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Session 2 Microbio19
Microbio -19- GI #3 Infection Hartley
| Question | Answer |
|---|---|
| What are the GI virus classified as | enteric virus trasmitted via fecal oral route |
| What are some of the enteric virus | Picornaviruses -poliovirus -coxsackievirus -echovirus -enterovirus -Hep A virus Rotavirus Norwalk agent related caliciviruses adenoviruses astroviruses |
| What are the followin Poliovirus 3 Coxsackievirus groups A and B 23/6 Echovirus 28 Human Enterovirus (68-71) 4 Hepatitis A Virus ~1 | picornaviruses that cause enteric infection with the number of serotypes that cause GI infection |
| What does a single round of viral replication of picorna virus consist of | attachment and entry tranlastion of polyprotein replication and shut down of host protein synthesis Cell Death and exit release of many new virions All takes about 6-8 hours |
| what is the source of infection with enteric picorna viruses | fecal/oral route |
| What is the progression of non-HAV picornaviruses | -transmission via fecal/oral route -infects intestinal epithelia and remains through disease progression -virus spreads to submucosal lymphoid tissues of the peyer's patches (or tonsils) and regional lymph nodes -Then spreads to reticuloendothelial sys |
| What is the reticuloendothelial system | a network of phagocytic cells residing in the spleen, liver, and bone marrow where they free the blood or lymph of foreign particles |
| What percent of NON-poliovirus and poliovirus infection are subclinical | 50% of non-polio enteric 90% of polio virus enteric infections are subclinical |
| When do you generally see symptomatic disease onset with enteric picorna virus infection | on second viremia and tissue spread |
| What are the three disease states of polio | abortive aseptic meningitis Paralytic Polio |
| What is abotive polio | nonspecific febrile illness that resolves in 2-3 days without CNS involvement |
| What is aseptic meningitis caused by polio | you get signs on meningeal involvement- stiff neck, pain, and stiffness in the back Rapid and Complete recovery in a few days |
| What are s/sx of paralytic polio virus | Starts as minor illness followed by meningeal irritaion then asymmetric flaccid paralysis with no sensory loss. All four limbs and respiratory muscles may become paralyzed and it may take 6 months to recover |
| How does severity of s/sx of polio virus tie in with age at infection | severity of s/sx increases with age at time of infection |
| how long after infection can you find polio virus in the stool | two months you can find polio in stool from beginning |
| What branch of immune response aids in immunity to polio and other picorna viruses | humoral response- patients with deficient cell mediated immunity have exacerbation of disease |
| What type of vaccines exists for polio which type is used in the US | both inactivated (IPV) and live attenuated (OV) IPV is used in the US |
| Do we have vaccines for the other picorna viruses other than polio | No vaccines for other serotypes of picorna |
| What is the tx for picorna virus infections | most are mild cases and resolve on their own Ig can be given in severe cases or immune deficient patients Supportive care for cardiac or CNS patients (polio virus paralytic patients) |
| What does a single round of viral replication of rotavirus consist of | Attachment and entry, release of outer shell Release of + RNA strands for translation New Capsid assembly and genome packaging Replication to make dsRNA budding into the ER and acquistion of outer layer to become infectious All this in less than 7 |
| what is the source of infection with rotavirus | fecal/oral route of infection from lack of sanitary practices |
| What is the progression of infection with rotavirus | 24-48 incubation period initial infection is of the mature villis tip cells of small intestines -Tip cell death leads to cell replacement by cells that cannot absorb nutrients leading to osmotic diarrhea |
| What are the s/sx of rotavirus infections | vomiting (1st symptom) abdominal cramps Watery diarrhea last 2-8 days |
| What infection typically accompanies rotavirus infections | respiratory tract infection |
| Why do you need to complete vaccination to rotavirus by 32 months of age | has potentially fatal complications in older age groups |
| what are the receptor targets for antibodies produced by humoral immunity that clear rotavirus from the body | VP4 and VP7 are the protiens of the viruses outer shell that are targeted |
| What is the tx for rotavirus infections | Treat with oral fluids most don't require IV rehydration |
| When can you detect rotavirus in the stool | only during active infection is shed in large amounts in the stool |
| what type of virus are Norwalk agent and Noroviruses | Calicivirus |
| what are the three serologically distinct types of norovirus | Norwalk Agent Snow Mountain Agent Hawaii Agent |
| What is the source of infection with norovirus | fecal/oral route |
| What types of outbreaks has noroviruses been associated with | Foodborne outbreaks Waterborne outbreaks Also associated with uncooked shellfish and some other seafoods which have had no known contamination with human fecal matter |
| why do you get osmotic diarrhea with norovirus infections | malabsorption of carbs and fats leads to diarrhea |
| What may be the cause of nausea associated with norovirus | gastric motor function gets delayed |
| HOw long does norovirus infection typically last | last 12-60 hours but effects last about 48 hours |
| What are s/sx of norovirus infeciton | NAUSEA vomiting (more common in kids) cramps watery diarrhea also may see headache fever chills and myalgias |
| which typically has more severe symptoms rotavirus or norovirus | norovirus |
| do you get lasting immunity to norovirus infections after you get them | no, but you get immunity from same strain for 2-3 months |
| What link is there between individuals and infectivity of norovirus | Link between ABO and Lewis blood groups and infectivity of virus |
| What is the tx for norovirus | no tx necessary disease is so short term, self limiting, and is not severe |
| How can you tell picornavirus infections from others | s/sx other than or in addition to vomiting and diarrhea like rashes, lesions, photophobia, tachycardia |
| Who typically is infected by rotavirus | children under 2 y/o and in temperate climates they occur in winter months |
| In what age group are calicivirus infections more common | Older Children and Adults |
| what can be a cause of traveler's diarrhea but not as common as e. coli | rotavirus |
| What type of diarrhea do picrona, rota, and calici viruses cause | cause watery diarrhea with little or no blood |
| how can you differentiate between protozoan outbreaks of diarrhea and caliciviruses | caliciviruses induce a short term diarrhea most protozoan outbreaks last longer |
| What causes jaundice | increase in serum bilirubin levels |
| how do viruses typically cause liver damage | generally cause liver damage through immune inflammation not direct cytopathic damage to hepatocytes |
| What is the prodrome phase of acute viral hep. | Fever, Vomiting, General Malaise, diarrhea, fatigue |
| What are the s/sx of classic hepatitis | jaundice and pruritis |
| What is fulminant hepatitis | classic hep w/ worsening jaundice signs of hepatic encephalopathy decreasing liver function fasting hypoglycemia easy bruising or bleeding |
| What should all patients with acute hepatitis be tested for | tested for clotting function |
| how is HAV spread | fecal/oral route or eating raw shellfish grown in contaminated waters |
| What is the progression of infection with HAV infections | 1- ingestion of contaminated food or water 2- viurs gets to liver 3- infection of liver 4- tissue inflammation and damage 5- excretion of virions with bile into the stool 6- viral clearance |
| What are some additional s/sx of HAV infections | most are asymptomatic 70% of kids 30% of adults Prodrome phase for 1 week -Diarrhea most common in kids Classic Hep A 80% of cases -dark urine, Clay colored stools tender hepatomegaly cervical lymphadenopathy |
| What is relapsing HAV | 2 or more cases of classic hep A within 6-10 weeks |
| What is cholestatic Hep A | 10% of cases classic Hep A with prolonged pruritis and persistant jaundice over several months |
| How common is Fulminant Hep A | .35% of symp cases |
| Hep E is similar to Hep A but what is one very important difference | Hep E can be fatal in pregnant women |
| Is there a vaccine for Hep E | yes advised for healthcare workers, some travelers, and food handlers provides life-long immunity |
| what tx can be done within two weeks of exposure to Hep E | passive immunization |
| What tx would you give to someone with Hep E symptoms | prohibit alcohol consumption |
| What type of virus is HEP B | HBC is ds DNA virus with gapped circle genome uses reverse transcription |
| what does the S gene code for in HBV | codes for the "major" envelope protein HBsAg |
| What does the C gene code for in HBV | C gene codes for two nucleocapsid proteins HBeAg and HBcAg |
| What does the X gene code for in HBV and what other problem may it cause | codes for HBxAg may contribute to carcinogenesis by binding to p53 |
| What body fluids contain HBV and can be source of infection | Blood, Saliva, semen, breast milk infact almost all body fluids most can be a source of infection |
| what is the progression of infection with HBV | 1- initial infection 2- viral replication in liver 3- immune inflammation and liver damage 4- clearance or progression to chronic infection |
| What is the prodrome associated with HBV | upper abdominal discomfort |
| What is cholestasis associated with HBV present as | infrequently jaundice may progress to pale stools and dark urine |
| What is chronic HEP B present as | may be asymptomatic until late stage when complications present may present as prolonged classic hep |
| What problem of HEP B is associated with transient rasshes, arthritis in small joints and glomerulonephritis | serum-sickness like disease that may occur in HEP B infections |
| what is the major complication associated w/ HBV | cirrhosis or progressive liver failure hepatic encephalopathy, reversal of sleep wake cycles, Hepatomegaly, splenomegaly all can lead to hepatocellular carcinoma |
| WHat significance can a mutation in C gene of HBV mean | HBeAG may not be synthesized or may be downregulated making infection harder to dx and more difficult to treat |
| which of the hepatitis viruses is a satellite virus | HDV- it is an incomplete virus and requires another virus for help |
| What virus does HDV often piggyback on | only occurs in HBV infected patients it need the HBV envelope protein |
| what are the two forms of infection with HDV | Coinfection and superinfection with HBV |
| which form of HDV infection presents as more severe acute hepatitis, poorer prognosis and rarely becomes chronic | Coinfection of HBV and HDV |
| Which form of HDV infection is more liekly to become chronic, may convert to asymptomatic state to a severe acute infection, High risk of HBV associated complications | Superinfection of HDV |
| IS there any vaccine for HDV | yes vaccine against surface antigen HBsAg |
| what is the tx for HDV | most acute cases are self limiting anitvirals, interferon Alpha and other drugs can be given if needed |
| Which hepatitis virus is a flaviviurs and is +ssRNA enveloped | HCV or HGV |
| what is the most common source of HCV infection and what are the rare sources | IV drug use Blood tranfussion before 1990 rare long term hemodialysis needle stick injury sexual contact perinatal transmission |
| What is meant by HCV chronic infections are periodic in nature | you have periods of massive inflammation followed by periods of almost normal liver size |
| what cells does HCV infect | will infect hepatocytes |
| When are most HCV infections diagnosed | most are dx when chronic problems manifest |
| What is acute HCV marked by | few or no symptoms very few manifest classic acute hepatitis around 20% of HCV is acute |
| What is chronic HCV marked by | still often asymptomatic prodrome after liver damage/cirrhoisis has occured Rare Rheumatic symptoms Rare Mucocutaneous symptoms |
| is there a vaccine for HCV | no HCV mutates rapidly hindering adaptive immune response |
| what is the tx for HCV | interferon alpha to promote sustained anti-viral response |
| What is the source of HGV infection | IV drug usem blood transfusion |
| Has HGV been proven to cause hepatitis | NO but it is found in 10-20% of patients w/o A-E hepatitis |
Created by:
smaxsmith
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