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MSII Micro Unit 6 > Enteric Viruses > Flashcards

Enteric Viruses Flashcards

1
Q

What are the enteric viruses?

A
  • reo- orthorecoviruses and rotaviruses
  • birna- Hep E
  • calici- noroviruses
  • picorna- Hep A, poliovirus, echovirus, Coxsackie A and B
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2
Q

What is the virology of reoviruses?

A
  • double protein capsid, segmented dsRNA genome
  • segmented genome -> reassortment
  • environmentally rugged -> fecal-oral transmission
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3
Q

What are the human infecting reoviruses?

A
  • orthoreoviruses (reoviruses for short)- cause mild GI symptoms
  • Rotaviruses: significant gastroenteritis- most common cause of serious communicable diarrheal disease in children
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4
Q

What is the pathogenesis of rotavirus?

A
  • 11 segments of dsRNA in double shelled capsid
  • infected is self limited, but fluid stool losses may be dramatic, risk of death from dehydration
  • most infections during the winter months
  • almost every child 5 years and younger will be infected at some point
  • primarily infects the cells of the small intestinal villi
  • impaired villus function leads to impaired hydrolysis of carbohydrates (malabsorption)
  • rotavirus nonstructural protein 4 (NSP4) acts like an enterotoxin, interfering with sodium transport pumps -> profuse watery diarrhea
  • virus is shed in high titers in stool starting before the onset of symptoms, continuing up to 10 days
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5
Q

What is the incidence of rotavirus?

A

US:

  • 2.7 million illnesses/year
  • 80,000 hospitalizations
  • 100 deaths
  • risk factor: group daycare

International:

  • 352,000-592,000 deaths/yr
  • 6% of all deaths among children <5yrs
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6
Q

Who does rotavirus infect?

A
  • disease primarily affects children 4-24 months
  • adults: a few days of nausea, anorexia, and cramping pain
  • newborn infants: seem more resistant
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7
Q

How does rotavirus present on exam?

A
  • history of exposure to other children with diarrhea
  • vomiting
  • anorexia
  • low grade fever
  • abdominal cramps
  • lethargy
  • dehydration: early physical symptoms in children may be unremarkable to parents
  • watery, bloodless diarrhea; may mask decreased urine output if diapered
  • hyperactive bowel sounds
  • sunken eyes
  • dry or sticky-appearing mucosa
  • rough skin
  • depressed sensorium
  • weight loss
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8
Q

How does rotavirus look on labs?

A

labwork is available:

  • latex agglutination
  • enzyme immunoassay
  • electron microscopy
  • culture
  • but is seldom needed for an individual patient
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9
Q

How do you treat rotavirus?

A
  • in most cases, no specific treatment
  • oral rehydration: no commercial soft drinks, sports drinks, commercial soup, boiled milk, no excessive free water intake
  • identification and treatment of dehydrated infants is most important
  • IV access may be required
  • pedialyte and rice-lyte
  • small, frequent feedings to dodge nausea
  • rotavirus vaccine (RotaShield) was released for general use in 1998-1999, but was discontinued after several cases of intestinal intussusception
  • RotaTeq and Rotarix vaccines are approved for and may help reduce severity of disease
  • no antiemetic or antidiarrheal meds
  • inpatient care is not usually needed
  • reinfection is common
  • health care workers can be vectors
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10
Q

What is the virology of norovirus?

A
  • positive sense single-stranded RNA viruses in the familt Caliciviridae
  • noroviruses cause 20% of all viral gastroenteritis in persons >24 months
  • Norwalk virus is the prototypical strain in the genus
  • Norwalk virus was identified by electron microscopy of stool samples from a 1968 gastroenteritis epidemic in Norwalk, Ohio
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11
Q

What is the virology of Norwalk Virus?

A
  • transmitted via the fecal oral route: personal contact, contaminated food (salad, cake frosting, clams, oysters, meats), contaminated water, particles aerosolized with vomiting
  • highly contagious: only ~100 viral particles required to establish infection
  • excretion of virus continues for weeks after recovery
  • can survive freezing and heating to 140F
  • infection may recurr
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12
Q

What is the pathogenesis of Norovirus?

A
  • infection damages microvilli in small intestine -> malabsorption
  • vomiting caused by change in gastric motility and delayed gastric emptying
  • 24-48 hr incubation
  • symptoms are short lived: 1-2 days -> less dehydration, fewer complications than rota
  • cruise ships are particularly vulnerable- frequent changes in passenger cohort, relative crowding, short cleaning periods at shore
  • also summer camps, nursing homes
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13
Q

How does Norovirus present on exam?

A

-headache, low fever, myalgias, dehydration may cause tachycardia, hypotension, anorexia, vomiting (profuse nonbloody nonbilious), abdominal cramps, watery diarrhea

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14
Q

How does Norovirus look on labs?

A
  • isolated cases do not require laboratory studies
  • if an international traveler, rule out parasites and/or cholera
  • in outbreaks, norovirus can be detected in stool by RT-PCR or electron microscopy
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15
Q

How do you treat Norovirus?

A
  • outpatient therapy is typically sufficient- oral rehydration, rest, handwashing
  • inpatient therapy for severe dehydration- IV hydration, electrolyte monitoring and replacement
  • reportable if 2 or more patients shared a common meal
  • usually self limited to 24-48 hours
  • antidiarrheal agents may be used sparingly in adults
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16
Q

What is the virology of enterovirus?

A
  • small naked icosahedral virions
  • single stranded positive sense RNA genome
  • envrionmentally rugged-> enteric infection by fecal- oral route
  • incubates 1-3 wk, excreted for 5-6 wk
  • primary replication in gut with viremia and spread to regional lymph nodes, leading to febrile illness and occasional CNS involvement
  • enteroviruses may display dual tropisms, replicating commonly in gut epithelium and lymphoid cells but also uncommonly in CNS neurons
  • > 90% of infections at home (asymptomatic or nonspecific febrile)- normal human immune system is well-adapted to handle threats from food
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17
Q

What are the human picornavirus infections?

A
  • Rhinovirus (common cold- only not enterovirus)
  • Polioviruses: polio
  • Coxsackie A: herpangina, hand-foot-and-mouth disease, acute hemorrhagic conjunctivitis
  • Coxsackie B: myocarditis and pleurodynia
  • Numbered Echoviruses: meningitis, pediatric febrile illness
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18
Q

What is the virology of poliovirus?

A
  • WHO Global Polio Eradication Initiative is in progress
  • 3 countries remain endemic: Afghanistan, Nigeria, and Pakistan
  • the last case of wild-type polio in the US was in 1979. Vaccine successful because:
  • virus infects only humans (no animal or environmental reservoir)
  • IgA + IgG immunity is protective against reinfection
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19
Q

What are the polio vaccines?

A
  • Inactivated- Dead, Salk vaccine: virus is dead, vaccine cannot cause polio, must be injected, used in first world
  • Attenuated- (weakened, Sabin vaccine, oral polio): virus is weak, vaccine infects patient and contacts with attenuated polio and (rarely) recovers virulence. Can be taken orally. Used in eradication efforts. Passive immunization also available
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20
Q

What is the pathogenesis of poliovirus?

A
  • begins as a fecal-oral enteric infection, using CD155 receptor to enter and infect epithelial/lmphoid cells in gut lining, then spreads to bloodstream and regional lymph nodes
  • problem: CD155 also found on gray matter CNS cells
  • enters CNS either by crossing the BBB (bloodstream) or by axonal transportation from a peripheral nerve (retrograde)
  • nerve death results both from lytic virus replication and overenthusiastic immune response
  • infection of the anterior horn motor neurons of the spinal cord (muscle symptoms) and brain stem (respiratory symptoms)
  • flaccid asymmetric weakness and muscle atrophy due to loss of motor neurons and denervation of their associated skeletal muscles
  • of acute poliovirus infections, 1-2% result in neurologic symptoms
  • the mortality from acute paralytic poliomyelitis is 5-10%; 20-60% if bulbar involvment
  • spread from person to person
  • greatest dissemination within families with poor sanitation or crowded circumstances
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21
Q

How does Nonparalytic Polio look like on Exam?

A
  • nonparalytic poliomyelitis or preparalytic poliomyelitis- generalized nonthrobbing headache, fever 38-40C, sore throat, anorexia, nausea, vomiting, muscle aches, symptoms may or may not subside in 1-2 weeks, non-specific symptoms- always check vaccination history
  • progression to CNS involvement: headache and fever, irritability, restlessness, apprehensiveness, emotional instability, stiffness of the neck and back
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22
Q

What does Paralytic poliomyelitis look like on exam?

A
  • risk factors: young age, advanced age, recent hard exercise ,tonsillectomy, pregnancy, immunosuppression
  • severe muscle pain, spasms, then weakness
  • weakness is asymmetric with lower lumns affected more than upper limbs
  • reflexes initially are brisk but then become absent
  • patients complain of paresthesias: numbness, tingling in the affected limbs without real sensation loss
  • paralysis remains for days or weeks before slow partial recovery over months or years
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23
Q

What are the tests for polio?

A
  • Lumbar puncture: fluid pressure (increased), pleocytosis, elevated protein, virus culture
  • virus recovery- throat washing, stool culture, blood culture, CSF
  • PCR differentiates wild type from vaccine strains
  • MRI may show localization of inflammation to the spinal cord anterior horns
  • electromyography will give characteristic findings
  • histology: spongiosis and inflammation of the grey matter
24
Q

What is the treatment of polio?

A
  • no specific treatment exists
  • supportive care required for survival and reduces disability
  • all patients should be placed on bedrest and monitoring in an isolation unit
  • patients who develop respiratory failure require immediate positive pressure ventilation
  • physical therapy plays an important role in rehabilitation
25
Q

What is the postpolio syndrome?

A
  • new history of decreased muscle strength, weakness, and atrophy
  • slow but gradual progressive weakness occurs decades after the acute attack
  • patients also report fatigue, muscle and joint pain and intolerance to cold
  • PPS is not infectious; it is increasing dysfunction in surviving motor neurons
  • overall prognosis is good with slow progression of weakness
  • lots of rest required
26
Q

What are the pathologies caused by Coxsackie A?

A

-Herpangina, Hand-Foot-And-Mouth Disease, Acute Hemorrhagic Conjunctivitis

27
Q

What is the pathogenesis of Herpangina?

A
  • acute febrile illness
  • small vesicular or ulcerative lesions on the posterior oropharyngeal structures
  • typically occurs during the summer
  • frequently in children, also young adults
  • incubation period 7-14 days
  • typically is a mild and self limited illness
  • complications rarely occur
  • clinical symptoms occur after viral replication at secondary sites of infection
  • Coxsackievirus A usually causes herpangina; less commonly, coxsackie B or other enteroviruses
  • enterovirus 71, can cause herpangina and has been associated with severe complications. Fatalities, mostly in infants aged 6-11 months, have been reported
28
Q

What does Herpangina look like on exam?

A
  • fever
  • malaise
  • sore throat
  • anorexia
  • abdominal pain
  • bilateral, anterior, cervical lymphadenopathy
  • infants may appear listless
  • oropharyngeal lesions: erythematous macules initially, vesicles ulcerate centrally, creating an erythematous halo, typically <5 mm, 2-12 lesions in a typical case, may persist for up to one week
29
Q

What does Herpangina look like on lab?

A
  • labwork not usually required
  • if labwork is indicated:
  • culture virus from swabs of the nasopharynx
  • serum antibodies of the Coxsackievirus may be measured after the onset of clinical symptoms
  • RT-PCR can be performed for enterovirus RNA of the throat, blood, CSF, urine, feces, and tissue specimens
30
Q

How do you treat Herpangina?

A
  • no specific therapy is indicated, no effective antiviral therapy exists
  • supportive treatment: hydration, antipyretics (eg acetaminophen, ibuprofen), topical analgesics (eg, topical lidocaine)
31
Q

What is the pathogenesis of Hand-Foot-And-Mouth Disease?

A
  • spread by fecal-oral route or contact with skin lesions and oral secretions
  • symptoms follow viremia and viral invasion of mucus membranes
  • widespread apoptosis likely results in the characteristic lesion formation
  • rarely, aspetic meningitis or myocarditis, interstitial pneumonitis, and pulmonary edema may occur
  • Coxsackie virus A is the usual cause, Enterovirus 71 has also caused outbreaks of HFMD with associated neurologic involvement in the western Pacific region
32
Q

How does Hand-Foot-And-Mouth Disease look like on exam?

A
  • incubation ~1 week, then sore mouth or throat, low fever
  • vesicular eruption in the mouth, hands, feet, buttocks, and/or genitalia
  • generally a mild self limited illness that resolves in 7-10 days
  • children younger than 10 years are most commonly affected
  • subsequent outbreaks among family members and close contacts
  • severe oral ulcerations may interfere with oral intake: dehydration is the most common complication
33
Q

How does Hand-Foot-And-Mouth Disease look like in labs?

A
  • laboratory studies are usually unnecessary
  • the virus can be isolated from cutaneous lesions, mucosal lesions, or stool samples. Oral specimens have the highest isolation rate
  • serologic testing (eg, acute and convalescent antibody levels) may be obtained
34
Q

What is the treatment of Hand-Foot-And-Mouth Disease?

A
  • treatment is supportive
  • ensure adequate fluid intake
  • IV hydration may be necessary if the patient has moderate-to-severe dehydration
  • fever may be treated with antipyretics
  • pain may be treated with standard doses of acetaminophen or ibuprofen
  • direct analgesia may also be applied to the oral cavity via mouthwashes or sprays
35
Q

What is the pathogenesis of Acute Hemorrhagic Conjunctivitis?

A
  • rapid-onset painful conjunctivitis
  • caused primarily by Coxsackie group A24 and enterovirus E70
  • reported most often in the southwestern US; more common in developing world
  • epidemic hemorrhagic conjunctivitis is prevalent in all age groups, highest prevalence in early teenaged years
36
Q

How is Acute Hemorrhagic Conjunctivitis Diagnosed?

A
  • laboratory testing impractical: rapid course, benign outcome
  • neutralizing assays with standardized antisera have been used
  • RT-PCR methods, which reduce the time needed for viral typing are coming up
37
Q

What is the treatment of Acute Hemorrhagic Conjunctivitis?

A
  • no treatment is available
  • usually self-limited
  • rarely, neurological sequelae: a poliolike paralysis has been reported in 1 case per 10,000
  • provide symptomatic treatment, while waiting for the disease to run its 5- to 7- day course
  • treatment with topical steroids should be avoided: risk of microbial superinfection of the cornea
38
Q

What does Coxsackie B cause?

A

-viral myocarditis

39
Q

What is the pathogenesis of viral myocarditis?

A
  • incidence of cardiovascular involvement after enteroviral infection is 1-4%
  • inflammatory disorder of the myocardium: necrosis of the myocytes, inflammatory infiltrate
  • incidence varies among countries: hygiene, socioeconomic conditions, medical services, immunizations
  • most common instigators: adenoviruses, enteroviruses
  • myocarditis-> pump failure, with cardiac enlargement
  • inflammation, muscle damage, lead to pulmonary edema and CHF
  • without treatment, may progress to end stage cardiac failure and death
  • infants and pregnant/immunocompromised patients are at higher risk
40
Q

What does viral myocarditis look like on exam?

A
  • in mild forms, there are few or no symptoms
  • in severe cases, patients may present with acute cardiac decompensation and progress to death despite supportive care
  • neonates and young children have higher mortality rates than older patients
  • patients can present with any type of dysrhythmia, heart failure is the most common presenting picture in all ages
  • chest pain: rare in young children, may be the initial presentation for older children, adolescents and adults. Chest pain may be due to myocardial ischemia or concurrent pericarditis
  • parents may refer to a recent, nonspecific, flulike illness, GI symptoms
  • initial symptoms in infants: irritability, lethargy, periodic episodes of pallor, fever, hypothermia, tachypnea (hyperventilation), anorexia, failure to thrive
  • older children also report lack of energy, general malaise
41
Q

What does Viral Myocarditis look like on labs?

A
  • complete blood count with differential- acute anemia (needs transfusion), lymphocytosis or neutropenia supports diagnosis of a viral infection
  • blood cultures: ruling out bacterial infection
  • sedimentation rate and C reactive protein: nonspecific markers of inflammation usually are elevated
  • creatinine kinase-MB isoenzyme (CK-MB) and troponin I: markers of myocardial damage may be elevated
  • viral cultures: nasopharyngeal and rectal swabs may help identify etiology
42
Q

What are the diagnostic tests for viral myocarditis?

A
  • Echocardiography: most cost-effective test used for evaluation of myocardial function, sensitive to heart dysfunction but not specific for viral myocarditis
  • chest radiography for cardiomegaly and pulmonary edema
  • radionuclide imaging and electrocardiography (ECG) will also yield characteristic results
  • endomyocardial biopsy- establishes diagnosis and classifies disease stage, relatively safe and effective in adults and older children, risk of perforation in very sick and infants, can prescreen using radionuclide imaging techniques before considering biopsy
  • in situ hybridization
  • PCR
43
Q

What are the histologic findings of viral myocarditis?

A
  • focal or diffuse interstitial infiltrate of mononuclear cells, lymphocytes, plasma cells, and eosinophils
  • necrosis and disarrangement of the myocytes
  • in the chronic and healing stages, myocytes are replaced by fibroblasts
44
Q

What is the treatment of viral myocarditis?

A
  • patient should be admitted to the hospital even if only mild signs of respiratory distress of congestive heart failure. Rapid progression may occur
  • maintain normal blood oxygen levels with supplemental oxygen as needed
  • bed rest is necessary during the acute phase and may slow the replication of the virus
  • the use of immunosuppressive agents is controversial
  • IV gamma globulin may be important in the treatment of acute myocarditis. It has been associated with improved left ventricular function and improved survival
  • Pleconaril is being tested in children with myocarditis
45
Q

What is the pathogenesis of pleurodynia?

A
  • pleurodynia (Devil’s Grip) is an uncommon complication of infection by coxsackievirus B or a few others- sudden occurrence of lancinating chest pain attacks, fever, malaise, headache
  • the striated muscle is the actual anatomic structure targeted by the coxsackievirus B and is responsible for the attacks of severe chest pain
  • pleurodynia and its sequale can be very serious
  • Coxsackie B, like other enteroviruses is transmitted by fecal-oral route- Handwashing!
46
Q

What is pleurodynia?

A
  • onset of chest pain is acute; during attacks, the pain is severe, intense, and excruciating, lasting seconds to a minute
  • pain is paroxysmal, occuring in attacks separated by minutes to hours
  • severe attacks can results in difficulty breathing
  • between attacks, patients usually have a constant, dull, pleuritic chest pain
  • the attacks usually persist for 3-5 days
47
Q

How does pleurodynia look on exam?

A
  • sore throat, rhinitis, and dry cough
  • headaches, fever, and malaise
  • nausea, vomiting, diarrhea, and in children, abdominal pain
  • fever and appropriate heart rate response (ie tachycardia)
  • pharyngitis, including herpangina
  • visible splinting of the chest during attacks
  • localized chest wall tenderness in the same area of pain
  • pleural friction rub
48
Q

How does pleurodynia look on lab?

A
  • viral cultures: usually from throat; alternatively blood or stool
  • fluorescent staining and neutralization assays: delineate the type of enteroviruses isolated from culture
  • RT-PCR for detect of viral RNA from specimens with a low viral load, including CSF, serum creatine kinase is usually elevated because of muscle necrosis
  • a chest radiography is usually obtained to exclude other causes of chest pain. In pleurodynia, the findings on chest radiography can be normal
  • if a biopsy is performed, nerosis of the striated intercostal muscles is visible on histology
49
Q

What is the treatment of pleurodynia?

A
  • no specific treatment exists
  • support with NSAIDs and analgesics
  • aspirin should be avoided in children (Reye syndrome)
  • patients must receive follow up care with their primary care providers to ensure that other potential coxsackievirus B-associated complications are diagnosed and managed in a timely manner
  • viral pleurodynia has been suggested as a trigger for immune-mediated sequale including: myocarditis, dermato-polymyositis, chronic fatigue syndrome, juvenile-onset diabetes type I
50
Q

What is the severity of a Coxsackie B infection in neonates?

A
  • the severity of Coxsackie B infection is highest in infants and young children
  • of infants who develop, 10% die usually within the first 4 weeks of life and most commonly from cardiac involvement
  • symptoms of cardiac failure different from adults
  • increased risk of cardiac perforation on biopsy
  • fulminant hepatic failure, sepsis syndrome, and meningoencephalitis are potential complications in this age group
  • presenting symptoms include poor fededing, lethargy, fever, irritability, hypoperfusion, and jaundice
  • history: recent maternal febrile illness?
51
Q

What is the pathogenesis of aseptic meningitis?

A
  • inflammation of the leptomeninges
  • aseptic means viral, NOT bacterial
  • viral meningitis is usually self-limited: complete recovery in 7-10 days
  • must rule out infection by bacteria or fungi: untreated outcomes are very bad
  • 85% of cases in developed world caused by enteroviruses
  • 10,000 cases of viral meningitis reported annually
  • after neonatal period, mortality less than 1%
  • long term effects possible (not proven): learning disabilities, neuromuscular impairments, deafness, altered language development
52
Q

What does aseptic meningitis look like on exam?

A
  • the classic tetrad in adults: fever, meningismus, irritability, photophobia
  • most adult patients report fever, headache, irritability, nausea, vomiting, stiff neck, rash, or weakness within the past 18-36 hours
  • symptoms may have a biphasic pattern: nonspecific flu-like symptoms and low grade fever ~48 hrs ago, fever returns with onset of neck stiffness and headache
  • rule out drug overdoses/interactions and CT disorders such as SLE
53
Q

How can you differentiate between different aseptic meningitis causes?

A
  • pharyngitis, pleurodynia, and gastroenteritis in enteroviral infections
  • Zosteriform eruption in VZV reactivation
  • maculopapular rash in measles and enteroviral infections
  • vesicular eruption in herpes simplex infections
  • herpangina in coxsackievirus A infections
  • herpangina in coxsackie A infections
  • pharyngitis, lymphadenopathy, and splenomegaly in EBV
  • immunodefiency and penumonia suggest adenovirus, CMV or HIV
  • parotitis and orchitis- mumps
54
Q

What are the tests for aseptic meningitis?

A
  • CSF- culture, gram stain and acid fast stain
  • PCR and RT-PCR testing for viral pathogen
  • CT scan and MRI rule out other intracranial pathogies (injury, encephalitis)
  • blood, feces, and throat swabs may be sent for viral serology and cultures
  • serum titers of antibodies against HIV and toxoplasma
  • EEG diagnoses encephalitis or atypical seizure disorders
55
Q

How do you treat aseptic meningitis?

A
  • treatment for viral meningitis is mostly supportive: rest, hydration, antipyretics, pain and anti-inflammatory medications
  • IV ampicillin and cephalosporin should be administered immediately if bacterial meningitis is suspected
  • patients with signs and symptoms of meningoencephalitis should receive empirin acyclovir early to curtail HSV encephalitis
  • seizures should be treated immediately with IV anticonvulsants
  • pleconaril is currently undergoing phase III trials for enteroviral meningitis
56
Q

How do you treat peds for asepti meningitis?

A
  • enteroviruses and HSV can cause septic shock in infants
  • initiate both broad-spectrum antibacterial coverage and acyclovir immediately
  • watch fluid and electrolyte balance
  • prognosis is usually excellent; majority of cases resolve 7-10 days
  • disease does not self-limit during the neonatal period, when viral meningitis can be fatal or associated with significant morbidity
  • ospithotonic positioning

MSII Micro Unit 6 (8 decks)

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