SEM photos of Argasidae Note mammillae in flexible exoskeleton mouthparts attached between legs not visible from above Life cycle Ixodidae egg larva nymph adult Larvae have 3 pairs of legs nymphs and adults 4 pairs Adult females feed once lay single large batch of eggs Argasid tick life cycle Can be quite variable between species but note Multiple nymphal stages as many as 8 in some species usually less Adults take many small blood meals 15 30 minutes Many reproductive cycles in female s lifetime Sexes can be distinguished in ixodid ticks by presence absence of a scutum Argasid ticks lack a scutum so determining sex harder Mating Soft ticks occurs off the host Hard ticks occurs on the host except for Ixodes where mating occurs both on and off the host Volume increases 10x water is extracted and returned to host so blood volume consumed 3 Female adults ixodid ticks take one large blood meal convert entire meal to 600 1000 eggs Ixodid hard ticks locate hosts by questing Ixodes holocephalus Engorged female Ixodid tick adult females attach feed for 10 14 days mls Ixodes eggs Larvae sometimes called seed ticks due to small size Note 3 pairs of legs Ixodes scapularis Deer tick Blacklegged tick Three host tick most ixodid ticks Two host tick eg Haemiphysalis One host tick eg Boophilus microplus The point is to discuss opportunities for horizontal transmission picking up pathogens from one host transferring to a different host later Often larvae nymphs use small hosts eg rodents adults large hosts A couple of adult ticks would kill a rodent Implications of tick life cycles Three host ticks Usually exploit small hosts eg rodents rabbits etc as larvae nymphs larger hosts deer cattle Related to blood meal volume one adult could kill a rodent less blood less eggs Switching between hosts host species increases opportunities for horizontal transfer of Same host exploited as larva nymph Only one opportunity for horizontal transmission unless vertical transmission also occurs Same host exploited by all life stages larva nymph do not drop off host to molt How can these ticks be disease vectors if all blood meals are taken from the same individual as adults pathogens Two host ticks One host tick Routes for transmission of pathogens Saliva Regurgitation Coxal Gland and Rectum Diseases associated with argasid ticks Ornithodoros pajahuella tick Bite of pajahuella tick Ornithodoros Bite causes swelling itch pain in sensitized patients Self resolving Tick Borne Relapsing Fever TBRF Western USA Pathogen Borrelia hermsi B parkeri B turicata Vector Ornithodoros hermsi O parkeri O turicata Africa mainly B duttoni vectored by O moubata complex Other species and vectors in Asia Initially high fever up to 106o F chills headache muscle and joint pain nausea dizziness Subsequent flush phase temp falls profuse sweating blood pressure may fall dangerously Intrinsic incubation period 2 18 days vomiting increase over 4 6 days then symptoms resolve Symptoms return each cycle 7 14 days neurological complications Mortality 1 8 locally infection rate can be high up to 38 in 1 year olds may be During the years 1990 2011 483 cases of TBRF were reported in the western U S with infections being transmitted most frequently in California Washington and Colorado More common in Africa Treatment tetracycline type antibiotics eg doxycycline Ornithodoros hermsi tends to be found at higher altitudes 1500 to 8000 feet where it is associated primarily with ground or tree squirrels and chipmunks Ornithodoros parkeri occurs at lower altitudes where they inhabit caves and the burrows of ground squirrels and prairie dogs as well as those of burrowing owls Ornithodoros turicata occurs in caves and ground squirrel or prairie dog burrows in the plains regions of the Southwest feeding off these animals and occasionally burrowing owls or other burrow or cave dwelling animals Why do symptoms relapse Antigenic variation Borrelia expresses an antigenic glycoprotein on it s surface About a dozen open reading frames ORFs for such proteins are in genome but only one promotor so only ORF linked to promotor is expressed Borrelia proliferate leading to onset and increase in symptoms Host develops immune response begins to kill bacteria symptoms abate A few Borrelia undergo genetic rearrangement different ORF linked to promotor begin to express a different surface antigen symptoms return cycles in untreated patients Host immune system initially doesn t recognize new antigen so bacterial population increases Host immune system begins to recognize new antigen cycle repeats 7 14 days cycle up to 10 Cycles continue until bacteria repeat old antigens for which host already has antibodies at that point immune system can eliminate infection Contrast with Trypanosoma brucei gambiense T b rhodesiensis causative agents of African sleeping sickness also use antigenic variation but have vastly larger repertoire of genes several thousand plus recombination results in supply of new antigens that never run out Diseases caused by or vectored by hard ticks Tick paralysis Lyme disease and related diseases Rocky Mountain Spotted Fever Monocytic Ehrlichiosis Granulocytic Ehrlichiosis Babesiosis Powassan and other viruses Deer ear heavily infested with Amblyomma americanum Severe infestations can lead to anemia reduced resistance to disease Ticks tend to aggregate Why Why 1 only certain areas of exposed skin so ticks accumulate there and 2 Some ticks esp Amblomma americanum secrete aggregation pheromone attract more ticks to feed Why Saliva inhibits hemostasis immune responses More ticks feeding in 1 spot better blood flow better suppression of immune response Tick Paralysis Ascending flaccid paralysis Caused by neurotoxin in tick saliva USA mainly Dermacentor andersoni D variabilis Often not diagnosed correctly can be can be confused with Guillain Barre syndrome botulism and myasthenia gravis Mortality rate up to 10 if untreated occasional cause of significant mortality in livestock Bigger issue in Australia Paralysis tick Ixodes holocephalus Resolves in hours following tick removal Lyme disease Named for Old Lyme Connecticut described in 1975 Causative agent Borrelia burgdorferi described in 1982 2 30 days after bite rash termed Erythema migrans usually appears not seen by 40 60 of patients If untreated progresses to muscle pain myalgia arthritis carditis neurological symptoms including facial paralysis mild encephalitis memory problems Responds well to tetracycline