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  1. Whipworms are:
    Trichuris trichuria
  2. Important anatomy of Trichuris trichuria
    Thin bodies with thick heads (whip-shaped)
  3. Life-cycle of Trichuris trichuria
    • -Females produce thousands of eggs a day
    • -Eggs excreted
    • -Eggs embryonate in soil (21 days)- Soil must be moist and shady
    • -Eggs swallowed, J1 hatch and enter crypts
    • -Penetrate the cells at the bottom of the crypts, then move to epithelial cells
    • -Grow to adults
    • -Thicker posterior end pokes out, think anterior stays embedded in cell
    • -Females die post reproduction, Males have coiled tales females swim through
  4. Epidemiology of Trichuris trichuria
    • Require poor sanitation:
    • -Poor sanitation (nightsoil)
    • -Warm climates/high rainfall/humid/moister/shade
    • -Found with A. lumbricoides
    • -Sources of infection: Nightsoil, geophagy
  5. Part of body infected by Trichuris trichuria
    • Juveniles infect small intestines
    • Adults infect all of gut and rectum
  6. Infective stage of Trichuris trichuria
  7. Pathology of Trichuris trichuria
    • -Need large number of worms
    • -Commonly seen only in children
    • -Symptoms of heavy infection
    • -Dysentery, anemia, growth retardation, finger clubbing, rectal prolapse
    • -Majority of pathology due to inflammation
  8. Geography of Trichuris trichuria
  9. Hosts of Trichuris trichuria
    • RH: Dogs
    • DH: Humans
  10. Diagnosis of Trichuris trichuria
    Worms/Eggs in stool, colonoscopy
  11. Treatment of Trichuris trichuria
  12. Chance of secondary infection in Trichuris trichuria
  13. Control of Trichuris trichuria
    Proper sanitation
  14. Prevalence of Trichuris trichuria
  15. Group most effected by Trichuris trichuria
  16. Important anatomy of Trichonella spiralis
    Smallest nematode parasite, largest intracellular parasite
  17. Life cycle of Trichonella spiralis
    • -Juveniles live in ‘nurse cells’ found in skeletal muscle
    • -Infected muscles eaten, juveniles in muscle cells eaten by new host
    • -Juveniles ‘activated’
    • -Undergo 4 molts in small intestines
    • -Thread through multiple connected cells
    • -Gives birth to juveniles (NOT EGGS)
    • -Juveniles enter hepatoportal system, liver, heart, lungs, arterial system, Body
    • -Migrate until they find skeletal muscle
    • -Penetrate individual fibers, convert them to ‘nurse cells’
  18. Epidemiology of Trichonella spiralis
    • -Humans are a dead end host (unless eaten)
    • -Several cycles depending on environment (most common is domestic via pigs)
    • -Pigs infected by eating other pig meat
    • -Make sure pork is fully cooked, freezing also works on the non-artic strains
    • -Mostly seen in less developed areas where control is less strict
  19. Part of body infected by Trichonella spiralis
    • Adults infect small intestines
    • Juveniles infect Eye/Tongue/Jaw, Diaphragm, Appendages
  20. Infective stage of Trichonella spiralis
    Juvenile (usually found in infected pork)
  21. Pathology of Trichonella spiralis
    • From adults: Non-specific gut illness, fever
    • Juveniles: Localized adema in hands/feet or other problems such as pneumonia (in lungs), encephalitis (brain), Nephritis (in kidneys), deafness (ears), others.
    • Formation of nurse cells can lead to aches
    • Can be fatal
  22. Geography of Trichonella spiralis
  23. Hosts for Trichonella spiralis
    • Dead End: Human
    • Reservoir/Definitive: Pigs and rats
    • Same animal can be DH and pseudo-IH
  24. How to diagnose Trichonella spiralis
    Hard to diagnose, Juveniles in feces, muscle biopsy
  25. Treatment of Trichonella spiralis
    Treat symptoms
  26. Control for Trichonella spiralis
    Monitor pig populations, freeze/cook meat
  27. Prevalence of Trichonella spiralis
    Worldwide, very common
  28. Most commonly effected groups of Trichonella spiralis
    Those in developing countries
  29. Important anatomy of Dicotophyme renale
    Very large nematode
  30. Life cycle of Dicotophyme renale
    • -Eggs need several weeks to months in water to embryonate (temp dependent)
    • -Eggs consumed by aquatic annelid, hatch to juveniles
    • -Develop to J3 in ventral blood vessels
    •        -Can be consumed by and enter a
    •       paratenic host at this point (encyst in       muscle or viscera)
    • -DH consumes annelid or PH
    • -J3 penetrates submucosa, migrate to liver
    • -Migrate to RIGHT kidney
    • -Maturation
    • -Eggs passed in urine
  31. Epidemiology of Dicotophyme renale
    Any large mammal can be host, humans are uncommon
  32. Part of body infected by Dicotophyme renale
  33. Geography of Dicotophyme renale
  34. Hosts for Dicotophyme renale
    • IH: Annelid
    • PH: Water creatures
    • DH: Humans and large mammals
  35. Diagnosing Dicotophyme renale
    Find eggs in urine , or find the form
  36. Treatment of Dicotophyme renale
    Remove the worm
  37. Prevalence of Dicotophyme renale
    Not a large problem for humans
  38. Important anatomy of Strongyloides stercoralis
  39. Life cycle of Strongyloides stercoralis
    • Female buries tail into respiratory system
    • Lay eggs into gut
    • Eggs hatch in transit, juveniles are passed with feces
    • 3 possible outcomes from here
    •   -Autoinfection: Juveniles molt all the way in rectum and re-infect. (Most common in immunosuppressed individuals)
    •   -Homogonic:J1 become filariform J3, penetrate and infect new host
    •          -No mating, only females, temp soil life
    •   -Heterogonic: J1 becomes free living adult, mating in soil, can produce more free living or filariforms
    •           -Mating and males seen here
    • After this J3 penetrate skin and enter bloodstream, heart, lungs, throat, swallowed
  40. Factor that determines type of Strongyloides stercoralis juvenile
    Temperature: 34 degrees and up free-living 34 degrees and lower filariform
  41. Epidemiology of Strongyloides stercoralis
    • Contact with contaminated soil
    • Once more nightsoil is a terrible idea
  42. Part of body infected by Strongyloides stercoralis
    Skin, lungs, gut
  43. Pathology of Strongyloides stercoralis
    • -Penetration: Slight hemorrhaging and swelling, possible
    • secondary infection
    • -Pulmonary, happens when juveniles enter lungs, burning chest, cough, ect.
    • -Gastrointestinal: Worms crawling through result in sloughing/patches of mucosa
    • -Usually asymptomatic
  44. Geography of Strongyloides stercoralis
    Generally tropics but can be seen in temperate climates
  45. Host for Strongyloides stercoralis
    DH: Human, possible others
  46. Diagnosis of Strongyloides stercoralis
    Worms in feces
  47. Treatment for Strongyloides stercoralis
  48. Control of Strongyloides stercoralis
    Stop shitting everywhere
  49. Prevalence and Groups affected for Strongyloides stercoralis
    Common, asymptomatic in soldiers, mental asylums
  50. Ancylostoma duodenae common name:
  51. Important anatomy in Ancylostoma duodenae
    Anterior end is curved (hook)
  52. Life cycle of Ancylostoma duodenae
    • -Mature and mate in small intestines
    • -Eggs passed with feces
    • -Eggs embryonate in feces (need air, warmth, moisture, shade)
    • -Grows to J3, becomes infective, punctures host
    • -Sensitive to freezing or desiccation
    • -Blood, Heart, Lungs, Glottis, Stomach, Small intestine, Becomes J4
    • -Matures in gut
    • -Produces eggs
  53. Epidemiology of Ancylostoma duodenae
    • -Mines, Shitting on things, wear shoes you stupid shits
    • -Warm, humid, shady soils
    • -Whites more heavily affected
    • -Can also be transferred by ingestion
    • -Synergism with A. lumbrocoides
  54. Part of body infected by Ancylostoma duodenae
    Primarily gut
  55. Infective stage of Ancylostoma duodenae
    Filareform J3
  56. Pathology of Ancylostoma duodenae
    • -Generally Asymptomatic, presentation depends on intensity
    • of infection
    • -Also on nutrition of host and species of worm
    • -Cutaneous Phase:
    • -Begins with penetration, mild
    • discomfort, can introduce secondary infection (ground itch)
    • -Pulmonary Phase:         
    • -Occurs when juveniles break out of lung capillary and enter bronchi/throat
    • -Hemorrhaging, but generally asymptomatic
    • -Intestinal Phase: Blood loss, anemia
    • -Heavy Infections:
    •     -Protein deficiency, mental/growth retardation
    • -Cutaneous larva migrans: Creeping
    • eruptions, non-human hookworms invade and cause skin problems as they wander. Do
    • NOT penetrate subcutaneous.
  57. Organs/Tissue infected by Ancylostoma duodenae
    Primarily gut
  58. Geography of Ancylostoma duodenae
  59. Host for Ancylostoma duodenae
    DH: Human
  60. Diagnosis of Ancylostoma duodenae
    Eggs and worms in feces
  61. Treatment of Ancylostoma duodenae
  62. Chance of secondary infection in Ancylostoma duodenae
  63. What are Ancylostoma duodenae also known as:
    Guardian of Children
  64. Ancylostoma caninum host and special
    Dogs, lies dormant until lactation then is passed transmammary
  65. Control for Ancylostoma duodenae
    Wear shoes, shit in toilets
  66. Prevalence of Ancylostoma duodenae
    High, still relevant in less developed areas, most commonly hits children
  67. Ancylostoma braziliense facts
    Hookworm of dogs and cats, common in south US, can be a source of cutaneous larval migrans
  68. Importnat anatomy of Ascardis lumbricoides
    Largest nematode
  69. Common name for Ascardis lumbricoides
    Intestinal roundworm
  70. Life Cycle of Ascardis lumbricoides
    • -Eggs in environment contain juveniles that undergo molting to J3
    • -Eggs containing J3 are consumed
    • -Egg hatches in small intestine, blood, heart, lungs, swallowed
    • -Mature in intestines, lay more eggs
  71. Epidemiology of Ascardis lumbricoides
    • -Infection from contamination, generally seen is stupid kids
    • -Un-cooked vegetables are important mechanical vector
    • -Certain individuals particularly susceptible
  72. Part of body infected by Ascardis lumbricoides
    Localized to gut, but can be systemic
  73. Geography of Ascardis lumbricoides
  74. Hosts of Ascardis lumbricoides
    • DH: Humans
    • PH: Chicken
  75. Diagnosing Ascardis lumbricoides
    • Juveniles in sputum
    • Eggs in feces
  76. Treatment of Ascardis lumbricoides
  77. Chance of secondary infection with Ascardis lumbricoides
  78. Which parasites eggs are extremely resilient to chemicals
    Ascardis lumbricoides
  79. Control for Ascardis lumbricoides
    Shit stuff
  80. Prevalence of Ascardis lumbricoides
    25% of the population
  81. Groups most likely to be hit by Ascardis lumbricoides
    Children putting shitty fingers in mouth
  82. Ascardis suum
    Very similar to Ascardis lumbricoides but does not breed so different species
  83. Life Cycle of Toxacara canis
    • -Adult worms live in gut of dog
    • -Produce eggs that are passed in feces, eggs are then consumed
    •              -If young pup without prior
    •               infection is infected then they                       complete standard                                        blood,heart,lung,stomach trip
    •                     -Juvenile completes                                      standard migration
    •              -If older dog migration is incomplete               and worms go dormant
    •                      -If said older dog become
    •                      pregnant, they reactivate,                              transplacentally infect pups
    •                             -Pup is born with infection -Rodents or other mammals can consume eggs and become paratenic hosts
    • -Can enter humans causing visceral larva migrans
  84. Epidemiology of Toxacara canis
    • -Low reported rates, expected to actually be much higher
    • -Very likely to infect children as they put shit in their mouth
    • -Sad connection that puppies+children=visceral larval migrans
  85. Parts of body infected in Toxacara canis
    • In dog: Standard route
    • In human: is systemic
  86. Infective stage of Toxacara canis
  87. Pathology of Toxacara canis
    • -Inflammatory response where ever they go; worst places are brain, eyes,
    • -Can get anywhere, severity depending on the place/intensity
    • -Often asymptomatic/misdiagnosed
  88. Geography of Toxacara canis
  89. Hosts of Toxacara canis
    • DH: Dog
    • PH: Small Mammals
    • AH: Humans
  90. Diagnosis of Toxacara canis
  91. Treatment of Toxacara canis
  92. Disease's caused by Toxacara canis
    Visceral larval migrans
  93. Control of Toxacara canis
    Stay away from dogs/wash hands
  94. Groups most commonly affected by Toxacara canis
  95. Toxocara cati
    Like Toxacara canis but effects cats and does transmammary not transplacentally
  96. Common name of Enterobius vermicularis
  97. Important anatomy of Enterobius vermicularis
    Thin, pin like
  98. Life cycle of Enterobius vermicularis
    • -Adults congregate in intestines,
    • but migrate as far up as the stomach and as far down as the anus
    • -Attach to mucosa and eat
    • epithelial cells/bacteria
    • -Females travel to anus as night as
    • lay eggs around butthole
    • -Females die after laying eggs and
    • males after copulation (more females generally seen)
    • -Eggs are consumed
    •           -Either re-infect via hand to mouth, or           hatch and crawl back in                                (retroinfection)
  99. Epidemiology of Enterobius vermicularis
    • -Clothing/Bedding/Everything rapidly become sources of infection
    • -Easily becomes impossible to disinfect everything
    • -Can also transfer on air currents but must ultimately be consumed
    • -White people more susceptible
  100. Part of body infected by Enterobius vermicularis
    Gastrointestinal tract
  101. Infective stage of Enterobius vermicularis
  102. Pathology of Enterobius vermicularis
    • -Generally asymptomatic
    • -High intensity can lead to disease
    • -Penetration of submucosa can be fatal
    • -Generally symptoms are irritants,
    • but variety of symptoms can be seen in heavily infected children
  103. Geography of Enterobius vermicularis
  104. Hosts for Enterobius vermicularis
    DH: Human
  105. Diagnosis of Enterobius vermicularis
    Watch butthole at night, scotch tape test
  106. Treatment of Enterobius vermicularis
    Mebendazole (treat whole household)
  107. Control of Enterobius vermicularis
    Can't really do so
  108. Prevalence of Enterobius vermicularis
    Worldwide and non-discriminate
  109. Common name for Onchocera volvulus
    'River Blindness'
  110. Life Cycle of Onchocera volvulus
    • -Adult worms live under the skin
    • where they become encapsulated by host
    • -Produce microfilariae (unsheathed)
    • which remain in skin
    • -Microfilariae taken up by black
    • flies (Simulium spp.)
    • -MF migrate to thoracic muscle of
    • fly, molt to J3s (J2=sausage stage)
    • -J3s move to mouth area
    • -Infect new host when they take
    • next meal
  111. Epidemiology of Onchocera volvulus
    • Simulium spp. Live in clear fast rivers with areas of high humidity and streamside vegetation
    • Disease associated with rivers
    • Location determined what part of body to be affected
    •    -Below waist in africa and above waist in S. America
  112. Infective stage of Onchocera volvulus
    J3 Microfilariae
  113. Pathology of Onchocera volvulus
    • -Adults: Less pathogenicàcreate
    • nodules (onchocercomas) over boney areas, not really harmful
    •          -Can sometimes cause elephantitis               or hanging groin
    • -Microfilariae
    •           -Inflammatory response in skin, can                be mild to severe (dermatitis) (from              wolbachia)
    •                     -Followed by lichenification                            -Elephant skin
    •           -MF migrate to eyes, die, form                      lesion, blindness (scleroses/keratitis of            eyes)
  114. Organs and tissues effected by Onchocera volvulus
    Skin and eyes
  115. Geography of Onchocera volvulus
    Africa and South Africa
  116. Hosts for Onchocera volvulus
    • DH: Human
    • Vector: Black fly
  117. Diagnosis for Onchocera volvulus
    Skin snip (don't get blood in it) for microfilariae
  118. Treatment for Onchocera volvulus
    Ivermectin (kills MF, disrupts transmissions)
  119. Chance of secondary infection in Onchocera volvulus
    Yes, Wolbachia
  120. Control for Onchocera volvulus
    Chemotherapy and Black fly control
  121. Prevalence of Onchocera volvulus
    Common in endemic areas
  122. Common name for Loa Loa
    African Eye Worm
  123. Life Cycle of Loa Loa
    • -Adults live in subcutaneous tissue
    • -Release MF into blood stream, are
    • found through-out body in day, congregate in lungs at night
    • -Taken up by deer flies
    • -Develop to Filariform J3 in fat of fly
    • -Transmitted to human on next blood meal
  124. Part of body infected by Loa loa
    Subcutaneous tissue and eyes
  125. Geography of Loa loa
  126. Hosts of Loa loa
    • DH: Human
    • IH: Deer fly
  127. Diagnosis for Loa loa
    MF in blood, worm in eye
  128. Treatment of Loa Loa
    • Surgical removal of worms
  129. Prevalence of Loa loa
  130. Life Cycle of Wuchreria bancrofti
    • -Adults in lymphatic ducts
    • -Females release microfilariae into lymph (ovoviviparous)
    • -Most end up in blood
    •     -Show periodicity
    •     -Most common in blood during middle of          night, when host sleeps
    •     -Hide out in deeper areas during day
    •      -Can be altered, seems to go off host        response
    • -Mosquito eats blood, consumes MF
    • -Develop in thoracic muscle to J3s
    • -Filariform J3s migrate to mouth area to infect new host
    •        -J3s are harmful to host mosquitos
    • -Migrate to lymphatic ducts to mature
  131. Epidemiology of Wuchreria bancrofti
    • -Can be carried by number of mosquito vectors
    • -Can be difficult to control mosquito breeding grounds, generally found on tropics
    • -More likely to infect if born in endemic areas
  132. Part of body infected by Wuchreria bancrofti
    Subcutaneous tissue, Lymphatic ducts
  133. Infective stage of Wuchreria bancrofti
    Filareform J3
  134. Pathology of Wuchreria bancrofti
    • -Asymptomatic Phase:
    •     -Generally many host show no symptoms   or microfilarimea, but are still infected
    •     -Can develop hydrocele
    •     -Those first infected as adults rarely show many symptoms
    •     -Those born in endemic areas are
    • often exposed to antigens as fetus and do not mount an appropriate immune
    • response

    • -Inflammatory Phase:
    •     -Disease from adult worm antigens, secondary infection
    •     -Lymphedema, other lymph-diseases
    •     -Also can lead to testicular issues

    • -Obstructive Phase:
    •     -Lymph varices, lymph scrotum, chyluria, elephantitis
    •     -Urine is milkly/bloody
    •     -Elephantoid organs are made up
    • mostly of connective tissue, granulomatous tissue and fat
    •             -Many heavy infections over long       time
  135. Organs effected by Wuchreria bancrofti
    Lymphatic regions, subcutaneous tissue
  136. Geography of Wuchreria bancrofti
    Mostly Africa, other tropical regions
  137. Hosts of Wuchreria bancrofti
    • DH: Human
    • Vector/IH: Mosquito
  138. Diagnosis of Wuchreria bancrofti
    Microfilariae in blood, PCR, ELISA, Rapid card test
  139. Treatment for Wuchreria bancrofti
    DEC (look for endemic Loa loa), manual treatment of elephant limbs
  140. Diseases caused by Wuchreria bancrofti
    Hydrocele, Elephantitis
  141. Control of Wuchreria bancrofti
    Mosquito control and preventative chemotherapy
  142. Prevalence of Wuchreria bancrofti
    Effects alot of people, Tropics
  143. Common name for Dicrofilaria immitis
  144. Life Cycle of Dicrofilaria immitis
    • -Mosquito eats microfilariae
    • -Filariform J3s develop in malpighian tubes
    • -Migrate through thorax to mosquito’s mouthparts
    • -Transmitted to host
    • -Develop and mature in RIGHT heart chambers
    • -Require wolbachia infection
  145. Epidemiology of Dicrofilaria immitis
    Mosquito vector
  146. Part of body infected by Dicrofilaria immitis
  147. Infective stage of Dicrofilaria immitis
    Filariform J3
  148. Pathology
    • -Respiratory insufficiency
    • -vomiting
    • -Chronic cough
    • -Cardiopulmonary failure and death if infection too bad
  149. Geography of Dicrofilaria immitis
  150. Hosts for Dicrofilaria immitis
    • DH: Dog
    • IH/Vector: Mosquito
  151. Diagnosis for Dicrofilaria immitis
  152. Treatment for Dicrofilaria immitis
    Preventative medication
  153. Dracunculus medinensis common name
    Guinea worm
  154. Important anatomy for Dracunculus medinensis
  155. Life Cycle of Dracunculus medinensis
    • -Gravid female migrates to skin of host
    • -Pressure forces a portion of the uterus out of the worm’s body where many juveniles
    • escape
    • -They form a blister that eventually bursts and results in freeing of juveniles
    • -Sections are used up and new ones are pushed to wound for more juveniles to be released
    • -Juveniles must enter water directly to survive
    • -Eaten by copepod
    • -Develop to J3 in copepod
    • -Copepod consumed by DH
    • -Juveniles burrow out of gut to surrounding tissue and migrate to extremities.
  156. Epidemiology of Dracunculus medinensis
    • Requires infected host to go in water with copepods and then someone to drink it
    • Paradoxically common in drought
    • Only helminthic parasite transfer with only drinking water
  157. Parts of body infected by Dracunculus medinensis
    Subcutaneous and cutaneous tissue
  158. Infective stage of Dracunculus medinensis
    J3 within a copepod
  159. Pathology of Dracunculus medinensis
    • -Emergent adult worms:
    •       -Release of metabolic waste by adult        worm can cause mild effects
    •       -Blister forms
    •       -Worm may pop out
    • -Secondary Bacterial Infection:
    •        -Good chance of bacterial infection worsening the blister, making an ulcer
    •        -Can be debilitating
    • -Non-emergent worm
    •        -Die inside, can cause arthritis
  160. Geography of Dracunculus medinensis
    Africa/Asia/Middle East
  161. Hosts for Dracunculus medinensis
    • DH: Human
    • IH: Copepod
  162. Diagnosis for Dracunculus medinensis
    Blister/Worm are good indicators
  163. Treatment for Dracunculus medinensis
    Yank it out
  164. Chance of secondary infection with Dracunculus medinensis
  165. Control of Dracunculus medinensis
    Very easy due to nature of disease, provide clean drinking water, educate and kill copepods and your good
  166. Lifecycle of Capillaria hepatica
    • -Females deposit eggs in liver parenchyma
    • -Host is eaten by a second host, consumes eggs
    • -This host is not infected as eggs must leave a body to embryonate (original host can
    • also die to accomplish this
    • -Eggs embryonate in soil
    • -Consumption of eggs
    • -Juveniles migrate to liver, mature
  167. Epidemiology of Capillaria hepatica
    Human feces not a source of contamination, carnivore feces instead
  168. Part of body infected with Capillaria hepatica
  169. Infective stage of Capillaria hepatica
  170. Pathology of Capillaria hepatica
    Worms in liver can result in loss of function
  171. Host of Capillaria hepatica
  172. Prevalence of Capillaria hepatica
    Not often a parasite of humans
  173. Common name of Nectar americanus
    American Killer (hookworm)
  174. Difference between Nectar americanus and another parasite
    Hookworms, basically the same, except first found in new world (came from old).
  175. Common name of Pediculus humanus humanus/capitus
    Lice (body and head respectively)
  176. Important anatomy of Pediculus humanus humanus/capitus
    Sucking lice
  177. Life Cycle of Pediculus humanus humanus/capitus
    Adult lives on hair/clothes (capitus/humanus) and feeds on host/attaches eggs

    • Eggs hatch and there are three nymphal instars before adulthood (incomplete
    • metamorphosis)
  178. Epidemiology of Pediculus humanus humanus/capitus
    • -Capitus common in tropics, humanus common in cooler climates
    • -Humanus came about with clothing
    • -Both likely evolved with us
    • -Transmission via contact
  179. Part of body infected by Pediculus humanus humanus/capitus
    Skin/Head on head
  180. Infective stage of Pediculus humanus humanus/capitus
    Adult, nymph or hair
  181. Pathology of Pediculus humanus humanus/capitus
    Minor annoyance, vagabound's disease
  182. Pthirus pubis
    Invade coarse hairs, cannot carry diseases
  183. Important anatomy of Ixodes scapularis
    Arachnids, hard ticks
  184. Life Cycle of Ixodes scapularis
    • -Eggs laid in early spring
    • -Larva (6 legs) hatch in summer
    • -Dormant through fall/winter
    • -Nymphs (8 legs) in spring/Summer
    • -Adults in fall/winter
    • -Lay eggs in spring
  185. Epidemiology of Ixodes scapularis
    • -Found in wisco
    • -Forested areas
    • -Important Factors in Tick-borne disease
    • 1). Longevity of ticks
    • 2). Long blood meals
    • 3). Large Populations
    • 4). Possiblity of transovarial spread.
  186. Pathology of Ixodes scapularis
    • 1). Anemia and possible exsanguination from high intensity
    • infection
    • 2). Dermatosis due to parts being left in or secondary infection
    • 3).Tick paralysis is temporary and from toxins when ticks bite at base of neck.
    • 4). Otoacarinsis:Ticks in ear
    • 5).Transmits a lot of kinds of disease
  187. Disease's caused by Ixodes scapularis
    Lyme Disease
  188. Xenopsylla cheopis common name
  189. Life Cycle of Xenopsylla cheopis
    • -Eggs laid on host
    • -Fall off host
    • -Hatch
    • -3 larval instars
    • -Pupa
    • -Adult
  190. Infective stage of Xenopsylla cheopis
  191. Diseases caused by Xenopsylla cheopis
  192. Mosquito genuses
    • Aedes--Floodwater--Lay eggs in soil--Carry Dengue
    • Culex--House--Eggraft
    • Anopheles--Dapple wing--Solo eggs in water
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