Flashcards in Micro Enteric Viruses 1 Deck (28):
double layered naked icosahedral capsid, segmented RNA genome (allows for reassortment) double stranded; environmentally rugged
fecal-oral, mostly peds (contaminated toys). attach, replicate in cell, epithelial cells die and fluids exit body as self limiting diarrhea with risk of dehydration
how does rotavirus attach to epithelial cell lining?
what does rotavirus primarily infect? what does this cause?
cells of the small intestinal villi - impaired villus function leads to impaired hydrolysis of carbs (malabsorption)
what causes the profuse watery diarrhea associated with rotavirus?
rotavirus nonstructural protein 4 (NSP4) that acts like an enterotoxin interfering with sodium transport pumps
who does rotavirus infect?
children 4-24 months. adults have a few days of nausea, anorexia, and cramping pain - newborn infants seem more resistant
exam for rotavirus
history of exposure; bloodless diarrhea young children with vomiting, anorexia, low fever, cramps, dehydration
most cases - no treatment. oral rehydration (pedialyte and rice-lyte)
-RotaTeq and Rotarix vaccines help reduce severity
-NO antiemetic or antidiarrheal
+ ssRNA, naked icosahedral capside, environmentall rugged, extremely contagious, low ID
norovirus clinical disease - symptoms and patients
gastroenteritis - older age cohort than rotavirus, fecal-oral (contaminated food), more vomiting
-infection damages microvilli in small intesting (malabsorption)
-vomiting caused by change in gastric motility and delayed gastric emptying
-typically lasts 24-48 hr
what are the implications of a short course with norovirus?
less dehydration (that combined with the older population of patients as compared to rotavirus)
profuse, non bloody vomiting; nausea, cramps, headache, low fever (mostly stay in gut), muscle aches, chance of dehydration
rest, rehydration, antidiarrheas in adults
what are the picornaviruses that cause enteric disease?
poliovirus, coxsackievirus, hepA
+ ssRNA genome; environmentally rugged
-includes both rhinoviruses (resp) and enteroviruses (polio, coxsackie, hepA)
primary replication in gut with viremia and spread to regional lymph nodes leading to febrile illness and occasional CNS involvement
-may have DUAL TROPISMS replicating in both epithelium and lymphoid cells
what are the two poliovirus vaccines?
inactivated: must be injected, used in first world where already irradicated
attenuated: weakened, taken orally, used in eradication effeorts
fecal-oral enteric infection using CD155 receptor to enter - infects epithelial/lymphoid cells in gut
CD155 and polio
how polio enters cells - present on both epithelial/lymph cells in gut AND on gray matter CNS cells
where does polio MC infect the CNS?
anterior horn motor neurons of spinal cord (muscle symptoms) and brain stem (respiratory symptoms)
signs of CNS involvement with polio
flaccid asymmetric weakness and muscle atrophy due to loss of motor neurons and denervation of associated skeletal muscle
risk factors for CNS progression with polio
young age, advanced age, recent hard exercise, tonsillectomy, pregnancy, immunosuppression
poliovirus diagnosis on exam:
nonparalytic poliomyelitis or -preparalytic: generalized nonthrobbing headache, fever, sore throat, anorexia, n/v, muscle aches - symptoms subside in 1-2 weeks
-progression to CNS involvement: headache and fever, irritability, restlessness, apprehensiveness, emotional instability, stiffness of neck and back
polio diagnosis: tests
lumbar puncture: fluid pressure increased, pleocytosis, elevated protein, virus culture
MRI: anterior horn inflammation
no specific treatment exisits - supportive care
-positive pressure ventilation for those with respiratory failure
-new history of decreased muscle strength, weakness, and atrophy
-decades after polio
-fatigue, muscle and joint pain, cold intolerance
-NOT infectious: increasing dysfunction of surviving neurons