Infectious diseases Flashcards

1
Q
  1. The clinical diagnosis of infective endocarditis (IE) can be made with 2 major criteria, 1 major criterion and 3 minor criteria, or 5 minor criteria. Which of the following is not a minor criteria for the diagnosis of IE?

A. History of injection drug use
B. Temperature >38C
C. Vegetation on transthoracic echocardiography (TTE)
D. Vascular phenomena
E. Immunological phenomena

A

C.
Major criteria include both blood cultures positive for infectious endocarditis and imaging positive for endocarditis. The specific blood culture criteria depend on the organisms and timing of the blood cultures. Imaging studies positive for IE include echocardiogram (either TTE or transesophageal echocardiography) with vegetation; abscess, pseudoaneuryms, or intracardiac fistula; Valvular perforation or aneurysm; and new partial dehiscence of prosthetic valve. Answer C is the correct answer because it is a major and not a minor criteria for the diagnosis of IE. The five minor criteria for the diagnosis of IE include predisposition to IE such as a predisposing heart condition or injection drug use (A); fever (B); vascular phenomena such as arterial emboli, septic pulmonary infarcts, infectious (mycotic) aneurysms, intracranial hemorrhage, conjunctival hemorrhages, and Janeway’s lesions (C); immunologic phenomena such as glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor (E); and microbiological evidence not meeting major criteria such as a positive blood culture not meeting major criteria or serological evidence of active infection with an organism consistent with IE.

(1) Habib et al. 2015 ESC Guidelines for the management of infective endocarditis: The Task Force of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur Heart J. 2015 Nov 21;36(44):3075-128.
(2) Li JS, Sexton DJ, Mick N, Nettles R, Fowler VG Jr, Ryan T, Bashore T, Corey GR. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis.Clin Infect Dis 2000;30:633–638.

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2
Q

A 32 year old G5P3013 with a history of IV drug use presents at 32 weeks with a fever and a new murmur and is diagnosed with endocarditis. Which of the following complications is most likely?

A. Stroke
B. Pulmonary embolism
C. Glomerulonephritis
D. Septic arthritis
E. Mycotic aneurysm

A

B.
Cardiac complications are the most common complications of infectious endocarditis, other septic complications do exist. IV drug users are at an increased risk of right-sided lesions including tricuspid valve endocarditis which predisposes patients to pulmonary complications such as septic pulmonary emboli, pneumonia, or lung abscess. Other septic complications of endocarditis include neurologic complications such as cerebrovascular accidents that can present as embolic strokes, cerebral hemorrhage, seizures, or meningitis. Renal complications can include glomerulonephritis due to immunoglobulin and complement deposition as well as infectious complications such as renal infarction or abscess. Mycotic aneurysms can occur in any vessel and lead to downstream sequelae in that organ system. Complications such as neurologic and renal complications as well as septic arthritis are more common with left-sided lesions.

Baddour LM, Wilson WR, Bayer AS, et al. Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Health Professionals from the American Heart Association. Circulation 2015; 132:1435.

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3
Q

Which of the following is correct regarding CMV IgM titers in pregnancy?
A. CMV specific IgM titers may not always present during an acute infection
B. CMV specific IgM titers are always present during reactivation (of a prior infection) or reinfection (with a new serotype)
C. CMV specific IgM titers do not always indicated the presence of acute primary infection
D. CMV specific IgM titers are only present with acute CMV infection

A

C.
In some pregnant women, CMV IgM may be present due to an infection in the past; only 10-30% of women with CMV-specific IgM will have a primary infection. Evaluation of a pregnant woman suspected of having a primary CMV infection should include initial testing for both CMV IgG and IgM antibodies. If the CMV IgG antibody result is negative, testing should be repeated in two to four weeks regardless of the initial IgM result. If the IgG is still negative, most likely the detection of CMV IgM antibody in the absence of IgG antibody is due to a false-positive IgM antibody test result.

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4
Q

A 22 year old G2P1 presents for her second trimester anatomy scan. The study reveals bilateral periventricular hyperechogenicities (calcifications). Her history is significant for flu symptoms several months ago. Part of the workup was obtaining CMV titers and she is CMV IgG positive. When reviewing her chart you noted that her IgG was negative 6 months ago. What is your diagnosis?
A. Cannot know diagnosis; will need CMV IgM avidity
B. Cannot know diagnosis; will need IgG avidity
C. Secondary CMV infection
D. Primary CMV infection
E. Not a CMV infection

A

D.
Primary maternal infection is diagnosed by seroconversion through the detection of CMV IgG antibodies in a woman who was previously IgG negative (seronegative). If seroconversion is absent or unknown, positive anti-CMV IgG and anti-CMV IgMcan either be a primary or secondary infection. In these cases Cytomegalovirus IgG avidity testing may be useful: A low avidity anti-CMV IgG represents an acute primary CMV infection. After 2-4 months, more mature, high avidity anti-CMV IgG is produced. High avidity usually means infection occurred more than six months ago. In other words, if a patient is less than 20 weeks with high avidity, primary infection is less likely and unlikely to be a cause of neonatal findings in the ultrasound.

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5
Q

A 19 year old G3P2 presents for her second-trimester anatomy scan. The study reveals fetal growth restriction, microcephaly, ventriculomegaly, echogenic foci in liver, and limb anomalies. What test will you order to confirm your diagnosis of maternal varicella zoster virus (VZV)?
A. Maternal vzv blood culture
B. Maternal blood vzv pcr
C. Anti-vzv IgM
D. Anti-vzv IgG
E. No testing is indicated

A

C.
Most pregnant women are screened for VZV by obtaining a detailed history; if unsure, it is recommended to obtain an anti-VZV IgG assay. If IgG antibody is positive, the patient is immune and there is no risk for the fetus. Diagnosis is confirmed with anti-VZV IgM antibody and a positive history of disseminated pruritic vesicular rash that progresses from vesicular to pustular. If a patient has no antibody against varicella, she should be cautioned caution to avoid exposure to those with vesicular eruptions. Maternal VZVT diagnosis is primarily clinical. If there is doubt about the clinical diagnosis, VZV infection may be rapidly confirmed through detection of viral DNA by PCR testing of skin scrapings from the base of the vesicle or through the detection of VZV antigen by immunofluorescence. VZV can also be cultured from vesicular fluid, although the virus replicates slowly and culture is less sensitive than direct detection techniques.

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6
Q

A 19 year old G3P2 presents for her second-trimester anatomy scan. The study reveals fetal growth restriction, microcephaly, ventriculomegaly, echogenic foci in liver, and limb anomalies. What test will you order to confirm your diagnosis of maternal varicella zoster virus (VZV)?
A. Maternal vzv blood culture
B. Maternal blood vzv pcr
C. Anti-vzv IgM
D. Anti-vzv IgG
E. No testing is indicated

A

C.
Most pregnant women are screened for VZV by obtaining a detailed history; if unsure, it is recommended to obtain an anti-VZV IgG assay. If IgG antibody is positive, the patient is immune and there is no risk for the fetus. Diagnosis is confirmed with anti-VZV IgM antibody and a positive history of disseminated pruritic vesicular rash that progresses from vesicular to pustular. If a patient has no antibody against varicella, she should be cautioned caution to avoid exposure to those with vesicular eruptions. Maternal VZVT diagnosis is primarily clinical. If there is doubt about the clinical diagnosis, VZV infection may be rapidly confirmed through detection of viral DNA by PCR testing of skin scrapings from the base of the vesicle or through the detection of VZV antigen by immunofluorescence. VZV can also be cultured from vesicular fluid, although the virus replicates slowly and culture is less sensitive than direct detection techniques.

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7
Q

A 19 year old G3P2 presents for her second trimester anatomy scan. The study reveals fetal growth restriction, microcephaly, ventriculomegaly, echogenic foci in liver, and limb anomalies. What test will you offer to confirm congenital varicella zoster virus (VZV) infection?
A. Maternal VZV culture
B. Maternal Blood VZV PCR
C. Polymerase chain reaction (PCR) testing of fetal blood or amniotic fluid for VZV DNA
D. Fetal skin biopsy
E. No testing is indicated

A

C.
A detailed anatomic ultrasound should be obtained to assess for fetal abnormalities consistent with congenital varicella syndrome (eg, microcephaly, limb hypoplasia, fetal growth restriction). If the ultrasound shows evidence of congenital varicella syndrome, the patient should be counseled regarding likely fatal disease. A sensitive test to confirm congenital VZV after abnormal ultrasound findings is amniotic fluid or fetal blood polymerase chain reaction (PCR) testing for VZV DNA.

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8
Q

A 19 year old G3P2 presents for her second trimester anatomy scan. The study reveals fetal growth restriction, microcephaly, ventriculomegaly, echogenic foci in liver, and limb anomalies. What test will you offer to confirm congenital varicella zoster virus (VZV) infection?
A. Maternal VZV culture
B. Maternal Blood VZV PCR
C. Polymerase chain reaction (PCR) testing of fetal blood or amniotic fluid for VZV DNA
D. Fetal skin biopsy
E. No testing is indicated

A

C.
A detailed anatomic ultrasound should be obtained to assess for fetal abnormalities consistent with congenital varicella syndrome (eg, microcephaly, limb hypoplasia, fetal growth restriction). If the ultrasound shows evidence of congenital varicella syndrome, the patient should be counseled regarding likely fatal disease. A sensitive test to confirm congenital VZV after abnormal ultrasound findings is amniotic fluid or fetal blood polymerase chain reaction (PCR) testing for VZV DNA.

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9
Q

What is the BEST next step in the evaluation of a patient with a known exposure to parvo B19 and who is found to be IgG-/IgM+ at 20 weeks of gestation?
A. Amniocentesis for parvo B19 polymerase chain reaction
B. Middle cerebral artery doppler studies of the fetus
C. IgG avidity testing on the mother against parvo B19
D. Amniocentesis for OD450 absorption
E. Repeat IgG/IgM titers in 2-4 weeks

A

B.
In pregnant patients exposed to parvo B19, serologic testing should be done to establish immune status. If there is evidence of a past infection (ie, IgG positive, IgM negative) no further tests will be necessary, as the patient is considered immune. In the case of a pregnant woman whose test results are negative for both IgM and IgG, repeated determination of IgM within 2 to 3 weeks after exposure is recommended to exclude seroconversion. Weekly ultrasound examinations for up to 12 weeks after maternal exposure should be performed in all patients with suspected or confirmed infection to evaluate for signs of fetal anemia or hydrops fetalis (ascites, pericardial effusion). Beyond 12 weeks after the potential infection, the risk virtually disappears. Doppler ultrasound measurements showing elevated peak systolic velocity values in the fetal middle cerebral artery accurately predict fetal anemia. Fetal blood sampling is warranted in the presence of hydrops to assess the degree of fetal anemia. Fetal management is dependent on gestational age, but intrauterine transfusion via cordocentesis for hydrops might improve fetal outcome. The risk of fetal death appears to be higher in fetuses managed expectantly than in those managed with intrauterine transfusion. In one study, approximately one-third of the cases of parvovirus-induced nonimmune hydrops resolved spontaneously, whereas 83.5% of transfused hydropic fetuses survived. The average time for hydrops resolution was 4 weeks.

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10
Q

Which of the following is NOT a classic finding for congenital CMV infection?***
A. Fetal growth restriction
B. Thrombocytopenia
C. Limb reductions
D. Microcephaly
E. Sensorineural hearing loss

A

C.
In the literature, definitions of symptomatic vs asymptomatic congenital CMV (cCMV) differ. In general, moderately to severely symptomatic cCMV is defined as the presence of multiple manifestations or central nervous system (CNS) involvement; mildly symptomatic cCMV is the presence of one or two isolated manifestations that are mild and transient; asymptomatic cCMV with isolated sensorineural hearing loss (SNHL) is defined the absence of apparent clinical symptoms other than hearing loss; and asymptomatic cCMV is defined as the absence of apparent abnormalities at birth and normal hearing. Approximately 10%-15% of babies with cCMV will be symptomatic at birth, and approximately half of those babies will have permanent sequelae. Of the remaining asymptomatically infected babies, approximately 10%-15% will have permanent sequelae. Symptoms associated with cCMV that can present at birth include thrombocytopenia, hepatosplenomegaly, fetal growth restriction, hepatitis, CNS and ocular disease, and SNHL. It has commonly been thought that primary infection in pregnancy results in more severe neonatal disease; however, some recent (2006-2013) evidence has introduced questions about this commonly accepted opinion. For example, some studies have shown that hearing loss may be similar in infants born to women who were seropositive or seronegative prior to pregnancy. In addition, the severity of infection likely depends on timing during pregnancy. CMV transmission is more likely to occur in the third trimester compared with the first, but more severe sequelae are associated with infection earlier in the pregnancy.

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11
Q

Which of the following ultrasound findings would NOT make you concerned for congenital varicella infection?
A. Scarring skin lesions
B. Cortical atrophy
C. Microphthalmia
D. Hydrops
E. Limb hypoplasia

A

D.
Varicella zoster virus (VZV), like CMV a member of the herpesvirus family, can lead to adverse pregnancy and infant outcomes when transmitted following acute maternal infection during pregnancy. Though preexisting VZV immunity has remained high in pregnant women both before and after the advent of VZV vaccination, immunity to VZV is standardly documented during early pregnancy. Infants with the highest risk of acquiring VZV are born to women with acute infection appearing between five days before and two days following delivery, as the infant is exposed to VZV at birth in the setting of limited or no placental VZV-specific IgG transfer. Rarely, VZV can be transmitted in utero during a primary maternal infection, and if this occurs in the first 20 weeks of pregnancy, fetal demise, fetal growth restriction, hydrops, limb deformities, microcephaly, and other neurologic defects can result from the congenital infection (congenital varicella syndrome).

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12
Q

In a pregnant patient with sepsis, which are the most common organisms that broad spectrum antibiotics should target?
A. Escherichia coli, Group A streptococcus, Group B streptococcus
B. Streptococcus pneumoniae and influenza
C. Clostridium difficile, Gardnerella vaginalis, Peptococcus spp., Bacteroides spp., Staphylococcus epidermidis, group B streptococcus, and Ureaplasma urealyticum
D. Methicillin-resistant Staphylococcus aureus

A

A.
The most frequently isolated organisms in maternal sepsis are Escherichia coli and group A and group B Streptococcus. It is important to start empiric broad-spectrum antimicrobial therapy until a specific pathogen is identified, allowing antibiotic choice to be driven by the presumed source. Initial coverage should include anaerobic and aerobic Grampositive and Gram-negative bacteria.

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13
Q

Why i it imperative to add clindamycin to penicillin in the treatment of Group A streptococcal sepsis?
A. Clindamycin covers penicillin-resistant strains of Group A streptococcus.
B. Clindamycin prevents co-infection with Clostridium difficile.
C. Clindamycin binds to penicillin-binding proteins on streptococcus to augment bacterial death.
D. Clindamycin directly impacts toxin production and is still efficacious when penicillin has reached its maximal efficacy, as when the burden of strep infection is high.
E. Clindamycin is not given for Group A streptococcus given the growing resistance rates.

A

C.
Clindamycin works because it combats the “eagle effect.”
Clindamycin works by binding to the 50s ribosomal subunit of bacteria.

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14
Q

A patient presents at 32 weeks of gestation without prenatal care. She has a fetal anatomical survey. The ultrasound shows hepatomegaly, placentomegaly, and polyhydramnios. After delivery, the neontate has lymphadenopathy, mucocutaneous lesions, osteochondritis, pseudoparalysis, rash, and snuffles. Additionally, hemolytic anemia and thrombocytopenia are noted. Which of the following is the most likely fetal infection?
A. Syphilis
B. Cytomegalovirus
C. Toxoplasmosis
D. Varicella
E. Rubella

A

A.
Prenatal ultrasound findings of fetal infections are often nonspecific. Hepatomegaly, placentomegaly, and polyhydramnios can be found in congenital syphilis, cytomegalovirus, toxoplasmosis, rubella, and parvovirus. In contrast, postnatal findings, such as snuffles and osteochondritis, are more specific to syphilis. Ultrasound findings of CMV include periventricular calcifications, cerebral ventriculomegaly, microcephaly, hyperechogenic bowel, growth restriction, ascites, hepatosplenomegaly, hepatic calcifications, polymicrogyria, cerebellar hypoplasia, pseudocysts, periventricular or adjacent to the occipital or temporal horn hyperechoic densities, amniotic fluid abnormalities (oligohydramnios or polyhydramnios), hydrops or placental thickening, enlargement. Ultrasound findings of toxoplasmosis include intracranial calcifications/densities, hydrocephalus, echogenic bowel, hepatosplenomegaly, intrahepatic calcifications/densities, growth restriction, ascites, pericardial and/or pleural effusions, hydrops, placental densities, and/or increased thickness. Ultrasound findings of varicella can show limb deformities, microcephaly, hydrocephaly, polyhydramnios, soft tissue calcification, and growth restriction. There are no specific ultrasound findings for congenital rubella syndrome, but a finding of fetal growth restriction should prompt evaluation for congenital viral infections, including rubella.

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15
Q

Which of the following findings are consistent with congenital measles?
A. Deafness, cataracts, growth restriction, congenital heart disease
B. Fetal anemia, hydrops, intrauterine demise
C. Growth restriciton, spontaneous abortion, intrauterine fetal demise, preterm birth
D. Intellectual delay, deafness, jaundice, microcephaly, growth restriction
E. Intrauterine fetal demise, growth restriction, limb abnormalities, cutaneous scars

A

C.
This answer reflects what we currently know about congenital measles.

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16
Q

Treatment options for congenital CMV

A

No.
While two small open-label and nonrandomized studies of high-dose (8g/day) valacyclovir have demonstrated potential benefit in reducing viral load in fetal blood and in preventing severe sequelae in high-risk fetuses (those showing ultrasound features of infection or with confirmed fetal CMV infection) based on historical controls, there are insufficient data at this time to recommend treatment of fetal CMV infection with oral valacyclovir. In addition, while 4 prospective observational studies demonstrated that administering CMV hyperimmune globulin to pregnant women with primary CMV infection reduced maternal-to-fetal transmission and reduced severity of congenital infection, a randomized trial did not demonstrate significant benefit of maternal CMV hyperimmune globulin administration. In addition, adverse maternal/obstetrical events were increased in the hyperimmune globulin group in this study. While additional RCTs are ongoing, there are insufficient data to recommend CMV hyperimmune globulin outside of a research protocol at this time. There is currently no CMV vaccine available for use in humans. A phase 2 vaccine trial including 464 CMV-seronegative women of childbearing age demonstrated only 50% efficacy at preventing CMV infection. At this point, the only potential interventions that may reduce the chance of primary maternal CMV infection in pregnancy and therefore the risk of fetal infection are behavioral risk reduction interventions, including handwashing with soap and water, avoiding contact with urine and oral and nasal secretions of young children, and careful cleaning of surfaces, toys, and utensils that come in contact with children’s urine or saliva.

17
Q

There has been an outbreak of parvovirus at several child care facilities in the area where you work. A pregnant woman at 34 weeks of gestation in your office has taken three days off to care for a child with a high fever and a slapped-cheek appearance who typically attends one of these daycare facilities. What is the next best step in the management of this patient?
A. Determine her immune status by testing for parvovirus B19 IgG and IgM.
B. Administer betamethasone in the event she also becomes ill and requires preterm delivery.
C. Begin monitoring with middle cerebral artery Doppler examinations.
D. Perform amniocentesis to determine if fetal infection is present.
E. Monitor for symptoms.

A

A.
The third trimester carries the lowest risk for fetal infection with parvovirus; however, cases have been reported. Up to 20% of immunocompetent patients will have an asymptomatic infection that may still result in fetal infection. Since the patient is asymptomatic and in the third trimester, determining her susceptibility would be the best first step, followed by monitoring for seroconversion if she is initially IgM, IgG negative.

18
Q

After attending a birthday party yesterday, your patient at 30 weeks of gestation learns that one of the individuals she spent time with had been ill and developed chickenpox (varicella) the next day. Your patient has no complaints at this time. After immediately sending antibody titers, you learn she is nonimmune/has negative serologies. What is the next best step in management of this patient?
A. Serial ultrasound to monitor for congenital VZV infection
B. Administration of VZIG
C. Admission to the obstetric unit for monitoring of symptoms
D. Initiation of prophylactic acyclovir
E. Weekly doppler studies to monitor for fetal anemia

A

B.
Congenital infection with varicella zoster virus (VZV) is associated with first-trimester exposure, not third trimester (Answer [A]). Third trimester VZV infection poses the greatest risk for neonatal disease, which can occur if the pregnant woman develops the disease from 5 days prior to delivery to 48 hours after and which can be lethal. Primary VZV in any pregnant woman is clinically significant due to the risk of maternal viral pneumonia/pneumonitis, but admission to the hospital is not recommended (Answer [C]). There is no known role for prophylactic acyclovir (Answer [D]) or any antiviral medication in this setting, other than VZIG (Answer [B]). VZIG should ideally be administered within 96 hours but up to 10 days to any nonimmune woman exposed to VZV. Fetal anemia is not associated with VZV but can be seen in CMV and parvovirus B19 infection; hence, answer D is not recommended.