cases that arise from ONE infectious host introduced into a susceptible population; R0 must be >/=1 for transmission to occur. If R0=<1, the disease will die out
  4. 4Why is R0 important?Determines: The rate at which a disease will spread through a population; The equilibrium level of infection; The age at which the host acquires infection; The effort required to control the disease. (Rate is measured per cycle of infection)
  5. 5Using R0 to target malariaThe whole system is most sensitive to mosquito survival rate; As it takes 10 days for an infected mosquito to become infective, and probability of survival is lower, there are very few infective mosquitoes over time
  6. 6Vectorial capacity, CC = R0 per day; Risk of transmission; most sensitive to feeding frequency and survival probability
  7. 790% of malaria deaths are in AfricaRelating to main vector; Anopheles gambiae survival probability is p=0.9 vs e.g. An. culicifacies p=0.7; So ~33% An. gambiae survive to infectiousness compared to ~3% An. culicifacies; An. gambiae highly anthrophilic vs An. culicifacies highly zoophilic
  8. 8Entomological Inoculation Rate (EIR)Bites from sporozoite-positive mosquitoes per person per day/year; In rural sub-Saharan Africa, ranges from ~10 to ~1000 infective bites per year
  9. 9Spleen rateLike prevalence; proportion of children aged 2-9 years with splenomegaly; can be >75% in holoendemic areas
  10. 10Hypoendemic malariaLittle transmission; most of the time is of little public health importance, spleen rate <10%; transmission often sporadic and self limiting; E.g. Central China and Mexico
  11. 11Mesoendemic malariaPresent in most places; generally important public health problem; transmission intensity varies widely locally and year to year; spleen rate 11-50% in children E.g. India and parts of SE Asia
  12. 12Hyperendemic malariaVery intense transmission, but seasonal; Primary public health problem; infection rates high, immunity important in controlling disease (asymptomatic common); spleen rate >50%; E.g. African Sahel
  13. 13Holoendemic malariaVery intense and perennial transmission, but may vary place to place and with season (wet regularly); Most common cause of hospitalisation; spleen rate >75%; Disease concentrated in young children and pregnant women; E.g. humid lowland tropical Africa
  14. 14R0 and endemicity-Stable perennial, R0 always >1; -Seasonal, R0 fluctuates above and below 1; -Unstable (epidemic), R0 normally <1 but increases >1 for long irregular intervals; -Perennial holoendemic, R0 may be >100
  15. 15R0 and stabilityClose to the threshold, R0 varies ~1, so malaria is unstable (epidemic) => vector control has great impact. Where R0>>1, malaria is stable, vector control may have little impact
  16. 16Discovery of P. knowlesi in humansConfirmed in 2004 by PCR; In Malaysia, cases of 'P. malariae' but with unusually high parasitemia; most likely monkey->mosquito->human transmission; may be >50% cases in some areas
  17. 17P. ovale subspecies, Curtisi & WallikeriLikely underestimated cases as thick film hard to ID; PCR ID's on small riobo. subunit - not found in some isolates; variants are sympatric - unique subspecies; P. o. wallikeri has longer latency
  18. 18Problems with diagnosisQuality varies greatly worldwide; Particular problems with zoonoses e.g. P. knowlesi and other species in apes
  19. 19Origin of human PlasmodiumWhole groups of related sp. only in apes; Pf. only small subset; suggested a single transition from apes to humans, which has expanded exclusively in humans (also likely with Pv)
  20. 20Erythrocytic schizogonyLysis releases immunogenic material and 'toxins' -> possibly haemozoin and GPI; immunogenic material likely MSP-1 &2, AMA-1
  21. 21PfEMP1Encoded by var; ~60 variants, exclusively expressed; specific adhesion properties; Highly polymorphic
  22. 22RosettingCOncequence of PfEMP1 expression on RBCs; PfEMP1 binds CR-1 on uninfected RBCs
  23. 23Syndromes of severe malariaSevere malarial anaemia; Cerebral malaria; PAM (in primigravid women in holoendemic areas)
  24. 24Cerebral malaria gradingCM-1: Only parasite sequestration in blood vessels; CM-2 Parasites and leukocytes (mainly monocytes/macrophages); CM-3 No parasite or leukocyte sequestration observed
  25. 25Immune response role in cerebral malariaIndividuals that generate a strong pro-inflammatory response to infected are more susceptible to CM
  26. 26Causes of severe malarial anaemiaLysis of infected RBCs; but mostly, inhibition/sub-optimal erythropoiesis through effects on EPO, by INFg, TNF, IL-10 and MIF
  27. 27PAMVAR2CSA (PfEMP-1) binding chondroitin sulfate A in intervillous space of placenta; pro-inflammatory responses
  28. 28Anti-malaria T cell effector mechanismsCD8+ TCs produce IFNg to kill infected hepatocytes and liver stages; CD4+ TCs produce IFNg to activate phpagocytes; Treg produce IL-10 and/or TGFb to dampen proinflammatory responses
  29. 29Anti-malaria Ab mediated effector mechanismsOpsonisation for enhanced phagocytosis; Inhibit liver invasion by sporozoites; inhibit invasion of RBCs; inhibit cytoadhesion; agglutination; neutralisation of 'toxins'
  30. 30Indicators of development of immunityPeak density <10 and slight reduction in prevalence with increasing age; early clinical immunity, developing later into anti-parasitic immunity
  31. 31Anti-parasitic immunityAbility to limit parasite growth and maintain subclinical infection; May inhibit liver or RBC invasion, opsonisation & phagocytosis, cytokine mediated cytotoxicity
  32. 32Clinical/anti-disease immunityAbility to tolerate considerable parasite burden without obvious clinical symptoms; May neutralise parasite 'toxins', secretion of anti-inflammatory cytokines
  33. 33Protection vs pathologyPartial immunity = pro-inflammatory without regulation; Clinical immunity = pro-inflammatory with anti-inflammatory IL-10 and TGFb
  34. 34Why does it take so long to develop immunity?Very large amount of foreign protein in blood keeps immune system busy; Ag polymorphism and variation - strain specific immunity (huge diversity; more than virus)
  35. 35Ag variation and polymorphismAll the highly immunogenic proteins of blood stages are polymorphic to some degree, e.g. MSP-2 >500 seqs, PfEMP-1; sexual stage recombination in gametes = continual reassortment of polymorphic loci
  36. 36IgG responses with increasing ageIgG responses seen to increase with age to many Ag (AMA-1, MSP-1, MSP-2...); some Ag more immunogenic than others; but are we looking at correct Ag variants to presume protective function?
  37. 37Variety of Ig responsesNot all Ab's respond in the same way between individuals - different responses to different proteins; individual repertoires; but screening has shown 'basic protective profiles' - protective responses to a key panel of Ag more likely to be present in immune individuals
  38. 38Length of Ab responses in childrenShort half life after acute episode (12-13 days), but this is similar for any Ab; but then a longer, more stable background remains with a longer half life once past clinical infection
  39. 39Impact of persistent infection on memoryPersistent, continuous inflammation may inhibit humoral memory - plasmablasts killed before fully developed by proinflammatory conditions
  40. 40Stage-specific immunityResponses to stage spec. Ag, e.g. TRAP, LSA1/2/3, MSPs; different mechanisms against extracellular and intracellular stages
  41. 41'Strain' specific immunityNo strains - each infection 'unique' due to Ag variation and polymorphism; clinical disease associated with infection of new genotype; Conserved Ag tend to be poorly immunogenic
  42. 42Live-attenuated vaccinesMost successful; irradiated sporozoites or under drug cover; but not practical - difficult to store and deliver; need high dose for protection
  43. 43RTS,SPf-CSP fused with Hep-B S Ag; repetitive B and T cell epitopes; Aim is to induce strong humoral response - should also elicit cell mediated responses
  44. 44Drug resistanceNow widespread; Pf resistant to chloroquine; beginnings of artemisinin resistance in Asia mostly due to illegal preparations and sub-optimal doses as monotherapy
  45. 45Merozoite digestive vacuole as a drug targetSite of hemoglobin breakdown - crystallised into non-toxin haemozoin; the target of chloroquine, quinine, mefloquine and maybe artemisinin; if haem monomers cannot be dealt with, there is toxicity, leading to disruption of the membrane
  46. 46Mechanism of chloroquine resistanceResistant parasites accumulate less drug by active efflux from target; have Pf chloroquine resistance transporter (PfCRT) - residue 76 from positive to neutral, allows chloroquine to pass through channel (also other quinine derivatives)
  47. 47P-glycoprotein homologue 1Another efflux pump, originally identified as cause of resistance; but more modulation - not sole determinant
  48. 48ArtemisininsHighly active, but short half life - multiple doses required; modifications improve efficacy - artesunate, artemether etc.; Endoperoxide is essential to activity - reacts with iron in haem
  49. 49Artemisinin resistanceMany proposed mechanisms; increased parasite clearance time on Thai-Cambodian border; drug levels are normal parasites persisted for 7 days and re-emerged 28 days post
  50. 50AntifolatesBlock synthesis or conversion of folate derivatives - used for DNA synthesis; target all life cycle stages; prophylactic and treatment
  51. 51Antibiotics against apicoplast35kb genome with essential genes; antibiotics target apicoplast ribosome; attacks all growing stages but only daughter cells; used alone or in combo
  52. 52Atovaquone against mitochondriaInhibits mitochondrial electron transport; Prophylactic and slow acting therapeutic; Kills only daughter parasites
  53. 53Current WHO treatment guidelinesACT for uncomplicated Pf (e.g. Artequin); Intravenous artesunate for severe malaria; Chloroquine for non-Pf; Primaquine also in Po and Pv; Combination therapies essential for slowing resistance
  54. 54Malaria control financingMajor fundraising increases, but still a huge unmet need
  55. 55Decline of efficacy from research to practiceEffect in trials may be 90%; Factor in access to healthcare, vaccine/drug availability, provider availability - may only be 50% effective in practice
  56. 56Challenge of treatment regulationDrugs available from clinics/pharmacies, but also shops & street vendors - most treatments are obtained from private sector in some countries, mostly unprescribed; Counterfeit and degraded drugs (<44% of anti-malarials in some countries fail QC tests)
  57. 57Targeting treatmentReducing wasted treatments by improving diagnostic accuracy; No prescription until +ve diagnosis (vs. presumtive treatment in the past); Over diagnosis a big problem - lack of expertise and supplies in clinics
  58. 58Over treatmentOften >90% slide or RDT negatives still receive treatment in some countries (e.g. Tanzania); lack of faith in diagnostic labs; easier to treat when presenting febrile; Prescribers desire to be seen to be doing something
  59. 59Treatment adherenceReduces with increasing complexity and duration of schedule; Also with increasing frequency & severity of side effects or adverse reactions
  60. 60Health system considerationsVery important - intervention effects are short lived unless followed by permanent services to adhere to interventions and deal with day to day work; Consider availability & accessibility, Human resources, priority setting, monitoring of programme effects, forecasting needs for supply chain
  61. 61Impact of ITNs/LLINsProbably now >3M lives saved
  62. 62ITN distribution and campaignsInitially by mass campaigns (often alongside other medical interventions); But between campaigns coverage can fall to low levels
  63. 63ITN coverage5-15 y.o. are the least covered group; Distribution needs to be continuous and targeted - e.g. pregnant women at antenatal classes, children at immunisation programmes; Also consider commercial opportunities
  64. 64Continuous ITN campaignsNeed BOTH antenatal clinics and Expanded Programme on Immunisation to supply; Coverage steady but less than universal; effective in some places, but supply chain issues
  65. 65Top-up ITN campaignsTheoretically ideal - no wastage, given only where needed; but operational problems experienced - abuse of system?
  66. 66Effects of net distributionDistribution of 2 nets per household leaves many unprotected - there are often many children in large households; Better as 1 net per 2 people
  67. 67Mass effect of ITNsDon't need much more than 40-50% coverage to have a great overall impact; Provides protection for non-users
  68. 68Tsetse fly feedingPool feeders; Males and females take blood - obligate; attracted to large, moving objects (like cattle)
  69. 69Tsetse fly groupsGlossina morsitans - Savanna/woodlands; G. palpalis - Riverine; G. fusca - Forest; Most known about morsitans - main vector for nagana
  70. 70Tsetse life cycleOne mating per life time; Single egg fertilised and live larvae produced after 9 days - nourished by milk gland; larvae burrow into ground to pupate; Adults emerge after 30 days
  71. 71Trapping TsetseOdour traps - e.g. human, cow, pig, monitor lizard; Preference depends on species - need to be considered;
  72. 72Tsetse host selection75-85% decline in catch when stationary- like moving objects; 96-99% decline in catch when with an ox - bovine preference over human; washing &/or deodorant no effect
  73. 73Insecticide control of TsetseGround spraying used in 1950s - DDT etc.; But ineffective against reinvasion, destruction of non-target species & environmental issues; Arial spraying - repeated to coincide with new adult emergence
  74. 74Sterile insect technique for TsetseRelease of large numbers of sterile males (irradiated); As females only mate one = v. effective; High cost and intensive, but effective on Zanzibar island
  75. 75Clinically important Triatomine bugsRhodnius, Panstrogylus and Triatoma
  76. 76Triatomine life cycleFemales produce 200-300 eggs in lifetime; Eggs hatch after 10-30 days; Five instars, each require a blood meal to mature to next stage; Full life cycle take between 4 months to 1 year
  77. 77Triatomine bug habitatsSpecies dependent; T. infestans often in rocky outcrops; Rhodnius sp. in palms or tree holes; Where life cycles stay in one habitat - easy to control; But where habitats overlap, much more difficult, e.g. moves between domestic environment and palms
  78. 78Geography of major T. cruzi vectorsCentral America - R. prolixus; Andean pact - R. prolixus; Southern cone - T. infestans; Rest of Brazil - T. sordida, T. brasiliensis; Generally R. prolixus Northern, T. infestans Southern
  79. 79Control of TriatominesAre slow reproducing and low number of offspring, low genetic diversity within populations (low resistance to insecticides) - easier to control; IRS most effective and first line control; House improvement - but expensive
  80. 80Phases of triatomine control programmesPreparatory - Mapping, sampling bugs, costing (V. important to ensure success); Attack - spray all houses and outhouses, respray 3-6 months later where reinfestation (ends when house index <5%); Vigilance - Surveillance of houses with community support via local centres, with rapid respraying
  81. 81Sampling triatomines for controlTimed manual collections - with forceps and torch at night; Passive collection - artificial resting sites to collect excrement, baited traps; Community assisted - photos and plastic bags for collection
  82. 82Insecticides against triatomines and applicationsDeltamethrin, Lambda-cyhalothrin. DDT ineffective; Can treat walls and solid roofs - not on palm roof; Fumigant canisters are effective but with little residual action
  83. 83The tick familiesIxodidae - Hard; Inflexible scutum; Argasidae - Soft; No scutum
  84. 84Ixodidae ticksMouthparts visible (hypostome); Scutum; Attach for days - one large blodmeal; Vectors of SPIROCHAETES, ARBOVIRUSES, RICKETTSIAE & BABESIOSIS
  85. 85Lyme diseaseBacteria on salivary glands of Ixodid ticks - I. ricinus principle vector in UK; Transmission 36-48 from onset of feeding; Neurological disorders, pain, chronic fatigue etc.; Easily treatable at early stages
  86. 86Rickettsial DiseasesRocky mountain spotted fever - Rickettsia rickettsii; Only humans and dogs show clinical symptoms; Principal vectors are Dermacentor andersoni, D. variabilis
  87. 87Arboviral DiseasesE.g. Colorado tick fever, Tick borne encephalitis, Crimean-Congo hemorrhagic fever; Various hard tick vectors
  88. 88Argasidae ticksSoft; No scutum or visible mouthparts; Take regular bloodmeals - whole meal in 20 mins; Important genera are Ornithidorus, Argas and Otobius
  89. 89Collecting ticksQuiescent ticks - direct searching of habitats; Questing and feeding ticks - Dragging and lures, Animal baits and CO2, Direct examination
  90. 90Control measures for ticksAvoidance, repellents, clothing; Insecticide treatment of animals and habitats
  91. 91Life cycle of mites4 stages; Few, large eggs; Hexopod larvae; 2 or 3 octopod nymphal stages; Adults
  92. 92Mites of clinical importanceDermatophagoides - house dust mite, triggers asthma; Sarcoptes scabei - causes scabies; Trombiculid mites/chiggers - transmit scrub typhus; Demodex- follicle mite, around eyelashes
  93. 93Dermaphgoides mitesTemperature and soft furnishings make homes ideal habitats; release mite allegens in faeces - asthma, eczema, rhinitis etc.; Can sample populations by vacuuming, for densities per unit weight; RDT and ELISA for allergens
  94. 94Sarcoptes scabeiObligate parasite; Females burrow into skin - ~50 eggs per burrow; Larvae excavate new burrows; Transmitted through skin contact; Typically found where skin is thinner; More serious in immunocompromised
  95. 95Sampling for Sarcoptes scabeiTake skin scrapings and examine microscopically
  96. 96Trombiculid mitesOnly larvae cause damage - fall on host and feed on cell tissue fluids through stylostome; Typically confined to rodents and insectivores in areas of vegetation in scrub land - humans infected when they enter these areas
  97. 97Culicine genera of medical importanceStegomyia (Yellow fever, dengue, encephalitis and Wuchereria & Bancrofti); Culex (Encephalitis & Wuchereria); Mansonia (Brugia); Haemogogus (Yellow fever in C & S America)
  98. 98Adult Culicine morphologyPalps shorter than proboscis; Males have more feathery palps and not club shaped
  99. 99Culicine eggs and layingStegomyia lay single eggs (but no floats) in small containers or depressions, and eggs can withstand dessication; Culex lay rafts of eggs; Mansonia glue eggs to underside of floating vegetation
  100. 100ArbovirusesAcquired during blood feeding; Selective tissue movement (fat body to nervous system to salivary glands and ovaries); Transovarial transmission to offspring can occur (vertical transmission); Infection of glands or NS can lead to modified probing/feeding behaviours
  101. 101StegomyiaTropical species breed in natural or man made containers; Major vector of arboviruses; Tropical distribution
  102. 102Stegomyia aegyptiUrban and peri-urban; Vector of yellow fever and dengue; Breeds in tree holes, tyres, storage jars etc.; Endo and exophilic; Bites early morning & late afternoon; Highly anthropophilic
  103. 103Stegomyia albopictusUrban and peri-urban; Relatively new vector of dengue; Container breeder
  104. 104Yellow FeverAfrica & tropical America; In Africa: Sylvatic cycle - Tree monkeys to mosquito to ground mokeys; Rural - Ground monkeys, mosquito, humans on plantation/forest edge (depends on cross over of vector); Urban - human, mosquito human
  105. 105Yellow Fever in S. AmericaSylvatic cycle - Between monkeys, but are poorly adapted to the virus, so often die; No link vector between forest and villages so not really rural; Uraban - Human, mosquito, human, often introduced by forest workers
  106. 106Dengue Fever4 distinct serotypes; SE Asia, Pacific, India and Americas; Primary vector is S. aegypti (secondary is S. albopictus in SE Asia); Virus adapeted to human transmitting mosquitoes; Reasons for global emergence not understood - population growth, export/import of tyres, poor response infrastructure?
  107. 107Stegomyia albopictusVector of Dengue in SE Asia; Container breeder; More widespread than S. aegypti - better cold tolerance; Bites man, mammals, birds; Endo-philic/phagic
  108. 108Dengue vaccinesNo liscened; Some under development; Live attenuated - some efficacy, higher in those with previous exposure
  109. 109Stegomyia aegypti controlClearing domestic breeding sites (containers); Screens over water tanks; Insecticide breeding sites; Repellents against day biting Steg.;
  110. 110ChikungunyaTransmitte by S. aegypti and albopictus; main reservoirs are monkeys; No vaccine or specific treatment; in africa, maintained in sylvatic cycle
  111. 111Culex speciesNight feeders; Breed in diverse aquatic habitats - pools, ditches, rice fields, man made containers, tree holes; Vectors of encephalitis viruses
  112. 112Encephalitis virusesComplex epidemiology and transmission cycles; Viremia in humans is low, so dead end host; Bird-mosquito cycles important for maintainence of transmission
  113. 113Japaenese encephalitisMain vector in Japan is Culex tritaeniorhynchus - breeding in paddies; Natural cycle involves birds; Spread from Japan and China
  114. 114Arbovirus characteristicsFor each virus = a specific main vector; Vertebrates can be dead end hosts, but if arthropods can be reinfected = amplifying host; Are mRNA based; Several families, e.g. Flaviviridae, Togaviridae; Are 'multihost' capable; Some currently available vaccines
  115. 115Categories of myiasis based on relationship with hostAccidental - e.g. ingestion of eggs/larvae with food; Facultative - e.g. species can develop on carrion & live hosts (often at wound sites); Obligate - e.g. species can only develop on live host
  116. 116Examples of accidental myiasis infection in humansRespiratory tract; Urogenital; Intestinal (Are some some evolved to live intestinally but only in herbivores)
  117. 117Major families of myiasis flyOstridae - All obligate & don't feed as adults, Respiratory or cutaneous; Calliporidae and Sarcophagidae - Obligate or facultative and all feed as adults, cutaneous only
  118. 118Oestridae (warble & bot flies)All found in nasal passage except 2 species, found in trachea; Often, if correct host can't be found, will lay in humans (particularly eyes)
  119. 119Hypodermatinae (Subfamily of Oestridae)All in dermal tissue; Eradicated in UK by use of pesticides
  120. 120Gastrophilinae (Subfamily of Oestridae)All found in digestive tract of herbivores; Infection by ingestion
  121. 121Cuterebrinae & DermatobiaCuterebrinae in mammals - Lay eggs somewhere host is likely to be, e.g. burrow entrance; Dermatobia in humans - D. hominis, lay eggs on other flies likely to contact humans, e.g. mosquitoes
  122. 122Sarcophagidae (flesh flies)Major obligate parasite of livestock; E.g. Wohlfahrtia
  123. 123Calliphoridae (blow flies)Wide range of mammalian hosts, including humans; Some sanguinivorous larvae - latch on for blood meal (also in birds)
  124. 124Scew worm flies (Calliphoridae)New world = Cochliomyia hominovorax; Old world = Chrysomya bezziana, likes to infect existing wounds/ulcers; distribution increased in Iraq with movement of cattle herds
  125. 125Why treat myiasis in animals?Pain and suffering; General malaise; Risk of bacterial infection; Risk of severe tissue destruction; Risk of death, especially in young animals
  126. 126Control of myiasis causing flies1. Control or eradication of fly population; 2. Avoidance of infestation - prophylaxis with repellents and insecticides; 3. Treatment, where other levels of control have failed
  127. 127Myiases vaccinesUnlikey - too big and too difficult
  128. 128Role of entomology in myiasis managementID of fly species involved; Knowledge of biology and distribution to determine infestation origin and prevent future infestations; estimation of the duration of infection
  129. 129Summary of myiasis fliesSummary of myiasis flies
  130. 130Myiasis diagnosisRemoved larvae should not be discarded - need to be retained for identification; Some larvae should be kept alive to be reared to adults for ID; Be aware of possible contamination (flies from other sources nearby)
  131. 131Life cycle of human lice3 instars of nyph; Eggs laid singly hairs (Pthris pubis & Pediculus capitus) or on clothing at seamsclos close to the body (Pediculus humanus)
  132. 132Blood feeding of human liceP. humanus - several times a day; P. capitus - every 5 hours; P. pubis - frequent (hard to know)
  133. 133Medical importance of Pediculus humanusVector of typhus (Rickettsia prowazeki), trench fever (Bartonella quintana) and louse-borne relapsing fever (Borrelia recurrentis)
  134. 134Pediculosis capitisHeadlice/nits; In UK, 1 in 10 primary school children infected; More common in girls; Heavy infestation = irritation, itching - saliva is toxic
  135. 135Pediculosis pubisBluish spots at bite; Associated with other sexually transmitted diseases
  136. 136Control for Pediculus humanusReplace/isolate, boil or wash clothes; Insecticidal treatments
  137. 137Control of Pediculus CapitisInsecticide resistance is increasing; Manual removal by combing best; No need to treat clothing or bedding
  138. 138Control of Pthris pubisWater based insecticide lotions
  139. 139Flea life cycleComplete metamorphosis; Eggs hatch 2-14 days; Larvae undergo 3 instars; Adults develop in cocoon - can lie dormant for up to a year: vibrations caused by a nearby host can trigger emergence
  140. 140Flea blood feeding behaviourMales and females are obligate blood feeders; Not host specific, but habitat specific and primary host is required to achieve sexual maturity; Saliva injected in bite
  141. 141Disease spread by fleasAll zoonoses; Mainly biting nuisance; Plague; Flea borne typhus; Tapeworms
  142. 142Tunga penetrans (Jigger flea)Pigs and man primary host; Burrows into skin to feed; Tropical Africa, Central and S America; High risk of secondary infection
  143. 143PlagueYersinia pestis spread by Xenopsylla sp.; Africa, Asia and S America; Develops in flea midgut
  144. 144Control of fleasInsecticide treatment of infested areas with residual sprays etc.: domestic areas, pets or other hosts; Vacuuming areas where egg laying occurs; Rodent control

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MSc Medical Parasitology FlashCards sobre Malaria, criado por tate0295 em 31-03-2015.
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