Enteric Viruses 1 + 2

Question 1

reoviruses virology

Answer 1

double protein capsid, segmented genome -> reassortment. fecal oral transmission. most common reovirus is rotovirus

Question 2

rotavirus pathogenesis

Answer 2

dsRNA. infection is self limited. mainly infects small cells of the small intestinal villi. leads to impaired hydrolysis of carbs. Rotavirus nonstructural protein 4 acts like an enterotoxin, messing with Na transport pumps leading to watery diarrhea.

Question 3

rotavirus exam

Answer 3

history of exposure to other kids with diarrhea. N/V. (not very severe vomiting) anorexia. low grade fever. dehydration. watery, bloodless diarrhea. may mask decreased urine output

Question 4

rotavirus lab

Answer 4

labwork is available: latex agglutination, enzyme immunoassay, electron microscopy, culture.

Question 5

rotavirus treatment

Answer 5

no specific treatment, just do oral rehydration. no excessive free water intake. IV access may be required. Pedialyte. No antiemetic or antidiarrheal medications

Question 6

norovirus virology

Answer 6

positive sense ssRNA. norwalk virus is prototypical strain.

Question 7

norwalk virus virology

Answer 7

fecal oral. highly contagious. excretion of virus continues for weeks after recovery. can survive freezing and heating to 140F.

Question 8

norovirus pathogenesis

Answer 8

infection damages microvilli in small intestine -> malabsorption. vomiting caused by change in gastric motility and delayed gastric emptying. short symptoms: 1-2 days. cruise ships vulnerable

Question 9

norovirus exam

Answer 9

low fever, anorexia, severe vomiting (nonbloody, nonbilious), cramps, watery diarrhea

Question 10

norovirus lab

Answer 10

isolated cases do not require lab studies. if international traveler, rule out parasites and/or cholera. in outbreaks, norovirus can be detected in stool by RT-PCR or EM

Question 11

norovirus treatment

Answer 11

outpatient therapy usually fine. rehydration, rest, wash hands. inpatient for severe dehydration. antidiarrheal agents used sparingly in adults

Question 12

primary viremia

Answer 12

successful virus travels in blood to seed replication sites. low levels of virus in the blood

Question 13

secondary viremia

Answer 13

new virus travels from replication sites to shedding sites. higher levels in the blood

Question 14

enterovirus virology

Answer 14

small naked icosahedral virions. ssRNA. fecal-oral. primary replication in gut with viremia, spread to regional lymph nodes, leading to febrile illness and occassional CNS involvement. “Dual tropisms” aka replicating in gut epithelium and lymphoid cells but also uncommonly in CNS neurons

Question 15

poliovirus virology

Answer 15

virus infects only humans. no animal or environmental reservoir. IgA + IgG immunity is protective against reinfection

Question 16

vaccine types for poliovirus

Answer 16

inactivated: virus is dead, vaccine cannot cause polio. used in first world.

Attenuated: virus is weak, infects patient, and contacts with attenuated polio and recovers virulence. used in eradication efforts.

Question 17

poliovirus pathogenesis

Answer 17

begins as fecal-oral infection, using CD155 receptor to enter and infect gut lining cells. CD155 also found on gray matter CNS cells. crosses BBB or uses axonal transport from peripheral nerve to get into brain. causes nerve death through lytic replication and over-reactive immune response

Question 18

poliovirus exam

Answer 18

nonparalytic poliomeyelitis or preparalytic poliomyelitis: headache, fever, sore throat, N/V, muscle aches. progression to CNS involvement is stiff neck/back, irritability

paralytic poliomyelitis: severe muscle pain, spasms, then weakness. asymmetric weakness with lower limbs more commonly affected. numbness, tingling. paralysis for days/weeks before slow partial recovery

Question 19

poliovirus tests

Answer 19

lumbar puncture. virus recovery through cultures. MRI may show inflammation in spinal cord anterior horns

Question 20

poliovirus treatment

Answer 20

no specific treatment exists. supportive care

Question 21

postpolio syndrome

Answer 21

decreased muscle strength, weakness, and atrophy. slow but gradual progressive weakness occurs decades after acute attack. not infectious.

Question 22

herpangina pathogenesis

Answer 22

acute febrile illness. small lesions on the posterior oropharyngeal structures. summer. symptoms occur after replication at secondary sites of infection. Coxsackievirus A usually causes herpangina. Enterovirus 71 can cause herpangina and has severe complications

Question 23

herpangina exam

Answer 23

fever, malaise, sore throat, anorexia, ab pain, cervical lymphadenopathy. oropharyngeal lesions. 2-12 lesions in a typical case. erythematous macules initially, ulcerate in the center

Question 24

herpangina lab

Answer 24

usually not required. culture virus from swabs of nasopharynx. serum antibodies of the coxsackievirus may be measured after the onset of clinical symptoms. RT-PCR

Question 25

herpangina treatment

Answer 25

no specific treatment. supportive therapy

Question 26

hand-foot-and-mouth pathogenesis

Answer 26

fecal oral, or contact with skin lesions and oral secretions. symptoms follow viremia and viral invasion of mucus membranes. apoptosis = characteristic lesion formation. rare meningitis, pneumonitis, and myocarditis. Coxsackie A is usual cause, but also been caused by enterovirus 71

Question 27

H, F, and M disease exam

Answer 27

sore mouth/throat, low fever. vesicular erruption in mouth, hands, feet, butt, genitalia. severe oral ulcerations may interfere with oral intake.

Question 28

HFM disease lab

Answer 28

lab usually unnecessary. virus can be isolated from lesions. oral specimens are the best

Question 29

HFM disease treatment

Answer 29

supportive

Question 30

acute hemorrhagic conjunctivitis pathogenesis

Answer 30

rapid-onset painful conjunctivitis. caused mainly by coxsackie A24 and enterovirus E70.

Question 31

acute hemorrhagic conjunctivitis diagnosis

Answer 31

lab testing impractical. neutralizing assays with standardized antisera have been used. RT-PCR coming

Question 32

acute hemorrhagic conjunctivitis treatment

Answer 32

none available. slef limited. rarely have neurological sequelae (poliolike paralysis.) DONT TREAT WITH TOPICAL STEROIDS

Question 33

viral myocarditis pathogenesis

Answer 33

inflammatory disorder of the myocardium: necrosis of myocytes, inflammatory infiltrate. common instigators are adenoviruses and enteroviruses. pump failure with cardiac enlargement. can lead to pulmonary edema and CHF

Question 34

what is a major causitive agent of viral myocarditis

Answer 34

coxsackie B. has one of its most severe presentations.

Question 35

viral myocarditis exam

Answer 35

in mild forms, no symptoms. severe: acute cardiac decompensation and progress to death. can present with any type of dysrhythmia. heart failure common. chest pain is rare in kids but common in adults. patients may refer to a recent nonspecific flulike illness with GI symptoms

Question 36

viral myocarditis lab

Answer 36

CBC. blood cultures. sed rate and C-reactive protein. markers of inflammation are usually elevated. Creatine Kinase/MB isoenzyme. viral cultures

Question 37

viral myocarditis hisological findings

Answer 37

focal or diffuse interstitial infiltrate of mononuclear cells, lymphocytes, plasma cells, and eosiniphils. necrosis and disarrangement of the myocytes. myocites are replaced by fibroblasts in the chronic and healing stages

Question 38

viral myocarditis treatment

Answer 38

admitted to hospital. rapid progression can occur. needs bedrest. maintain normal blood oxygen levels. controversial use of immunosuppressive agents.

Question 39

pleurodynia pathogenesis

Answer 39

uncommon complication of coxsackie B. sudden occureence of lancing chest pain attacks. fever, malaise, headache. striated muscle is the actual anatomic structure targeted by coxsackie B, and is responsible for severe chest pain

Question 40

pleurodynia exam

Answer 40

headaches, fever, malaise. N/V, diarrhea, and ab pain in kids. herpangina. pleural friction rub.

Question 41

pleurodynia lab

Answer 41

viral cultures. chest X ray can show normal findings. biopsy will show necrosis of striated intercostal muscles

Question 42

pleurodynia treatment

Answer 42

no specific treatment exists. support with NSAIDs and analgesics. only life threatening if the patient is a newborn

Question 43

aseptic meningitis pathogenesis

Answer 43

inflammation of leptomeninges. aseptic means viral. 7-10 days usually. must rule out infection by bacteria or fungi.

Question 44

aseptic meningitis exam

Answer 44

tetrad: fever, meningismus, irritability, photophobia. symptoms may have a biphasic pattern. younger the patient, the less obvious the viral meningitis symptoms will be. take intense history. some signs are specific to certain agents

Question 45

aseptic meningitis treatment (adults/all)

Answer 45

mostly supportive. IV ampicillin and cephalosporin if bacterial meningitis is suspected. acyclovir. seizures treated with IV anticonvulsants

Question 46

aseptic meningitis treatment (pediatric)

Answer 46

can cause septic shock in infants. give antibacterial coverage and acyclovir. watch fluid and electrolyte balance.