Exam 3 - Vector-borne Diseases Flashcards
when is the overall prevalence of tick infestation highest in the USA?
may & June – second peak in October
what replication-incompetent bacteria relies on fleas & ticks to be transmitted?
bartonella spp.
what protozoal parasite uses an insect as both vector & definitive host?
hepatozoon
what agents are obligate intracellular parasites?
ehrlichia, anaplasma, rickettsia spp.
genus borrelia spirochetes
T/F: obligate intracellular parasites can’t survive outside of the host or vector & therefore, aren’t directly contagious
true – extremely well-adapted to survive
because you typically can’t culture obligate intracellular pathogens to diagnose them, what tests are used instead?
serology or molecular diagnostics
how are infections caused by obligate intracellular parasites treated?
must get drugs into the cells to kill the pathogen – or prevent the transmission in the first place
general tick-borne syndrome involves what agents?
ehrlichia, rickettsia, anaplasma, & borrelia
what is the common presentation of general tick-borne syndrome?
tick was attached for 48 hours or more – clinical signs appear 7-21 days later
what are the common initial signs associated with general tick-borne syndrome?
fever, lethargy, lameness, shifting leg lameness, polyarthritis, polymyositis, acute thrombocytopenia, & may wax/wane in severity
acute signs associated with general tick-borne syndrome are generally rapidly responsive to what antibiotic?
doxycycline
why is shifting leg lameness seen in animals with general tick-borne syndrome?
muscle stiffness, soreness, or pain from systemic inflammatory disease or just achiness
true neutrophilic polyarthritis – may be reactive to systemic inflammatory disease or may be direct spread within connective tissues
what 3 mechanisms are associated with acute thrombocytopenia in animals with general tick-borne syndrome?
- increased consumption – fever, inflammatory cascade during bacteremia/parasitemia, vasculitis
- concurrent immune-mediated destruction in some cases – could be specific or bystander
- impaired function also likely – bleeding occurs at platelet counts higher than typically seen with spontaneous bleeding
T/F: anemia is a common feature of general tick-borne syndrome
false – but when present, anemia of chronic inflammatory disease & is non-regenerative
what major clinical syndromes are associated with vector-borne diseases in humans?
spotted fever group, STAR, tick-borne relapsing fever (borrelia turicatae), r. typhi, & r. prowazekii
what is the primary vector of rickettsia rickettsii?
dermacentor species
what are the possible reservoirs for rickettsia rickettsii?
dermacentor, small mammals, rodents, & birds
where is the highest seropositivity of dogs with rickettsia rickettsii?
eastern time zones
where are human cases of rocky mountain spotted fever most prevalent?
southeast united states
rickettsia rickettsii causes clinical disease in what species?
dogs & people
what are the target cells of r. rickettsii?
vascular endothelial cells – ‘spotted’ appearance
typically, mild thrombocytopenia – likely immune-mediated or secondary to vasculitis
diffuse vasculitis often progresses to DIC
what is the prognosis of rocky mountain spotted fever?
acute disease only!!!
dead or better in days to weeks – extremely rapidly treatment responsive
T/F: in rocky mountain spotted fever, exposure-induced immunity is protective for 3 years or more
true
what ticks transmit ehrlichia canis?
r. sanguineus & d. variabilis
what serves as the reservoir for e. canis?
wild & domestic canids
why is ‘canine monocytotropic ehrlichiosis’ another name for e. canis infections?
monocytes/macrophages are the preferred target cells
what are the 3 phases seen with e. canis infections?
- acute – 2-4 weeks, thrombocytopenia, multisystemic signs
- subclinical – months to years to indefinitely (splenic hideout), may remain mildly thrombocytopenic
- chronic – pancytopenia
when are specific IgM & IgG antibodies seen in e. canis infections?
IgM by 4-7 days post-infection
IgG by 15 days post-infection
T/F: antibodies for e. canis are not protective
true
what are some possible vectors for ehrlichia chaffeensis?
amblyomma, dermacentor, ixodes, & haemaphysalis
what are some possible reservoirs for ehrlichia chaffeensis?
white tail deer, possums, coyotes, raccoons
ehrlichia chaffeensis causes clinical disease in what species?
people & dogs
what are the target cells of ehrlichia chaffeensis?
monocytes & neutrophils – perhaps more uveitis seen, milder than e. canis but similar disease
what is the only proven vector of ehrlichia ewingii?
amblyomma americanum
what is the reservoir of ehrlichia ewingii?
white tailed deer
ehrlichia ewingii causes disease in what species?
dogs & people
what is another name for ‘ehrlichia ewingii’?
canine granulocytotropic ehrlichiosis – target cells are neutrophils & eosinophils
visually looks like a. phagocytophilum
where is anaplasma phagocytophilum especially common?
northern midwest USA
what tick species transmits anaplasma phagocytophilum?
ixodes
what are the reservoirs of anaplasma phagocytophilum?
small mammals & deer
anaplasma phagocytophilum causes clinical infection in what species?
dogs, horses, & people
what is the target cell of anaplasma phagocytophilum?
neutrophils
what are the common clinical abnormalities of an animal with anaplasma phagocytophilum?
acute illness with notable lameness – muscular pain and/or neutrophilic polyarthritis
typically, low platelets & low eosinophils
antibody titers persist but don’t protect against re-infection
what is the suspected vector of anaplasma platys?
r. sanguineus
anaplasma platys causes clinical disease in what species?
dogs
what disease does anaplasma platys cause?
infectious cyclic thrombocytopenia – 1–2-week cycle of platelet parasitism, clearance & drop in count (<20K)
only 1% of platelets are parasitized – platelet clearance must include immune-mediated component
what ticks transmit borrelia burgdorferi?
ixodes species & amblyomma
why is it important to know borrelia burgdorferi has many reservoirs?
many reservoirs mean ticks can become infected as larvae, nymphs, or adults
what reservoirs are important for larvae & nymphs when considering borrelia burgdorferi? what about adults?
rodents, small mammals, lizards
adults – deer, large mammals, & lizards
borrelia burgdorferi causes clinical disease in what species as hosts of adult ticks?
dogs & people
how is the lifecycle of ixodes tick species different in the south from the north?
we have lizards who are cold blooded & can’t amplify disease well, so lower prevalence of lyme
in endemic areas of b. burgdorferi, many dogs & people are exposed, but there are few clinical cases of disease – why?
takes»_space; 24 hours to infect after tick attachment & also likely natural host resistance
what are the clinical signs of b. burgdorferi infections?
direct migration through connective tissues
fever, malaise, polyarthritis, typically acute, self-limiting but some poorly understood chronic immune-mediated complications leading to severe protein-losing nephropathy in certain dogs
how is b. burgdorferi treated?
antibiotics – very responsive
what is the disease process of lyme nephritis?
severe membranoproliferative glomerulonephritis causing severe proteinuria that is associated with lyme seropositivity
T/F: lyme nephritis is a direct result of lyme infection
false – it is an immune-mediated disease
what major clinical signs are associated with r. rickettsii?
high fever, acute severe illness, & often petechiae