Vector Borne Diseases

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vector

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organism that transmits a pathogen

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arthopod vectors

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transmits a wide array of blood borne pathogens form viruses to multicellular organisms

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the periods of vector

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- Arthropods acquire pathogens when they feed on infected hosts and then transmit the pathogen to naïve hosts later during a future blood meal. However, this process is not instantaneous. After a host animal is infected, it is NOT immediately infectious to subsequent vectors.
- Similarly, after a pathogen enters the vector, a defined incubation period must elapse before the vector is capable of transmitting the disease. This period varies for different pathogens and vectors.
- In addition, when an infected vector feeds on a host, transmission is often not instantaneous and requires a minimal feeding period.

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vector borne infection facts

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-affect people living in poor tropical countries
-many are zoonoses and humans are incidental, dead end hosts
-pathogens alter their gene expression as they grow and adapt to the environment within the vector. specific pathogen species are only transmitted by specific vector species
-highly seasonal
the mode of maintenance of a pathogen in a vector population is defined as vertical transmission

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Rickettsia rickettsia (Rocky Mountain Spotted Fever) characteristics

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- obligate intracellular parasite
-replicates in tick's salivary gland
-infected ticks can spread infection to their eggs (transvarial transmission)
-vector is the American Dog Tick
-humans, dogs, and rodents are resovoirs

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Rickettsia rickettsia (Rocky Mountain Spotted Fever) virulence factors

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• Attachment of rickettsiae to receptors on vascular endothelial cells
• "Induced endocytosis" and internalization in endosome
• Rapid escape from endosome-lysosome vesicle by rickettsia-specific phospholipase
• Rickettsiae released by "exocytosis" at ends of host filapodia (perhaps via phospholipase activity)

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Rickettsia rickettsia (Rocky Mountain Spotted Fever) pathogenesis

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• Clinical disease:
- tick takes a long blood meal; regurgitates organisms into bloodstream
- chills, fever, headache, rash occur within 1-2 weeks
- rash is erythematous * maculopapular * petechial (extremities * trunk)
- Untreated RMSF progresses to fulminant vasculitis, especially of endothelial cells as well as the vascular smooth muscle cells of kidney, heart, skin, brain and subcutaneous tissues. Typical treatment: doxycycline.

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RMSF Presentation

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Petechiae that can evolve into purpura
Rapid inflammation of the vasculature (fulminant vasculitis)
Vasculitis of endothelial cells and smooth muscle cells in various organs
Can lead to DIC

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RMSF treatment

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Depletes host cell’s ATP supply

“More of the bad and less of the good”
Increase in toxic peroxides and decrease in antioxidants
Leads to cell membrane damage

Platelets that stick to these damaged endothelial cells can quickly lead to DIC which can lead to shock

>Treatment is doxycyline

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malaria characteristics

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-Transmitted by female Anopheles mosquitoes
-They only feed at night
-No animal reservoir
-There is asexual reproduction of malaria in man D) This makes mosquitos the definitive host

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malaria life cycle

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Asexual Replication in liver and RBCs
“Falciparum Ain’t Never Scared!”
It doesn’t hide out in the liver like other species causing it to be the most severe

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malaria clinical disease

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-Prepatent period- Patient is asymptomatic as parasite replicates in the liver
-Paroxysm- Develop chills and then fever as the parasite is bursting from infected RBCs
-In falciparum, the placenta is susceptible to infection

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Falciparum Pathogenesis

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-Falciparum is most severe
-Infects RBCs of all ages
-RBCs become “sticky” once infected
-Does not relapse like other species (P. vivax and ovale)

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malaria treatment

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-No vaccine yet
-Mosquito control devices such as mosquito nets
-Chloroquine- highly resistant
regions are on the rise
-the best way to diagnose malaria- looking at a blood smear and taking a good travel history

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human granulocytic ehrlichiosis (anaplasmosis) characteristics

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- different cell tropism
>ehrilichia chaffensis in monocyte
> anaplasma phagocytophilum in PMN
-do not have transovarial transmission
- vector: lone star tick

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human granulocytic ehrlichiosis (anaplasmosis) virulence factors

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-Inhibits phagosome lysosome fusion
-Host defense= Iron sequestering
-Can steal host’s ATP supply

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human granulocytic ehrlichiosis (anaplasmosis) diagnosis and treatment

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-Observing morulae within the cell
-Mostly diagnosed by detection of antibody or antigen by PCR
-Treatment is doxycyline