infectiont5 Flashcards
multi system infection, NS infections
akiThe primary target cells of the Flaviviruses are, where do they replicate
what happens after target is reached
monocyte-macrophages inc dendritic cells, esp suffer cells. will replicate in lymphnodes first and then infect macrophages to send virus into system/organs
induce INFa and cytokine production= prodromal sx
neutralizing vs non neutralizing antibodies
NON-NEUTRALIZING ANTIBODIES PROMOTE INFECTION.-Fc receptors on cell attach Flavivirdae and will enhance the infection(encourage macrophage uptake and induce more cytokine release and will recruit T lymphocytes
NEUTRALIZING ANTIBODIES CAN BLOCK DISEASE. -these will tag a micro for immune destruction
yellow fever endemic countries
vector and resovior
South America, Africa
vector is mosquito but the resovior is non human promates
what gets the most damage in yellow fever
hepatocellular apapotosis and necrotic cells make the councilman bodies
mucosa surfaces have massive hemmorages
jaundice hurts kidney-all scene in severe form
other notable sx: conjunctival injection, bradycardia
dengue endemic countries
asia, africa, South America, US
same for zika
positive torniquette test
dengue
rash on palms and soles
Zika, Ricketsia(both also have conjunctivitis)
The virus replicates in the fibroblasts of the dermis and disseminates through the bloodstream to several tissues.
chikungonia
saddleback fever
chikungonia
along with severe distal joint pain
obligate intracellular
bacteria:
ricketsia, chlamydia
protozoa: leishmania, brucella
(both for the reticuloendothelial system[MAC], toxoplasma
obligate, intracellular bacteria
Small, Gram –ve rod, non-motile, pleomorphic coccobacilli
ricketsia
Gems stain
ricketsia, borellia
target cells of ricketsia…who has similar target
what happens after the target is reached
Infect vascular endothelium (systemic and pulmonary circulation)…similar target is lepto
inc vascular permeability, T cell mediated immunity, INFg, TNFa, cytokines= edema, hypovolemia, vasculitis, digital necrosis
indirect FA (IFA) and enzyme immunoassays (EIA) used for
ricketskia testing and borellial
should follow with confirmatory western blot assay
spirochete
borellia, lepto, trep palledum(syphillus)
adheres to integrins, proteoglycans, glycoproteins on host cells or tissue matrices
disseminated borellia
at first will multiply locally at bite sight and induce inflammation locally
protozoan from snad fly
leishmania
endemic visceral leishmania
india, africa
promastigote injected into skin, pages by macrophages, transform to amastigote which will go infect other cells(which cells?). Vector takes in amastigote and will change back to promastigotes
leishmania
likes to go for the reticuloendothelial system, sleen, liver, and bone marrow
parasitophorous vacuoles
helps leishmania survive intracellularly( blocks phase lysosomal formation in macrophages)
Leishmanolysin fuction
Facilitates complement and NATURAL KILLER CELL inactivation
Prevents antigen cross-presentation to T cells
G –ve, short rods “Coccobacilli”
* Aerobic, facultative, non-spore forming and catalase +ve
* Nutritionally fastidious: will not grow on blood or other common media; requires supplemental compounds (Fe2+, cysteine)
Francisella tularensis
tularemia sx
if via injection there will be an ulcer on the skin.
if via inhalation will present like pneumonia(like tb pneumonia- dry could, pleuritic chest pain)
if ingested-exudative tonsillitis, bloody diarrhea. of typhoidal fever sx
if inoculated into eyes -purulent conjunctivitis, corneal ulceration, lymphadenopathy
intermittent fever, abdonimal enlargement, pancytopenia
leishmania(visceral)
if cutaneous form will present with huge lesion
intermittent fever also seen with brucella