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January

Question: 1

You receive a call from one of your colleagues in general pediatrics who asks your advice about purulent
conjunctivitis in a 2-year-old child in clinic who attends daycare. You and the fellow walk over to general
pediatric clinic to examine the child. The child is afebrile and non-ill-appearing except for mild bulbar
(Figure 1a) and palpebral erythema of both eyes, with copious purulence (Figure 2a).

Of the following, the MOST likely etiology of the conjunctivitis in this child is

A. Chlamydia trachomatis

B. Haemophilus influenzae

C. Neisseria gonorrhoeae

D. Staphylococcus epidermidis

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Figure 1a. Bulbar
conjunctiva
Reprinted with permission from LaMattina K and Thompson L. Pediatric
Conjunctivitis. Disease-a-Month. 2014;60(6): 231-238. DOI:
10.1016/j.disa.month.2014.03.002

Figure 2a. Child in the

vignette.

January
Print
Question: 1

Of the following, the MOST likely etiology of the conjunctivitis in this child is
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INCORRECT
Correct Answer: B Average Correct: 77.50%
A. Chlamydia trachomatis

B. Haemophilus influenzae

C. Neisseria gonorrhoeae

D. Staphylococcus epidermidis
The child in the vignette has bacterial conjunctivitis caused by Haemophilus influenzae. Acute
bacterial conjunctivitis is one of the most common forms of bacterial conjunctivitis in children.
Bilateral gluing of the eyes on waking has been shown to be the most predictive


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factor of bacterial etiology in conjunctivitis; it usually begins in one eye, often progressing to the
second eye, and is a leading cause of children being absent from daycare or school (Figure 2b).

Most cases are mild and self-limited, lasting as few as 2 to 3 days or up to 2 to 3 weeks. In
addition to copious amounts of purulence, the palpebral conjunctiva papillae often are inflamed;
papillae are dilated vessels surrounded by edema and inflammatory cells and may coalesce and
form giant papillae. This is a finding most characteristic of bacterial or allergic conjunctivitis, or in
contact lens overwear (Figure 1b).

In patients with suspected conjunctivitis, a bacterial cause is more likely with disease onset during
winter months, if there is purulent discharge, and if there are prominent papillae in the palpebral
conjunctiva. In children, bacterial conjunctivitis is more common than viral and is mainly caused by
H influenzae, S pneumoniae, and M catarrhalis; Staphylococcus epidermidis is not a reported
cause of bacterial conjunctivitis.
Outbreaks of bacterial conjunctivitis have been linked to nontypeable strains of Streptococcus
pneumoniae, often with bilateral conjunctivitis. The clinical course is usually mild, with resolution of
symptoms after initiating topical antibiotics and no ocular sequelae.

Inclusion conjunctivitis is a bilateral follicular conjunctivitis caused by Chlamydia trachomatous,

serotypes D through K. It is more common in newborns, 5 to 12 days after birth, causing redness
of the eye(s), swelling of the eyelid(s), and purulence (Figure 3).

Chlamydia also can cause a unilateral, chronic follicular conjunctivitis with mucopurulent
discharge in sexually active adolescents, associated with preauricular lymphadenopathy,
urethritis in males, and vaginitis in females.

Hyperacute bacterial conjunctivitis is usually caused by Neisseria gonorrhoeae and leads to

severe hyperpurulence with pseudomembrane formation and preauricular lymphadenopathy. Its
onset is sudden, rapid, and is accompanied by yellow-green discharge that returns even after
being wiped away from the eye(s). N gonorrhoeae occurs in sexually active adolescents/adults or
a sexually abused child. Gonococcal conjunctivitis also occurs in newborns 2 to 4 days after birth,
leading to red eyes, thick pus, and swelling of the eyelids (Figure 4, Figure 5).

Both chlamydial follicular conjunctivitis and hyperacute N gonorrhoeae conjunctivitis can lead to
vision loss if not treated promptly.
Conjunctivitis or pink eye is a common eye condition with inflammation of the mucous membranes
that cover the front of the globe, known as the bulbar conjunctiva, and lining of the inside of the
eyelids, known as the palpebral conjunctiva. In the pediatric population, diagnosis and treatment
are complicated by the challenge of performing an eye examination of and administering treatment
to a child with an irritated ocular surface. History-taking becomes a crucial element to appropriate
diagnosis, as duration, associated pain, and other systemic complaints will aid in sorting through
the vast differential of red eye, as well as to determine whether consultation with an ophthalmologist
or other specialist is indicated. Findings such as significant eye pain, visual blurring, and/or
photophobia may indicate a serious eye condition.

Viral conjunctivitis is commonly associated with mild-to-moderate discharge and early morning
crusting and often begins in one eye and progresses to the second eye within days. Infection
spreads easily and rapidly between people and can result in epidemics. Typical infection is mild
and resolves in 7 to 14 days without treatment; there are usually no long-term effects.

Epidemic keratoconjunctivitis (EKC) is a more severe type of conjunctivitis commonly caused by

adenovirus serotypes 8, 19, or 37; EKC has characteristic clinical features which include sudden
onset of acute unilateral follicular conjunctivitis, watery discharge, hyperemia, chemosis, and
ipsilateral preauricular lymphadenopathy (Figure 6).

Epidemic keratoconjunctivitis is highly contagious; nosocomial outbreaks from contaminated

medical devices are not uncommon. Infection can take 2 to 3 weeks or longer to completely
resolve and eye involvement may range from diffuse, fine, superficial keratitis to epithelial defects
to subepithelial opacities, leading to corneal scaring. Epidemic keratoconjunctivitis, as well as
chemical conjunctivitis, often causes the follicles, which are translucent collections of plasma cells
and lymphocytes in the normal tarsal conjunctiva epithelium to become erythematous and/or
enlarged (Figure 7).

In addition to adenovirus-associated epidemic keratoconjunctivitis, other causes of viral

conjunctivitis are common:

Common cold, flu, or other respiratory infection — conjunctivitis often occurs with respiratory
infections. Pharyngoconjunctivial fever — conjunctivitis as well as a fever and pharyngitis can
occur with this syndrome, which is most commonly caused by infection with adenovirus
serotypes 3, 4, and 7. Acute hemorrhagic conjunctivitis — can accompany central nervous
system involvement and is associated with enterovirus 70 or 71 and coxsackievirus A24 (Figure
8).
Herpetic keratoconjunctivitis —associated with herpes simplex virus on the skin and eye; it may
affect only one eye (Figure 9). Varicella-zoster virus —associated chicken pox with eye
involvement, or zoster (shingles) with eye and skin involvement in a dermatomal distribution
(Figure 10). Rubella (3-day measles) and rubeola (9-day measles) — conjunctivitis
accompanied by rash, fever, and cough.

Bacteria are believed to account for 50% to 75% of acute infectious conjunctivitis, although the
presence of normal ocular flora makes this estimate controversial. The most common pathogens
causing bacterial conjunctivitis include Staphylococcus aureus, Streptococcus pneumoniae,
Moraxella catarrhalis, Pseudomonas aeruginosa, and Haemophilus influenzae. Neisseria
species are known to cause hyperacute conjunctivitis, and both Chlamydia and Bartonella may
cause distinct forms of conjunctivitis. Depending on the cause of bacterial conjunctivitis, some
patients may have additional symptoms or conditions, such as the following:

Chronic bacterial conjunctivitis — often develops along with another inflammatory condition
such as blepharitis that promotes bacteria growing in the eyelid; flaky debris and warmth along
the lid may also be present. Symptoms may last for at least 4 weeks with recurrences.
Trachoma — chronic follicular conjunctivitis caused by chlamydial serotypes A through C,
characterized by a severe follicular reaction of the superior tarsal conjunctiva, which may
develop into scarring. Patients may present with vision loss due to the development of corneal
cicatrization, which leads to scarring in the conjunctiva and cornea; repeat infections occur in
children younger than 10 years of age and are common in developing countries.

Bartonella henselae is a common cause of Parinaud oculoglandular syndrome, a unilateral

granulomatous conjunctivitis with ipisilateral preauricular and submandibular adenopathy, and a
decrease in visual acuity if there is coexisting neuroretinitis (Figure 11).

Infectious conjunctivitis must be distinguished from noninfectious causes; allergic conjunctivitis

occurs frequently, especially among people with other allergic conditions, such as hay fever,
asthma, and eczema. It usually occurs in both eyes and folliculitis is commonly present; allergic
conjunctivitis can occur seasonally or year-round due to indoor allergens, such as dust mites and
animal dander. Allergic conjunctivitis may result from exposure to certain drugs and cosmetics,
clears up once the allergen or irritant is removed or after treatment with allergy medications, and
may be present when contact lenses are worn too long or not cleaned properly. Systemic diseases
are associated with conjunctivitis and include Kawasaki syndrome (Figure 12), leptospirosis,
tularemia, dacryocystitis, periorbital cellulitis, orbital cellulitis, Zika virus (Figure 13), and
endophthalmitis.

Other noninfectious causes of a red or painful eye include: corneal abrasion, subconjunctival
hemorrhage, pinguecula, keratoconjunctivitis sicca (dry eye), hordeolum, keratitis, uveitis, acute
angle-closure glaucoma, chemical conjunctivitis, contact lens wear,
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foreign bodies in the eye, and indoor and outdoor air pollution (chemical vapors, fumes, smoke,
or dust).
PREP Pearls

Bilateral gluing of the eyes on waking has been shown to be the most predictive factor of
bacterial etiology in conjunctivitis.

Follicular conjunctivitis is often seen in viral, allergic, and chlamydial conjunctivitis.

Viral conjunctivitis is commonly associated with mild-to-moderate discharge and early

morning crusting and often begins in one eye and progresses to the second eye within days.

Suggested
Readings

LaMattina K, Thompson L. Pediatric conjunctivitis. Disease-a-Month. 2014;60(6):231-238.

Narayana S, McGee S. Bedside diagnosis of the “red eye”: a systematic review. Am J Med.
2015;128(11):1220-1224. doi: http://dx.doi.org/10.1016/j.amjmed.2015.06.026

US Centers for Disease Control and Prevention. Conjunctivitis (pink eye). US Centers for
Disease Control and Prevention website. http://www.cdc.gov/conjunctivitis/index.html

January
Print

Question: 2
During the routine screening of a 2-year-old refugee from Africa, HIV testing resulted as
positive and confirmed by the HIV fourth-generation assay. The child is underweight but
otherwise asymptomatic. His CD4 count is 750 cells/mm ; the viral load is pending.
Of the following, the MOST appropriate next step in the management of this patient is to
CORRECT
Average Correct: 79.07%
3
A. delay initiation of antiretroviral drugs
B. initiate 3 antiretroviral drugs
C. initiate azithromycin prophylaxis
D. initiate trimethoprim-sulfamethoxazole prophylaxis
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The current guidelines for the use of antiretroviral agents in pediatric HIV infection
emphasize early initiation of antiretroviral (ARV) therapy consisting of 3 drugs from at
least 2 different classes in HIV infected children and adolescents. The patient in the
vignette fulfills criteria for starting therapy without delay (Table). The goals of early
therapy include enhanced survival, reduction in opportunistic infections and their
complications, improved growth and neurocognitive function, and improved quality of
life. Studies have
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demonstrated decreased morbidity, mortality and hospitalizations with early initiation of
ARV therapy. In general, when to initiate therapy depends on the severity of disease
and the risk of disease progression, along with the presence of comorbidities. However,
in treating asymptomatic patients, clinicians may be able to preserve immune function
and suppress viral replication. Infants younger than 12 months of age are likely to have
rapidly progressing disease, and treatment in this age group regardless of symptoms,
CD4 count, or viral load has been shown to decrease mortality and improve
neurodevelopmental outcome. In HIV-infected children aged 12 months or older, about
50% develop moderate immunosuppression, while 20% develop severe
immunosuppression. For children 1 to 6 years of age, treatment is recommended in
those who are symptomatic or have opportunistic infections, or are immunodeficient
with CD4 less than 500 cells/mm , along with those who may be less clinically ill but
have CD4 counts 500 to 999 cells/mm , and/or viral load greater than 100,000
copies/mL. Given the patient’s CD4 count, initiation of azithromycin or
trimethoprim-sulfamethoxazole prophylaxis is not indicated at this time
(https://aidsinfo.nih.gov/contentfiles/lvguidelines/pedoitablesonly.pdf).
Risk factors for maternal-to-child transmission include higher maternal viral load, the
duration of exposure (rupture of membrane duration, breastfeeding, timing of caesarean
delivery in relation to labor), maternal breast lesions and/or infant candidiasis. Risk
factors for adolescents include intravenous drug use and sexual exposure (higher risk in
men who have sex with men). Minority race or ethnicity has also been linked to higher
rates of HIV acquisition.
In infants infected through maternal to infant transmission, symptoms typically present
by 12 to 18 months of age. Without therapy, 15% to 20% of these children die by 4
years of age (rapid progressors), whereas 80% to 85% of slow progressors with
delayed symptoms onset survive beyond 5 years of age.
In any individual with nonperinatally acquired HIV, acute retroviral syndrome occurs 7 to
14 days following viral acquisition. This initial mononucleosis-like illness phase lasts 1 to
6 weeks. With seroconversion comes a decrease in plasma viremia. In most patients,
CD4 counts decline gradually over years. Increasing plasma viremia correlates with
decreasing CD4 counts. With decreasing CD4 counts, symptomatic disease emerges.
Both the CD4 count and viral load should be used as prognostic markers for disease
course. There are long-term nonprogressors who remain asymptomatic without
immunologic decline for many years. Elite controllers have undetectable viral load and
maintain normal CD4 counts. The typical progression to AIDS defining conditions based
on age is seen in the Figure, with Pneumocystis jirovecii peaking at 3 to 6 months of
age, while other conditions are more evenly distributed over the first 2 years of life.
33
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When making the decision to initiate therapy, one must weigh the risks (ie, toxicities, resistance)
versus the benefits and carefully assess the ability of the family and patient to adhere to the
medication regimen, as noncompliance will lead to the emergence of resistant virus. It is
important to address the barriers to adherence prior to starting antiretroviral therapy.

PREP Pearls

Early initiation of antiretroviral drugs in children can lead to improved survival and
enhanced quality of life.

One must weigh the risks versus the benefits and assess the potential for compliance when
starting antiretroviral therapy.

Initiate 3 or more antiretroviral drugs.

Suggested
Readings

American Academy of Pediatrics. Human immunodeficiency virus infection. In: Kimberlin DW,
Brady MT, Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee on Infectious
Disease. 30th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2015:453- 476.

National Institutes of Health. Guidelines for the prevention and treatment of opportunistic
infections in HIV-exposed and HIV-infected children. AIDSinfo website.
https://aidsinfo.nih.gov/guidelines/html/5/pediatric-oi-prevention-and-treatment- guidelines/0

National Institutes of Health. Guidelines for the use of antiretroviral agents in pediatric HIV
infection. AIDSinfo website. http://aidsinfo.nih.gov/contentfiles/lvguidelines/pediatricguidelines.pdf
Reitz MS Jr, Gallo RC. Human immunodeficiency viruses. In: Bennett JE, Dolin R, Blaser MJ, eds.
Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 8th ed.
Philadelphia, PA: Saunders Elsevier; 2015:2054-2065.
Table. Treatment Recommendations for Initiation of Therapy in Antiretroviral-Naive,
HIV-Infected Infants, and Children.
Panel's Recommendations for Initiation of Therapy in Antiretroviral-Naive, HIV-Infected
Infants and Children
Panel's Recommendations
Recommend
Urgent Treatmenta
Combination Antiretroviral Therapy (cART) Should Be Initiated Urgently in All HIV-Infected
Children with any of the Following: Age <12 Months:
• AI for infants age <12 weeks
• AII for infants 12 weeks–12 months Age ≥1 year:
• CDC Stage 3-defining opportunistic illnesses (AI*)
• CDC Stage 3 immunodeficiency (AI*):
o Aged 1 to <6 years, CD4 countc<500 cells/mm3 o Aged ≥ 6 years, CD4 countc<200 cells/mm3
Recommend
cART Should Be Initiated in HIV-Infected Children Aged ≥1 Year with any of the
Treatmentb
Following:

• Moderate HIV-related symptoms (AII)

• Plasma HIV RNA >100,000 copies/mLd(AII) CDC Stage 2:
• Age 1 to <6 years, CD4 countc 500–999 cells/mm3(AII)
• Age ≥6 years, CD4 countc 200–499 cells/mm3 (AI* if CD4 count <350 cells/mm3; AII* if CD4
count 350–499 cells/mm3)
Consider
cART Should Be Considered for HIV-Infected Children Aged ≥1 Year with:
Treatmentb
• Mild HIV-related symptoms (see Table 7) or asymptomatic and CDC Stage 1 (see Table 6):
• Ages 1 to <6 years, CD4 countc ≥1000 cells/mm3(BIII)
• Age ≥6 years, CD4 countc ≥500 cells/mm3(BIII)
Rating of Recommendations: A = Strong; B = Moderate; C = Optional R ating of Evidence: I = One or more
†
randomized trials in children with clinical outcomes and/or validated endpoints; I* = One or more randomized trials in
adults with clinical outcomes and/or validated laboratory endpoints with accompanying data in children† from one or
more well-designed, nonrandomized trials or observational cohort studies with long-term clinical outcomes; II = One

or more well-designed, nonrandomized trials or observational cohort studies in children† with long-term outcomes; II*
= One or more well-designed, nonrandomized trials or observational studies in adults with long-term clinical outcomes
with accompanying data in children† from one or more similar nonrandomized trials or cohort studies with clinical
outcome data; III = Expert opinion † Studies that include children or children/adolescents, but not studies limited to

post-pubertal adolescents
Note: Adherence should be assessed and discussed with HIV-infected children and their caregivers before initiation
of therapy (AIII). a Within 1–2 weeks, including an expedited discussion on adherence b More time can be taken to

fully assess and address issues associated with adherence with the caregivers and the child prior to initiating therapy.
Patients/caregivers may choose to postpone therapy, and on a case-by-case basis, providers may elect to defer
therapy based on clinical and/or psychosocial factors. c CD4 counts should be confirmed with a second test to meet

the treatment criteria before initiation of cART. d To avoid overinterpretation of temporary blips in viral load (which can

occur, for example, during intercurrent illnesses), plasma HIV RNA level
>100,000 copies/mL should be confirmed by
a second level before initiating cART. Reprinted with permission from Panel on Antiretroviral Therapy and Medical
Management of HIV-Infected Children. Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection
Figure. Human Immunodeficiency Virus
Infection

AIDS-defining conditions, by age at diagnosis for perinatally acquired AIDS cases, reported
through 2001, United States.

The incidence of Pneumocystis jiroveci ( formerly P carinii) pneumonia (PCP) in children with
perinatally acquired AIDS peaks at 3 to 6 months of age. The age at diagnosis for the other
AIDS-defining conditions is much more evenly distributed during the first 2 years of life.
Because PCP occurs early, prophylaxis is recommended for all perinatally HIV-exposed children,
beginning at 6 weeks of age. The occurrence of PCP in children may indicate missed
opportunities for testing pregnant women, the use of zidovudine or other antiretroviral therapies
to prevent transmission, or therapy (including PCP prophylaxis) for HIV-exposed children.

The Centers for Disease Control and Prevention has a high-priority initiative to reduce HIV
transmission from mothers to children by promoting voluntary maternal testing prenatally
(intrapartum if women do not receive prenatal care) and zidovudine therapy. Courtesy of
Centers for Disease Control and Prevention

Reprinted with permission from the American Academy of Pediatrics. Human

Immunodeficiency Virus Infection. In: Kimberlin DW, Brady MT, Jackson MA, Long SS, eds.
Red Book: 2015 Report of the Committee on Infectious Disease. 3 0th ed. Elk Grove Village,
IL: American Academy of Pediatrics; 2015:453-476.

January
Print

Question: 3

A 17-year-old female adolescent comes to your office with a history of abrupt onset that morning of fever
to 39.1°C in association with complaints of vomiting, sore throat, headaches, diffuse myalgias, and joint
achiness. She also noted a rash developing on her arms and legs.

She works in a pet store and reports over the last week being scratched by a kitten and bitten by a pet
rat in the store. She remembers seeing a small, raised lesion at the site of the rat bite initially that healed
over several days. The kitten reportedly scratched her on the right forearm without biting her. She states
that she cleaned both sites promptly with soap and water after the incidents occurred.
She has been previously well and reports no ill contacts. Immunizations are reportedly up to date.
She is said to have had an urticarial reaction with difficulty breathing during amoxicillin exposure in
the past. Past medical history is otherwise unremarkable,

Physical examination reveals an ill-appearing adolescent. Vital signs show a temperature of 39°C, heart
rate of 104 beats/min, blood pressure of 96/60 mm Hg, and respiratory rate of 20 breaths/min. Other
examination results include:

Head, ears, eyes, nose, and throat: pharynx mildly injected, without exudates Neck: Supple,
without significant lymphadenopathy appreciated. Lungs: Clear Cardiovascular: Regular
rhythm, without murmur, rub, or gallop Abdomen: Mild distension, (+) bowel sounds, mild
diffuse tenderness without rebound, without organomegaly Extremities: without joint swelling
Neurologic: No focal abnormalities
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Skin: Papulovesicular lesions on extensor surfaces of distal extremities and palms and soles
(Figure)

Of the following, the BEST choice of an antibiotic for treatment of this patient’s illness is

A. azithromycin

B. ciprofloxacin

C. clindamycin

D. doxycycline
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Figure. Distal rash
characteristics

American Academy of Pediatrics. In: Kimberlin DW, Brady MT,

Jackson MA, Long SS, eds. Red Book: 2015 Report of the
0th ed. Elk Grove Village, IL:
Committee on Infectious Disease. 3
American Academy of Pediatrics; 2015:666-667 and Courtesy of
George Nankervis, MD
January
Print

Question: 3

She has been previously well and reports no ill contacts. Immunizations are reportedly up to date.
She is said to have had an urticarial reaction with difficulty breathing during amoxicillin exposure in
the past. Past medical history is otherwise unremarkable,

Assessment Review & Tools

Skin: Papulovesicular lesions on extensor surfaces of distal extremities and palms and soles
(Figure)

Of the following, the BEST choice of an antibiotic for treatment of this patient’s illness is
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Correct Answer: D Average Correct: 72.09%
A. azithromycin

B. ciprofloxacin

C. clindamycin

D. doxycycline
The abrupt onset of illness with fever, systemic illness, and a distal extremity rash within a week
after a rat bite is most consistent with a diagnosis of rat bite fever caused by Streptobacillus
moniliformis. As in this case, the initial bite mark heals without residual inflammation. The
treatment of choice is penicillin G parenterally, but in a patient with serious penicillin allergy, as
noted in this case, doxycycline is an effective agent. Streptomycin and gentamicin are other
alternatives for treatment of rat bite fever in a penicillin-allergic patient. Ampicillin or ceftriaxone
are effective alternatives to penicillin in the treatment of this infection when penicillin allergy is not
a concern.

Azithromycin, clindamycin, and ciprofloxacin have not been demonstrated to be effective against
S moniliformis.

Nearly all domestic and wild rats carry S moniliformis in the upper respiratory tract and infection
can be transmitted by rodent bites or scratches. Other rodents (eg, mice, gerbils, squirrels,
weasels) and rodent-eating animals (eg, cats, dogs) may also transmit the infection. Infection after
ingestion of contaminated unpasteurized milk, water, or food causing outbreaks of infection have
been reported and the illness has been called Haverhill fever in that setting. Spirillum minus
causes a similar illness, but is characterized by a distinctive rash of red purple plaques and
ulceration at the site of the bite. Infections with this organism occur primarily in Asia.
uestion Continue 

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Comment n
o
Diagnosis of this infection may be difficult as the organism grows slowly (up to 3 weeks in
culture) and requires special medium enriched with 15% rabbit blood. When possible, sodium
polyanethol sulfonate (SPS)-free blood culture media (anaerobic blood culture bottle) should be
used, as SPS inhibits growth of S moniliformis. No serologic tests are available and the
diagnosis is often made clinically.

Untreated, symptoms of the infection often resolve over 2 to 3 weeks, but fever may relapse
for weeks or months. Additionally, complications including tissue and organ abscesses,
endocarditis, septic arthritis, pneumonia, myocarditis, and meningitis may occur; untreated,
the mortality rate is approximately 10%.

PREP Pearls

Rat bite fever may occur after a bite or scratch from a domestic or wild rodent.

The acute illness typically begins within a week of the bite and is characterized by
abrupt onset of fever, systemic illness, arthralgias, and myalgias.

Penicillin is the drug of choice for treatment of rat bite fever. Doxycycline and
aminoglycosides are alternatives for treatment in the penicillin-allergic patient.

Suggested
Readings

Adam JK, Varan AK, Pong AL, McDonald EC. Fatal rat-bite fever in a child – San Diego county,
California, 2013. MMWR Morbid Mortal Wkly Rep. 2014;63(50):1210-1211.
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6350a8.htm

American Academy of Pediatrics. Rat bite fever. In: Kimberlin DW, Brady MT, Jackson MA, Long
SS, eds. Red Book: 2015 Report of the Committee on Infectious Disease. 30th ed. Elk Grove
Village, IL: American Academy of Pediatrics; 2015:666-667.

Elliot SP. Rat bite fever and Streptobacillus moniliformis. Clin Microbiol Rev. 2007;20(1):13- 22.
doi: http://dx.doi.org/10.1128/CMR.00016-06
January
Print

Question: 4

You are seeing a 14-year-old adolescent for an infected dog bite wound of his left hand. Two days ago
while he was playing with his friend’s dog, he was bitten when he tried to take away the dog’s food bowl.
He sustained a deep bite to the dorsal and palmar surface of his hand with bleeding. Yesterday, he
developed a fever up to 39°C with chills, body aches, and malaise. Physical examination is significant for
a tired-appearing adolescent with a temperature of 39.2°C, pulse of 100 beats/min, respiratory rate of 20
breaths/min, and blood pressure of 80/40 mm Hg. His left hand is very swollen and tender to palpation
with erythema of the entire dorsal and palmar surfaces spreading up onto his wrist and down to his
fingers. There is a bloody discharge from the wound sites with some purplish discoloration around the
bites. Of note, he had his spleen removed 2 years ago after he ruptured it in an all-terrain vehicle
accident.

Of the following, the organism that is MOST likely the cause of the patient’s condition is

A. Capnocytophaga canimorsus

B. Eikenella corrodens

C. Pasteurella multocida

D. Staphylococcus aureus
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January
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Question: 4

Of the following, the organism that is MOST likely the cause of the patient’s condition is
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INCORRECT
Correct Answer: A Average Correct: 69.77%
A. Capnocytophaga canimorsus

B. Eikenella corrodens

C. Pasteurella multocida

D. Staphylococcus aureus
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Assessment Review & Too

The patient in the vignette has an infection of his dog bite that has progressed to sepsis. All the
organisms listed may be isolated from patients with infected dog bites, however, the presence of
asplenia is a major predisposing factor for the development of sepsis with Capnocytophaga
canimorsus.

Skin and soft-tissue infections (SSTIs) are defined as infections of the epidermis, dermis, or
subcutaneous tissue. Skin and soft-tissue infections range from mild infections (eg, pyoderma,
folliculitis) to severe life-threatening infections, such as necrotizing fasciitis. The pathogenesis of
SSTIs usually involves direct inoculation of pathogens through skin punctures or other mechanisms
that result in a break in the skin barrier (eg, lacerations, bite wounds, scratches, traumatic wounds,
burns, catheter insertions, and surgery), but can also be associated with skin conditions such as
dermatitis and eczema. Other routes of penetration include contiguous spread from deeper foci or
adjacent sites (eg, osteomyelitis), hematogenous seeding, and occasionally there is no obvious
source of infection. Involvement of pores in the epidermis may lead to folliculitis, furuncles,
carbuncles, and impetigo. Infection of the superficial layers of skin and upper dermis may result in
erysipelas, while involvement of the dermis and/or subcutaneous tissues results in cellulitis.
Involvement of deeper skin structures (eg, fascia and muscles) may lead to fasciitis and myositis.
Skin and soft-tissue infections may present with diverse clinical manifestations. Typical clinical
manifestations include warmth, erythema, edema, induration, and pain at the affected site.
Systemic signs and symptoms such as fever, tachycardia, tachypnea, and hypotension may also
be present in more severe infections. Pain out of proportion to clinical presentation or skin
anesthesia and the presence of bullous lesions with violaceous lesions or other skin color changes
may also be present in infections, causing severe damage of the deep layers of skin such as with
necrotizing fasciitis and/or myositis.

Skin and soft-tissue infections are primarily diagnosed through clinical examination.
Uncomplicated SSTIs usually are localized with no signs or symptoms of systemic toxicity, while
complicated SSTIs may include signs and symptoms of systemic involvement with fever, ill or
toxic appearance, sepsis syndrome, or life-threatening infection.

Laboratory investigations help to confirm the diagnosis and elucidate characteristics of specific
etiologies. Identification of the causative organism will also guide the choice of antibiotic therapy
and can help to establish the prognosis for the infection. Tests that may be done include blood
cultures, tissue swab with culture, needle aspiration, radiograph, ultrasonography, computed
tomography, or magnetic resonance imaging. Bacteriologic examination from needle aspirates, skin
biopsy, and blood culture are mostly low yield tests in establishing the diagnosis in patients with
intact skin lesions without areas of fluctuance. In the absence of systemic symptoms, such as fever,
blood cultures produce a very low yield and are positive in less than 5% of cases. If a skin swab is
obtained from an area of
intact skin and it is positive, it is also difficult to determine if the positive culture represents a
pathogenic agent or merely skin colonization. However, in cellulitis with fluid collections or
exudates, open wounds, skin breakdown, sites of active drainage, and in necrotizing fasciitis, skin
swabs or swabs of material from the wound or fluid collection are very helpful in identification of
one or several pathogens in over 65% of the cases. Needle aspiration remains a controversial test
as to its utility and different approaches exist as to how it should be obtained. Some studies
recommend a leading edge aspirate, while others recommend a central aspirate. However, the
evidence from most studies demonstrates no added benefit to using either method. Needle
aspirations are most useful in patients who present with skin infections associated with fluid
collections. Radiographic studies are useful in determining the extent of the infection and the
presence of drainable collections of fluid.

Most SSTIs are caused by Gram-positive bacteria, primarily Staphylococcus aureus and group A
streptococci (GAS); in addition, enterococci, various enterobacteriaceae, and anaerobes may be
found in complicated mixed SSTIs, especially those involving the skin below the waist. For the
treatment of most SSTIs, antimicrobial agents (eg, β-lactams, glycopeptides, oxazolidinones, and
clindamycin) that are effective against S aureus and GAS should be included in the treatment
regimen. Other organisms may cause SSTIs based upon various risk factors. The Table shows
different risk factors for SSTIs, the most common associated pathogens causing infection, and the
commonly recommended treatment regimens.

Complications that may be associated with SSTIs include lymphadenitis, myositis/necrotizing

fasciitis, gangrene, osteomyelitis, bacteremia, endocarditis, septicemia, or sepsis. Studies have
found that having diabetes as a comorbid condition increases the risk for the development of SSTI
complications. Skin and soft-tissue infection-associated complications were found to be 5 times
higher and SSTI-associated hospitalizations were 4 times higher in patients with diabetes
compared to those without diabetes. Other comorbid conditions that predispose to complications
with SSTIs include: immunosuppression, peripheral vascular disease, obesity, dialysis-dependent
chronic renal disease, blunt or penetrating trauma, surgical incisions, varicella, perforation of the
gastrointestinal tract, malnutrition, soft tissue trauma, and iron overload states with deferoxamine
therapy. Infections, especially severe infections with GAS and MRSA, seem to place the patient at
a higher risk for the development of necrotizing fasciitis and/or myositis. Cellulitis of the groin and
perineal area may become necrotic resulting in Fournier’s gangrene. Severe otitis externa with
Pseudomonas aeruginosa especially in a diabetic may result in malignant otitis externa with
necrosis of the walls of the external auditory canal. Meleney’s synergistic gangrene may occur in
infections of surgical wounds postoperatively caused by a combination of S aureus,
enterobacteriaceae, and anaerobic streptococci.
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PREP Pearls

Skin and soft-tissue infections (SSTIs) are defined as infections of the epidermis,
dermis, or subcutaneous tissue that range from mild to severe life-threatening
infections.

Most SSTIs are caused by Gram-positive bacteria, primarily Staphylococcus aureus and
group A streptococci, however, a variety of other organisms may cause SSTIs based on a
variety of risk factors. This needs to be taken into consideration when choosing the best
antibiotic regimen for treatment.

Suggested
Readings

Bernard P. Management of common bacterial infections of the skin. Curr Opin Infect Dis.
2008;21(2):122-128. doi: http://dx.doi.org/10.1097/QCO.0b013e3282f44c63

Brook I. Microbiology and management of soft tissue and muscle infections. Int J Surg.
2008;6(4):328-338. doi: http://dx.doi.org/10.1016/j.ijsu.2007.07.001

Eisenstein BI. Treatment challenges in the management of complicated skin and soft-tissue
infections. Clin Microbiol Infect. 2008;14 Suppl 2:17-25. doi:
http://dx.doi.org/10.1111/j.1469-0691.2008.01922.x

Gabillot-Carré M, Roujeau JC. Acute bacterial skin infections and cellulitis. Curr Opin Infect Dis.
2007;20:118-123.

Ki V, Rotstein C. Bacterial skin and soft tissue infections in adults: A review of their
epidemiology, pathogenesis, diagnosis, treatment and site of care. Can J Infect Dis Med
Microbiol. 2008;19(2):173-184. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605859/

Moran GJ, Abrahamian FM, LoVecchio F, Talan DA. Acute bacterial skin infections:
developments since the 2005 Infectious Diseases Society of America (IDSA) guidelines. J Emerg
Med. 2013;44(6):e397-e412. doi: http://dx.doi.org/10.1016/j.jemermed.2012.11.050

Suaya JA, Eisenberg DF, Fang C, Miller LG. Skin and soft tissue infections and associated
complications among commercially insured patients aged 0 -64 years with and without
diabetes in the U.S. PLoS One. 2013;8(4):e60057. doi:
http://dx.doi.org/10.1371/journal.pone.0060057

January
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Question: 5

You are asked to consult on a 5-year-old girl who underwent renal transplantation 10 days ago. Five
days ago, her central venous catheter was removed because it developed a disruption and could not be
repaired. In the last 4 days, she has required 4 separate peripheral intravenous catheters because each
time a new one is placed, she develops phlebitis. Her primary care team ‫ ﻫﻮ‬has been treating the
episodes of phlebitis with intravenous cefazolin. Her only other medications are mycophenolate and
intravenous ganciclovir. Review of the pre-transplant cytomegalovirus (CMV) status of the patient and
donor show discordance: the patient was CMV seronegative and the donor was CMV seropositive. The
transplant team started ganciclovir prophylaxis immediately after the transplant surgery. The patient has
not had fever. On physical examination, the patient’s current intravenous catheter site is warm,
erythematous, and exquisitely painful to light touch. An erythematous linear streak extends from the
catheter site along the vein for approximately 10 cm. The site where a catheter was removed yesterday
remains erythematous, but the patient’s mother explains that it is already much improved. The other 2
catheter sites are well healed, with no residual evidence of phlebitis. The wound from the transplant
surgery shows no signs of inflammation. The remainder of the girl’s physical examination is normal.

Of the following, the statement that BEST explains the reason that the ganciclovir is causing the
problem with the peripheral intravenous catheter sites is that the medication is

A. causing an allergic reaction

B. causing a chemical reaction

C. contaminated with a mold

D. contaminated with coagulase-negative staphylococci

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January
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Question: 5
You are asked to consult on a 5-year-old girl who underwent renal transplantation 10 days ago. Five
days ago, her central venous catheter was removed because it developed a disruption and could not be
repaired. In the last 4 days, she has required 4 separate peripheral intravenous catheters because each
time a new one is placed, she develops phlebitis. Her primary care team has been treating the episodes
of phlebitis with intravenous cefazolin. Her only other medications are mycophenolate and intravenous
ganciclovir. Review of the pre-transplant cytomegalovirus (CMV) status of the patient and donor show
discordance: the patient was CMV seronegative and the donor was CMV seropositive. The transplant
team started ganciclovir prophylaxis immediately after the transplant surgery. The patient has not had
fever. On physical examination, the patient’s current intravenous catheter site is warm, erythematous,
and exquisitely painful to light touch. An erythematous linear streak extends from the catheter site along
the vein for approximately 10 cm. The site where a catheter was removed yesterday remains
erythematous, but the patient’s mother explains that it is already much improved. The other 2 catheter
sites are well healed, with no residual evidence of phlebitis. The wound from the transplant surgery
shows no signs of inflammation. The remainder of the girl’s physical examination is normal.

Of the following, the statement that BEST explains the reason that the ganciclovir is causing the
problem with the peripheral intravenous catheter sites is that the medication is

A. causing an allergic reaction

B. causing a chemical reaction

C. contaminated with a mold

D. contaminated with coagulase-negative staphylococci

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Correct Answer: B Average Correct: 82.98%

The pH of ganciclovir for injection is 11. The alkaline nature of the medication can be quite
irritating to the vein causing a painful inflammatory chemical phlebitis. Allergic reactions to
ganciclovir are uncommon, but when they do occur, are associated with a generalized eruption or
urticaria, not self-limited phlebitis. It is very uncommon for medications for injection to become
contaminated with bacteria or mold, but such contamination could cause a localized, and later, a
disseminated infection. Neither is likely in this case since the sites of phlebitis improved quickly
when the catheters were removed. Cefazolin would not be expected to treat either a
coagulase-negative staphylococcal or fungal phlebitis.

Adverse effects during ganciclovir treatment are quite common because the medication has a
fairly narrow therapeutic index. The most common and expected adverse effect is dose-dependent
bone marrow suppression. Some degree of hematologic toxicity, such as neutropenia, anemia, or
thrombocytopenia, is seen in the majority of patients treated with the medication. Regular
laboratory monitoring is important because altogether. When neutropenia occurs, it typically
resolves within a week of stopping therapy.

Less common adverse reactions to ganciclovir include gastrointestinal adverse effects such as
nausea, vomiting, diarrhea, abdominal pain, or raised liver enzymes. Rapid administration of
intravenous doses may result in elevated plasma concentrations and a greater likelihood for
toxicity. Dilution to concentrations less than 10 mg/mL is necessary to minimize the risk for pain
and phlebitis because of the alkaline nature of the drug for injection. Even with dilution, some
patients experience mild to moderate chemical irritation at the infusion site. Ganciclovir should not
be administered intramuscularly or subcutaneously.

Ganciclovir is a synthetic analogue of 2′-deoxy-guanosine that has activity in vitro against herpes
simplex type-1, herpes simplex type-2, varicella-zoster virus, cytomegalovirus (CMV), and
Epstein-Barr virus. The major distinction of ganciclovir from other antiviral agents is its potent
activity against CMV. Oral bioavailability is limited to less than 10%, but the valyl ester
valganciclovir has approximately 60% bioavailability and is rapidly converted to ganciclovir by
intestinal and hepatic esterases following absorption.
When taken up by infected cells, ganciclovir is first phosphorylated to produce ganciclovir
monophosphate by a viral kinase encoded by the CMV gene UL97. Host cellular kinases then
catalyze two additional phosphorylation steps to yield ganciclovir triphosphate, a competitive
inhibitor of deoxyguanosine triphosphate (dGTP). Concentrations of ganciclovir triphosphate are
10-fold higher in virus-infected cells compared with uninfected cells. The triphosphate form serves
as a poor substrate for DNA chain elongation, thereby disrupting viral DNA synthesis and blocking
replication.

Recent evidence confirmed the earlier observation that antiviral treatment for symptomatic
congenital CMV infection was associated with improved hearing outcomes. Moreover, 6 months of
treatment with oral valganciclovir modestly improved developmental outcomes when compared
with a shorter treatment course of 6 weeks. Approximately one-fifth of infants included in that study
developed moderate-to-severe neutropenia during treatment.

Ganciclovir is specifically indicated for both induction and maintenance treatment of CMV retinitis in
immunocompromised patients, and for the prevention of CMV infection in transplant recipients. In
addition to its published benefits in the treatment of congenital CMV infection, ganciclovir has also
been shown to be effective in the treatment of active CMV pneumonitis, gastroenteritis, and
retinitis, but outcomes are dependent on the patients’ primary illness and overall degree of immune
suppression. As such, patients treated with ganciclovir have variable clinical responses to
treatment. Ganciclovir treatment of primary CMV pneumonitis following renal transplantation shows
the highest success. While ganciclovir treatment in bone marrow transplant patients with CMV
pneumonia reduces viremia and clears CMV from the respiratory secretions, mortality from CMV
disease in this context remains high.

PREP Pearls

Ganciclovir for injection is very alkaline, so it can cause local chemical irritation to the vein

Bone marrow suppression is the most common and expected adverse effect seen during
treatment with ganciclovir and may become severe enough to warrant dose reduction or
stopping the medication altogether.

Suggested
Readings
Kimberlin DW, Jester PM, Sánchez PJ et al. Valganciclovir for symptomatic congenital
cytomegalovirus disease. N Engl J Med. 2015;372:933-943. doi:
http://dx.doi.org/10.1056/NEJMoa1404599

January
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Question: 6

You are asked to see a 14-year-old previously healthy adolescent who presented with a 1-week history of
a rash on his back and neck. He has been otherwise well without any systemic symptoms. On physical
examination, he appears well and has several scattered scaly patches on his neck, back, and upper trunk
(Figure 1). The patches are white, tan, and pink in color and some are coalescing. A KOH preparation
from scrapings of one of the patches is done and is shown in Figure 2.

Of the following, the organism that is MOST likely responsible for this infection is

A. Microsporum canis

B. Pityrosporum orbiculare

C. Trichophyton rubrum

D. Trichophyton tonsurans
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Figure 1. Scaly
patches
Reprinted with permission from the American Academy of Pediatrics. In: Kimberlin
DW, Brady MT, Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee
on Infectious Disease. 30th ed. Elk Grove Village, IL: American Academy of Pediatrics;
2015:622-624. Copyright © Edward Marcuse, MD.
Figure 2. KOH preparation from scaly patches. Reprinted with permission from the
American Academy of Pediatrics. In: Kimberlin DW, Brady MT, Jackson MA, Long SS,
0th ed. Elk
eds. Red Book: 2015 Report of the Committee on Infectious Disease. 3
Grove Village, IL: American Academy of Pediatrics; 2015:622-624
Reprinted with permission from the American Academy of Pediatrics. In: Kimberlin DW, Brady MT,
Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee on Infectious Disease. 3 0th
ed. Elk Grove Village, IL: American Academy of Pediatrics; 2015:622-624.

January
Print
Question: 6

Of the following, the organism that is MOST likely responsible for this infection is

A. Microsporum canis

B. Pityrosporum orbiculare

C. Trichophyton rubrum

D. Trichophyton tonsurans
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INCORRECT 
Correct Answer: B Average Correct: 47.92%

The patient in the vignette most likely has pityriasis versicolor (formerly known as tinea versicolor),
based on the characteristic findings of fine scaly, and well-demarcated skin patches, which can be
of varying colors, including brown, tan, pink, or white. These patches are most commonly found on
the neck, upper back, and trunk, and in infants and children, are also commonly seen on the face
and bilateral temple region. This superficial skin infection is more common in boys than girls,
commonly affects adolescents and young adults, and is seen more often during the summer and in
humid and warm climates.

Pityriasis versicolor is caused by Pityrosporum orbiculare, previously known as Malassezia furfur,

a lipophilic yeast which is part of the normal skin flora. Overgrowth of the organism, related to
genetic and environmental factors such as moist heat and lipid-containing sebaceous secretions,
are thought to play a role in pathogenesis. Transformation of the organism from the yeast phase
into the mycelial phase, which then invades the stratum corneum, also is important in
pathogenesis. Microsporum canis, Trichophyton tonsurans, and Trichophyton rubrum are
common causes of dermatophytic infections. T tonsurans is the most common cause of tinea
capitis, while T rubrum is the most common cause of tinea corporis. M canis is a less common
cause of tinea capitis in the United States, but more common in the Mediterranean area. These
agents typically cause individual, rather than multiple, lesions with central clearing and raised
scaling borders. The KOH preparation typically reveals hyphae with multiple branch points, rather
than the “spaghetti and meatball” appearance.

The diagnosis of pityriasis versicolor can be made by scraping a scaly lesion and performing a
KOH preparation. Microscopic examination of this preparation will reveal a typical “spaghetti and
meatball” pattern, which signifies the mycelial and round yeast forms, respectively.

Topical antifungal creams and selenium sulfide lotion/shampoo are generally effective treatments.
Clotrimazole and ketoconazole are 2 common effective topical antifungal agents used. These
agents are usually applied for 2 to 3 weeks for best results. Selenium sulfide shampoo/lotion
typically is used for 5 to 7 days applied for 10 minutes and then showered off. Topical therapy
appears to be equivalent or superior to systemic therapy. Thus, systemic therapy is reserved for
resistant cases or extensive involvement. Systemic agents used to treat pityriasis versicolor,
although not approved by the US Food and Drug Administration for this indication, that have been
shown to be effective include fluconazole

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Pop-up blocker may need to be disabled
and ketoconazole. Return of the normal skin pigment may take months despite clearance of the
infection. There is no standard therapy for recurrent cases, although some experts recommend
monthly topical or oral therapy with the aforementioned agents.

PREP Pearls

Pityriasis versicolor manifests as fine, scaly, well-demarcated macules and patches on the
skin that can be white, tan, brown, or pink in color, and most commonly are found on the
neck, upper trunk, and back.

Pityrosporum orbiculare, previously known as Malassezia furfur, is the cause of

pityriasis versicolor.

Topical antifungal creams and shampoo are generally effective treatments for pityriasis
versicolor.

Suggested
Readings

American Academy of Pediatrics. Pityriasis versicolor (tinea versicolor). In: Kimberlin DW, Brady
MT, Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee on Infectious
Diseases. Elk Grove Village, IL: American Academy of Pediatrics; 2015:622-624.

Gupta AK, Kogan N, Batra R. Pityriasis versicolor: a review of pharmacological treatment

options. Expert Opin Pharmacother. 2005;6(2):165-178. doi:
http://dx.doi.org/10.1517/14656566.6.2.165

Hu SW, Bigby M. Pityriasis versicolor: a systemic review of interventions. Arch Dermatol.

2010;146(10):1132-1140. doi: http://dx.doi.org/10.1001/archdermatol.2010.259
February
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Question: 1

A 16-year-old adolescent girl presents with a 3-week history of itching and skin peeling between her toes
with new development of small pustules in the last week. She swims competitively year- round and is a
lifeguard at the local community center. Examination reveals excoriated, erythematous skin with fissures
between the second, third, and fourth toes and scaling, along with several small vesicles (Figure).

Of the following, the MOST appropriate treatment for this infection is

A. gentian violet

B. nystatin

C. sodium thiosulfate

D. terbinafine

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Assessment Review & Tools

3/20/2017 February | 2017.prepid.courses.aap.org
Figure: Reprinted with permission from American Academy of Pediatrics. In: Kimberlin DW, Brady MT, Jackson MA, Long SS, eds. Red
Book: 2015 Report of the Committee on Infectious Disease. 30th ed. Elk Grove Village, IL: American Academy of Pediatrics;
2015:784786.

February
Print

Question: 1

Of the following, the MOST appropriate treatment for this infection is

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INCORRECT
Correct Answer: D Average Correct: 86.67%
A. gentian violet

B. nystatin

C. sodium thiosulfate

D. terbinafine

The patient in the vignette has tinea pedis (also known as athlete’s foot), which should be treated
with topical therapy, provided tinea unguium is not also present. Of the options listed, terbinafine
is the best therapeutic choice. Terbinafine is applied twice daily for 1 week, not to exceed 4 weeks
in duration. Sodium thiosulfate in the form of a lotion is used


Assessment Review & Tools

to treat tinea versicolor. Nystatin and gentian violet are both used to treat mucocutaneous
candidiasis, the latter of which is reserved for refractory cases, as purple staining of skin and
clothing occurs with use.

Much overlap exists among the indications for use of the topical antifungal agents, with topical
azoles providing good tinea and candidiasis coverage. Topical ketoconazole is also indicated for
use in the setting of seborrhea. Other topical antifungal agents such as terbinafine and tolnaftate
are indicated for treatment of tinea infections, while nystatin and gentian violet are only indicated for
treatment of candidiasis. There is a wide variety of formulations and strengths available for topical
use and length of treatment is dependent upon these preparations (Table).

In addition to prescribing topical antifungal treatments for tinea pedis, education regarding
prevention of recurrence should be provided during the healthcare visit. Education may include
discussion of proper foot hygiene (eg, drying between toes, use of absorbent antifungal foot
powder, frequent airing of affected areas, and avoidance of occlusive footwear and nylon socks or
other materials that prevent moisture dissipation).

PREP Pearls

Education for prevention of recurrent cutaneous fungal infections should occur

alongside antifungal treatment.

Gentian violet may be used for topical Candida albicans infections recalcitrant to topical
nystatin, clotrimazole, and miconazole, but purple skin discoloration may occur.

American Board of Pediatrics Content

Specification(s)

Know the use of topical drugs/treatments for superficial fungal infections (clotrimazole,
ketoconazole, miconazole, cystatin, tolnaftate, terbinafine, gentian violet, sodium thiosulfate)

Suggested
Readings

American Academy of Pediatrics. Tinea pedis and tinea unguium. In: Kimberlin DW, Brady MT,
Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee of Infectious Diseases.
30th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2015: 784-786.
http://redbook.solutions.aap.org/chapter.aspx?sectionid=88187254&bookid=1484

Rotta I, Otuki MF, Conegero Sanches AC, Januario Correr C. Efficacy of topical antifungal drugs
in different dermatomycoses: a systematic review with meta-analysis. Rev Assoc Med Bras.
2012;58(3):308-318.
Table. Topical Antifungal Agents, Formulations, and Applications for Common Cutaneous Fungal
Infections.
Drug Indication Formulations Application Clotrimazole Mucocutaneous candidiasis, tinea pedis,
tinea cruris, tinea corporis
Cream, solution, troche Topical-Twice daily
Troche-5 times daily Vaginal candidiasis= 7-day, 3-day, and 1-dose
formulations available
Ketoconazole Mucocutaneous candidiasis, tinea pedis, tinea
cruris, tinea corporis, seborrhea
Cream, gel, foam, shampoo Shampoo- twice weekly for 4 weeks
Topical- 1 to 2 times daily
Miconazole Vulvovaginal candidiasis, tinea pedis, tinea
cruris, tinea corporis
Ointment, cream powder, solution,
spray powder, spray lotion
Tinea pedis/corporis= Twice daily for 4 weeks Tinea cruris= Twice daily for 2 weeks Vaginal
candidiasis= 7-day, 3-day, and 1 dose
formulations available
Nystatin Mucocutaneous candidiasis Cream, ointment, powder,
intravaginal tablet
Infants-4 times daily on each side of mouth Cutaneous-2 to 4 times daily Vaginal- 1 tablet at
bedtime daily for 2 weeks
Tolnaftate Tinea pedis, tinea cruris, tinea corporis, tinea
manuum, tinea versicolor
Cream, spray, gel, spray lotion,
powder, spray powder
2 to 3 times daily for 2 to 4 weeks
Terbinafine Tinea pedis, tinea cruris, tinea corporis, tinea
versicolor
Cream, gel, solution 1 to 2 times daily depending on formulation for
one week
Gentian violet Mucocutaneous candidiasis Solution 0.25% to 2% Infants- 3 to 4 drops under the
tongue or on the
lesion after feedings for 3 days Children/Adults- 2 to 3 times daily for 3 days
Sodium thiosulfate Tinea versicolor Lotion 25% Twice daily for weeks to months
Courtesy of A Myers, MD

February
Print
Question: 2
A 29-day-old extremely low birthweight baby in the neonatal intensive care unit (NICU)
had 4 days of positive blood cultures. On day 24 of life, she developed
thrombocytopenia (platelet count, 61 x 10 3 /μL [61 x 10 9 /L]) and apnea with
bradycardia; white blood cell count was 25 x 10 3
/μL (25 x 10 9
/L) with 15% bands, 80% segmented neutrophils, and 5% lymphocytes. Vancomycin
and ceftazidime were started. The blood cultures grew a Gram-positive,
catalase-negative coccobacillus in pairs and chains, which the microbiology laboratory
had trouble identifying. Cerebrospinal fluid cultures were negative. Repeat blood
cultures over the next 4 days continued to grow the bacterium and the percutaneous
intravenous central catheter was removed. The laboratory reported the minimum
inhibitory concentrations (MIC) in mg/mL of the isolate as follows: vancomycin greater
than256, penicillin 0.125, ceftriaxone 12, clindamycin 0.19, and meropenem 3. The
antibiotic was changed to ampicillin, the subsequent blood cultures were sterile, and
infection was treated successfully.
Of the following organisms, the ones MOST likely to have intrinsic vancomycin
resistance that may be responsible for this patient’s infection are
A. Abiotrophia, Bacillus, Peptostreptococcus
B. Aerococcus, Micrococcus, Stomatococcus
C. Corynebacterium, Clostridium, Listeria
D. Gemella, Leuconostoc, Pediococcus
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Question: 2
A 29-day-old extremely low birthweight baby in the neonatal intensive care unit (NICU)
had 4 days of positive blood cultures. On day 24 of life, she developed
thrombocytopenia (platelet count, 61 x 10 3 /μL [61 x 10 9 /L]) and apnea with
bradycardia; white blood cell count was 25 x 10 3
/μL (25 x 10 9
/L) with 15% bands, 80% segmented neutrophils, and 5% lymphocytes. Vancomycin
and ceftazidime were started. The blood cultures grew a Gram-positive,
catalase-negative coccobacillus in pairs and chains, which the microbiology laboratory
had trouble identifying. Cerebrospinal fluid cultures were negative. Repeat blood
cultures over the next 4 days continued to grow the bacterium and the percutaneous
intravenous central catheter was removed. The laboratory reported the minimum
inhibitory concentrations (MIC) in mg/mL of the isolate as follows: vancomycin greater
than256, penicillin 0.125, ceftriaxone 12, clindamycin 0.19, and meropenem 3. The
antibiotic was changed to ampicillin, the subsequent blood cultures were sterile, and
infection was treated successfully.
Of the following organisms, the ones MOST likely to have intrinsic vancomycin
resistance that may be responsible for this patient’s infection are
A. Abiotrophia, Bacillus, Peptostreptococcus
B. Aerococcus, Micrococcus, Stomatococcus
C. Corynebacterium, Clostridium, Listeria
D. Gemella, Leuconostoc, Pediococcus
INCORRECT
View Peer Results Correct Answer: D Average Correct: 60.00%
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Gemella, Leuconostoc, and Pediococcus organisms are catalase-negative,

Gram-positive cocci that display intrinsic high-level vancomycin resistance which is
unrelated to the acquired vancomycin resistance observed in enterococci and
staphylococci. The baby in the vignette had sepsis from Leuconostoc species, however,
any 1 of these 3 organisms could be the causative bacteria.
The remaining bacteria in the response choices are Gram-positive bacteria that do not
possess intrinsic resistance to vancomycin. Catalase is a test mainly used to distinguish
staphylococci from streptococci. Bacillus, Corynebacterium, Listeria, and Micrococcus
are catalase-positive; Abiotrophia, Aerococcus, Clostridium, and Peptostreptococcus
are catalase-negative. Stomatococcous may be weakly catalase-positive or -negative
(Figure).
Gemella species are facultative anaerobic Gram-positive diplococcus, which are
obligate fermentative, producing either a mixture of acetic and lactic acids in the
absence of oxygen,
or an equimolar mixture of acetic acid and CO 2
, when oxygen is present. While the cellular morphology of most Gemella species
resembles that of streptococci, some form Neisseria- like diplococci that may also be
arranged in tetrads and clusters and may appear to be Gram-variable.
Leuconostoc and Pediococcus are bacteria well known to food microbiologists and the
food and dairy industry because these species occur in various foods and on
vegetation. They are known as lactic acid bacteria because they produce lactic acid as
the principle by- product of sugar fermentation. Leuconostoc are responsible for the
fermentation of sugars in fresh cabbage, transforming it into sauerkraut, as well as the
cause of the stink when creating a sourdough starter. Similarly, they are part of the
symbiotic colonies of microbes involved in the fermentation of kefir, a fermented milk
beverage. Pediococcus bacteria are usually considered contaminants of beer and wine,
although their presence is sometimes desired in beer styles such as lambic. Certain
Pediococcus isolates produce diacetyl, which gives a buttery or butterscotch aroma to
some wines (such as chardonnay) and a few styles of beer. Pediococcus species are
often used as probiotics, in silage (fermented, high- moisture stored fodder that can be
fed to ruminants or used as a biofuel feedstock for anaerobic digesters), and as
beneficial microbes in the creation of cheeses and yogurts.
Gemella, Leuconoctoc, and Pediacoccus species are part of the normal oral,
gastrointestinal tract, and vaginal flora of humans and many other mammals, and are
uncommon causes of disease in humans. Infective endocarditis, meningitis, pneumonia,
sepsis, and abdominal andocular infections have been reported in immunocompromised
and cancer patients, infants with short bowel syndrome, and preterm extremely low
birthweight neonates.
Standard commercial identification kits are often unable to identify Leuconostoc, Gemella, and
Pediococcus organisms, frequently being misidentified as a viridans streptococci. When
vancomycin resistance is identified, there should be a high index of suspicion for one of these
organisms. The mechanism of resistance to vancomycin involves the alteration of the peptidoglycan
synthesis; there is also cross-resistance to teicoplanin. Organisms are generally susceptible to
penicillin and aminoglycosides, but the minimum inhibitory concentrations should be confirmed in
the microbiology laboratory. Most resistance to glycopeptide antibiotics among other Gram-positive
organisms is acquired resistance, generally observed in enterococci with recent spread to
Staphylococcus aureus.

PREP Pearls

Gemella, Leuconostoc, and Pediococcus species are catalase-negative, Gram-positive

cocci that display intrinsic high-level vancomycin resistance.
Organisms are generally susceptible to penicillin and aminoglycosides, but the
minimum inhibitory concentrations should be confirmed in the microbiology
laboratory.

Standard commercial identification kits are often unable to identify Leuconostoc, Gemella,
and Pediococcus organisms, with them frequently being misidentified as a viridans
streptococci. 7

These organisms are part of the normal oral, gastrointestinal tract, and vaginal flora of
humans and many other mammals, and are uncommon causes of disease in humans.

American Board of Pediatrics Content

Specification(s)

Understand the clinical significance of infections with Pediococcus, Leuconostoc, or

Gemella species, and the antimicrobial susceptibilities

Suggested
Readings

Barton LL, Rider ED, Coen RW. Bacteremic infection with Pediococcus: vancomycin-resistant
opportunist. Pediatrics. 2001;107(4):775-776.
http://pediatrics.aappublications.org/content/107/4/775

Carano N, Agnetti A, Allegri V, et al. Infective endocarditis following body piercing: presentation of
one case due to Gemella morbillorum and review of the literature. Med Sci Monit.
2010;16(10):CS124-CS218. http://www.medscimonit.com/download/index/idArt/881184

Lee MR, Huang YT, Lee PI, et al. Healthcare-associated bacteremia caused by Leuconostoc
species at a university hospital in Taiwan between 1995 and 2008. J Hosp Infect.
2011;78(1):45-49. doi: http://dx.doi.org/10.1016/j.jhin.2010.11.014

Figure. Identification of gram-positive cocci by catalase result. Courtesy of K

Moffett, MD
February
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Question: 3

You are evaluating an 18-month-old child for a 3-day history of fever and rash. The rash was initially
described as papular, but has evolved with the development of vesicular lesions on a erythematous base.
There has been continued development of new lesions. The child has been previously well. He attends a
childcare center 5 days per week.

The mother has elected to delay live vaccines for this child due to her concern over their possible
association with autism.

Physical examination reveals an uncomfortable, but nontoxic child. His temperature is 39.1°C and his other
vital signs are stable. Examination is otherwise notable for an erythematous pharynx with vesicular lesions on
the palate, as shown in Figure 1 and Figure 2.

The nurse from the patient’s childcare center calls requesting advice for managing those exposed to this
child.

Of the following, the MOST appropriate control measure to advise would be to

A. administer varicella vaccine for exposed children and staff without evidence of immunity

within 3 to 5 days of the exposure

B. exclude children from this classroom from attending the center from 10 to 21 days after
this exposure

C. provide varicella-zoster immune globulin (VariZIG) for all children younger than 1 year of

age in the classroom

D. start acyclovir beginning 7 days after the exposure for all unvaccinated children in the

classroom
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Assessment Review & Tools

Figure 1. Erythematous pharynx with vesicular lesions
on the palate in the patient in the vignette.

Reprinted with permission from the American Academy of Pediatrics.

In: Kimberlin DW, Brady MT, Jackson MA, Long SS, eds. Red Book:
2015 Report of the Committee on Infectious Disease. 3 0th ed. Elk
Grove Village, IL: American Academy of Pediatrics; 2015:845-860.
http://redbook.solutions.aap.org/chapter.aspx?sectionId=88187270&b
ookId
Figure 2. Erythematous and vesicular lesions in the
patient in the vignette

Reprinted with permission from the American Academy of

Pediatrics. In: Kimberlin DW, Brady MT, Jackson MA, Long
SS, eds. Red Book: 2015 Report of the Committee on
Infectious Disease. 3 0th ed. Elk Grove Village, IL: American
Academy of Pediatrics; 2015:845-860.
http://redbook.solutions.aap.org/chapter.aspx?sectionId=881
872 70&bookId=1484&resultClick=1#91042010

February
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Question: 3

The mother has elected to delay live vaccines for this child due to her concern over their possible
association with autism.

The nurse from the patient’s childcare center calls requesting advice for managing those exposed to this
child.

Of the following, the MOST appropriate control measure to advise would be to

A. administer varicella vaccine for exposed children and staff without evidence of immunity

within 3 to 5 days of the exposure

B. exclude children from this classroom from attending the center from 10 to 21 days after

this exposure

C. provide varicella-zoster immune globulin (VariZIG) for all children younger than 1 year of

age in the classroom

D. start acyclovir beginning 7 days after the exposure for all unvaccinated children in the

classroom


INCORRECT
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Correct Answer: A Average Correct: 75.56%

The child in the vignette clearly has varicella (chickenpox) based on the picture of the rash and the
evolution of sequential crops of vesicular lesions. Varicella-zoster virus in cases of chickenpox is highly
contagious via infected secretions transmitted onto mucosal surfaces of susceptible individuals. Direct
contact with vesicular lesions or airborne spread may also occur, but less commonly than by contact
with infected secretions. Based on this high degree of contagion, control measures to prevent
additional spread of the virus in the child care setting are recommended.

Varicella is now an uncommon disease in childhood and in child care settings. Children with varicella
should be excluded from child care until all lesions have crusted, which usually occurs on the sixth day
after onset of rash. Immunized children with breakthrough varicella with only maculopapular lesions can
return to childcare or school if no new lesions have appeared within a 24-hour period. All staff members
and parents should be notified when a case of varicella occurs; they should be informed about the
greater likelihood of serious infection in susceptible adults and adolescents and in susceptible
immunocompromised people. There also exists for the potential for fetal sequelae if infection occurs in
a pregnant woman. Less than 5% of adults born in the United States may be susceptible to
varicella-zoster virus. Adults without evidence of immunity should be offered 2 doses of varicella
vaccine unless contraindicated. Susceptible childcare staff members who are pregnant and exposed to
children with varicella should be referred promptly to a qualified physician or other healthcare
professional for counseling and management.

The American Academy of Pediatrics and US Centers for Disease Control and Prevention (CDC)
recommend use of varicella vaccine in nonpregnant immunocompetent people 12 months of age or
older without evidence of immunity within 3 days, but up to 5 days after exposure to varicella. During a
varicella outbreak, people who have received 1 dose of varicella vaccine should, resources permitting,
receive a second dose of vaccine, provided the appropriate interval has elapsed since the first dose (3
months for children 12 months through 12 years of age; at least 28 days for people 13 years of age
and older). Of the measures listed in the vignette, vaccine for susceptible staff within 3 to 5 days of the
exposure (provided they do not have contraindication to receipt of the vaccine) is the correct response.
A second dose of vaccine should be given more than 28 days after the initial vaccination. For adults,
the Advisory Committee on Infectious Diseases defines evidence of immunity to varicella to include:

1. Documentation of receipt of age-appropriate varicella vaccination 2.

Laboratory confirmation of disease or evidence of immunity
3. Birth before 1980 4. Healthcare provider diagnosis or verification of varicella or
herpes-zoster infection

Although the incubation period for varicella infection is 10 to 21 days excluding all children, including
those with appropriate vaccination status, would not be indicated to control further spread.

Prophylactic antiviral therapy with acyclovir beginning 7 to 10 days after exposure may attenuate, if
not prevent, development of clinical disease, but has not been as well studied as vaccine for control
of an outbreak after exposure.

Varicella–zoster immune globulin (VariZIG) as soon as possible after exposure (ideally within 96 hours
and up to 10 days) may prevent or modify the course of infection after exposure, but is recommended
for immunocompromised patients, neonates whose mothers have varicella from 5 days before to 2
days after delivery, premature neonates exposed postnatally, and susceptible pregnant women. If
VariZIG is not available, immune globulin intravenous may be utilized.

PREP Pearls

Varicella vaccination of susceptible healthy individuals administered within 3 to 5 days after

exposure to an active case of chickenpox can be used to control an outbreak of varicella.

Antiviral therapy with acyclovir may be useful in susceptible individuals exposed to a case of
varicella when administered beginning 7 to 10 days after the exposure, but is less well studied for
outbreak control.

Varicella-zoster immune globulin (VariZIG) may be useful in preventing or ameliorating

disease in high-risk individuals.

American Board of Pediatrics Content

Specification(s)

Make recommendations for child-care center attendees and staff members for control of varicella

Make recommendations to a child-care center for control of varicella-zoster infection

Suggested
Readings

American Academy of Pediatrics. Infectious diseases—epidemiology and control. In: Kimberlin DW,
Brady MT, Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee on Infectious
Disease. 30th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2015:137- 147.

February
Print

Question: 4

A 9-year-old girl who was adopted from an orphanage in Asia at 18 months of age is referred to you for
further evaluation of abnormal findings on an ophthalmologic examination after complaining of progressively
worsening blurry vision in her left eye over a 4-month period. Findings of the ophthalmologic examination of
her left eye include anterior uveitis, interstitial keratitis, and a small pupil that constricts slowly with direct light.
The remainder of her physical examination is completely normal. By history, the patient was found
abandoned shortly after birth and lived in a poor, rural orphanage until she was adopted. Screening
laboratory tests performed at the time of adoption showed a negative tuberculin skin test, negative hepatitis B
serology, negative HIV, and negative stool examination for ova and parasites. Since being adopted, the
patient has been doing well with no hospitalizations or surgeries. She has no pets and no history of travel
outside the United States. There is no history of consumption of raw meats or unpasteurized milk or cheese.

Of the following, the tests that would help to establish the diagnosis in this patient is

A. cerebrospinal fluid, serum, and urine histoplasma antigen

B. cerebrospinal fluid venereal disease research laboratory and serum treponemal test

C. Toxoplasma cerebrospinal fluid polymerase chain reaction and serum antibody titers

D. tuberculin skin test and interferon-γ release assay

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Question: 4
A 9-year-old girl who was adopted from an orphanage in Asia at 18 months of age is
referred to you for further evaluation of abnormal findings on an ophthalmologic
examination after complaining of progressively worsening blurry vision in her left eye over
a 4-month period. Findings of the ophthalmologic examination of her left eye include
anterior uveitis, interstitial keratitis, and a small pupil that constricts slowly with direct light.
The remainder of her physical examination is completely normal. By history, the patient
was found abandoned shortly after birth and lived in a poor, rural orphanage until she was
adopted. Screening laboratory tests performed at the time of adoption showed a negative
tuberculin skin test, negative hepatitis B serology, negative HIV, and negative stool
examination for ova and parasites. Since being adopted, the patient has been doing well
with no hospitalizations or surgeries. She has no pets and no history of travel outside the
United States. There is no history of consumption of raw meats or unpasteurized milk or
cheese.
Of the following, the tests that would help to establish the diagnosis in this patient is
A. cerebrospinal fluid, serum, and urine histoplasma antigen
B. cerebrospinal fluid venereal disease research laboratory and serum treponemal test
C. Toxoplasma cerebrospinal fluid polymerase chain reaction and serum antibody titers
D. tuberculin skin test and interferon-γ release assay
INCORRECT
View Peer Results Correct Answer: B Average Correct: 55.56%
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The patient described in the vignette has an abnormal ophthalmologic examination with findings of left
eye anterior uveitis, interstitial keratitis, and a small pupil that constricts slowly with direct light. Infection
with Histoplasma, syphilis, tuberculosis, and Toxoplasma all may have ocular findings associated with
them, however, the pupillary abnormality Argyll Robertson pupil is classic for syphilis and is not found
with the other infections. This patient is presenting with a neurosyphilis syndrome of tertiary syphilis.

Genital vesiculoulcerative diseases (GVUD) are sexually transmitted diseases that have a major
impact on morbidity and mortality in many countries, partially because of their ability to enhance the
rate of sexual transmission of HIV. The different causes of GVUD are shown in Table 1.

For all these infections, presumptive treatment should be given to all patients from endemic areas
who have been clinically diagnosed with the disease.

Genital herpes is most commonly caused by herpes simplex virus types 1 and 2 (HSV-1, HSV-2) and is
a lifelong infection that may result in painful and recurrent genital lesions (Figure 1) and systemic
complications. Genital HSV transmission is usually the result of close contact with a person who is
shedding virus at a peripheral site, at a mucosal surface, or in genital or oral secretions. The person
may be asymptomatic and are unaware that they are infected. Infection occurs by inoculation of virus
onto susceptible mucosal surfaces or through small cracks in the skin.

The first episode of primary genital herpes is associated with prolonged duration of symptoms, lesions
(10 to 12 days), and viral shedding. In 70% of women and 40% of men, first-episode genital herpes is
accompanied by fever, headache, malaise, and myalgias. Pain, itching, dysuria, vaginal and urethral
discharge, and tender inguinal lymphadenopathy are the predominant local symptoms and persist for
several days after the appearance of the systemic symptoms. Lesions may be present in varying
stages, including vesicles, pustules, painful erythematous ulcers, crusting, or re-epithelialization.
Multiple small ulcers often coalesce into one larger ulcer. The mean time from the onset of a primary
genital HSV lesion to complete healing is 19.5 days for women and 16.5 days for men. Both HSV-1 and
HSV-2 can cause symptomatic or asymptomatic rectal and perianal infection. Herpes simplex virus
proctitis is usually associated with rectal intercourse. Symptoms include anorectal pain, discharge,
tenesmus, and constipation. Ulcerative lesions are present in the distal 10 cm of the rectal mucosa.
Extragenital lesions commonly develop during the course of primary genital herpes and are more
common in women than in men. These lesions most frequently occur in the buttock, groin, or thigh
area, however, the fingers and eyes can also be involved. The clinical diagnosis of genital herpes is
both insensitive and nonspecific, especially in areas endemic for other GVUD because the appearance
of the lesions may be similar. Therefore, the clinical diagnosis should be confirmed by laboratory
testing, which includes HSV isolation in cell culture or real- time PCR assay.
Infants acquire HSV infection through contact with HSV-infected secretions, usually at the time of
delivery. Ninety percent of neonatal herpes is perinatally acquired, 5% to 8% is congenital, and a few
infections are acquired postnatally. Of the 70% of neonatal HSV infections caused by HSV-2, almost
all result from contact with infected genital secretions during delivery. The highest risk for transmitting
HSV in the perinatal period occurs during the acquisition of HSV near the time of labor. Neonatal
HSV-1 infections may also be acquired through postnatal contact with healthcare workers or
immediate family members who have symptomatic or asymptomatic orolabial HSV-1 infection. Infants
born by cesarean delivery to women before the rupture of membranes or by vaginal delivery to women
with no evidence of recent HSV infection are at minimal risk for the development of HSV infection.

The goal of management of genital herpes with antiviral drugs is to ease the signs and symptoms of
genital herpes. In randomized placebo-controlled trials, antiviral therapy resulted in faster resolution of
symptoms, lesion healing, decreased viral shedding, and prevention of new lesions. However, the
antiviral drugs do not eradicate latent virus or affect the risk, frequency, or severity of recurrences after
the drug is discontinued. Episodic treatment of recurrent herpes is useful in patients with multiple
recurrences. Effective episodic treatment of recurrent herpes requires initiation of therapy within 1 day
of lesion onset or during the prodrome that precedes some outbreaks. Suppressive therapy reduces
the frequency of genital herpes recurrences by 70% to 80%, especially in patients who have frequent
recurrences (defined as > 6 recurrences per year).

An estimated 60% to 70% of HIV-infected individuals in the United States and nearly 80% to 95%
in Africa are seropositive for HSV-2. The relative risk for HIV seroconversion among patients with
genital herpes varies from 1.2 to 8.5.

Acyclovir may be administered orally to pregnant women with their first episode of genital herpes or
severe recurrent herpes, but intravenous therapy should be used in patients with severe HSV infection.
Acyclovir treatment late in pregnancy reduces the frequency of caesarean deliveries among women
who have recurrent genital herpes by diminishing the frequency of recurrences at term. Caesarean
deliveries should be considered for women with recurrent genital herpes at the onset of labor.
Recurrent genital herpes at any other time during pregnancy is not an indication for caesarean delivery.

Granuloma inguinale (Donovanosis) is a mildly contagious, chronic progressive infection usually of the
genital region caused by the encapsulated, Gram-negative bacterium Klebsiella granulomatis that is
endemic in many parts of the world including India, Papua New Guinea, the Caribbean, Brazil, the
Guyannas, South Africa, Zambia, Vietnam, and in Australian aboriginals. It is a rare disease in the
United States, with fewer than 100 cases reported annually. The disease is assumed to be sexually
transmitted, however, extragenital lesions and lesions in young children indicate alternative modes of
spread. Donovanosis begins as small firm, painless, subcutaneous nodules or papules that gradually
increase in size and ulcerate. The ulcerated lesions become hypertrophic, beefy red, granulomatous,
and friable with rolled
edges and a characteristic velvet-like surface. Untreated lesions may either spontaneously resolve or
persist and slowly spread (Figure 2). Donovanosis may also manifest as ulcerogranulomatous,
hypertrophic, sclerotic, and necrotic lesions. Inguinal nodes are involved and infection may spread to
the overlying tissues, resulting in either abscess formation (pseudobubo) or ulceration. Complications
include hemorrhage, genital lymphedema, genital mutilation and cicatrization, development of
squamous cell carcinoma, and rarely, hematogenous dissemination to bone, joints, and viscera.
Donovanosis must be distinguished from other causes of GVUD. Diagnosis can be established by
demonstration of Donovan bodies in the tissue smears and/or histopathologic examination of biopsy
specimens and by isolation of K granulomatis in culture. Treatment of Donovanosis should be
continued for at least 3 weeks and until all lesions have completely healed. Healing typically proceeds
inward from the ulcer margins. Relapse can occur 6 to 18 months after apparently effective therapy.
Some experts recommend the addition of an aminoglycoside to the treatment regimens if improvement
is not evident within the first few days of therapy. Patients with both donovanosis and HIV infection
should receive the same treatment regimens as those who are HIV negative, however, consideration
should be given to the addition of a parenteral aminoglycoside to the treatment regimen. Donovanosis
is associated with an increased risk of acquiring and transmitting HIV.

Chancroid (granuloma venereum) infection is found mainly in the tropics and subtropics and only
occurs sporadically in the developed world, usually in individuals who have recently returned from
chancroid endemic areas or occasionally within the context of localized urban outbreaks associated
with commercial sex work. It is caused by the Gram-negative coccobacillus, Haemophilus ducreyi.
Chancroid starts as a tender erythematous, nonindurated papule that may develop 4 to 7 days after
exposure which then becomes a pustule. The pustules rupture after 2 to 3 days to form shallow painful
ulcers that have granulomatous bases and purulent exudates. The ulcer edge is typically ragged and
undermined and bleeds easily when scraped (Figure 3). Chancroid can present atypically with multiple
ulcers that coalesce to form a giant ulcer. Naturally occurring chancroid is usually more prevalent in
men compared to women. Lesions typically occur on the prepuce and frenulum in men and on the
vulva, cervix, and perianal area in women. Painful, tender, inguinal lymphadenopathy occurs in up to
50% of cases and the lymph nodes may develop into buboes. The lymphadenopathy is usually
unilateral and tends to be more prevalent in men. If not aspirated or drained, fluctuant buboes can
rupture spontaneously. It may be spread to other extragenital anatomical sites by auto-inoculation, and
lesions may be seen on the inner thighs, breast, and fingers. Since there is an overlap in the
presentation of chancroid with other GVUD, the diagnosis should be confirmed by demonstration of
Gram-negative coccobacilli on Gram-stained smear and isolation of H ducreyi in culture of scrapings
from the ulcer base or of pus aspirated from the suppurative lymph nodes. Like other GVUD, chancroid
facilitates the transmission of HIV. HIV has been detected in chancroid ulcer material obtained from
both men and women and chancroid ulcers contain numerous CD4-positive T lymphocytes, which may
increase the susceptibility of an individual infected with chancroid to subsequent infection by HIV.
Mixed infections with other agents, including HSV and Treponema pallidum are well described. In the
absence of effective antimicrobial therapy, the ulcerations can take several weeks to months to
resolve. Treatment with appropriate antimicrobial therapy usually results in symptomatic improvement
within 3 days and cure of the infection within 7 days. The time required for complete healing depends
on the size of the ulcer. In addition, healing is slower for some uncircumcised men who have ulcers
under the foreskin. Clinical resolution of fluctuant lymphadenopathy is slower than resolution of the
ulcers and may require needle aspiration or incision and drainage. Pregnant women should be treated
with either the erythromycin or ceftriaxone regimens.

Lymphogranuloma venereum (LGV) is a systemic disease caused by 1 of 3 invasive serovars L1, L2,
or L3 of Chlamydia trachomatis. It is endemic in several tropic areas, including East, West, and
Southern Africa, Madagascar, India, South-East Asia, Papua New Guinea, and some Caribbean
islands. Since 2003, there have been a series of LGV outbreaks reported in several European cities,
starting in the Netherlands, and occurring mostly among HIV-positive men who have sex with men.
There are 3 distinct stages to LGV. The first stage is the development of an evanescent genital ulcer or
papule at the site of inoculation. The primary lesion is transient and often overlooked given that the
lesion is in the form of a painless papule, pustule, or shallow erosion. It is found on the coronal sulcus
of males and on the posterior vaginal wall, fourchette, or on the vulva, and occasionally on the cervix
of females. Lymphadenopathy commonly develops from a few days to weeks (10 to 30 days) after the
primary lesion and heralds the secondary stage. The most common clinical manifestation of LGV
during this stage is tender inguinal and/or femoral lymphadenopathy that is typically unilateral (66% of
cases). When both inguinal and femoral lymph nodes are involved, they may be separated by the
inguinal ligament, the so called “groove sign,” which is considered pathognomonic of LGV but only
occurs in 15% to 20% of cases. The lymph nodes become matted with considerable periadenitis and
bubo formation. The nodes may ulcerate and discharge purulent material from multiple points, creating
chronic draining fistulae (Figure 4). The secondary stage is also marked by systemic manifestations
that include fever, headache, and myalgias. Women often also have backache and pelvic pain from
enlarged, inflamed pelvic lymph nodes. Meningitis may also occur. The vast majority of patients
recover after the secondary stage without sequelae, however, some patients progress to have a
chronic third stage of disease that is marked by persistent or progressive spread of the infection into
the anogenital tissues, resulting in a chronic inflammatory response and destruction of tissues in the
involved areas. This leads to fistulae, strictures, and a chronic granulomatous enlargement and
ulceration of the vulva, scrotum, and penis. Rectal disease results in LGV proctocolitis that leads to
chronic, colorectal/anorectal fistulas and strictures, urethral strictures, perianal abscess, ischiorectal
abscess, and fistulas.

Diagnosis of LGV is difficult and requires a combination of high clinical suspicion and supportive
tests. LGV can be suspected with positive chlamydial serology, isolation of C trachomatis from the
infected site or histologic identification of Chlamydia in infected tissue. Treatment is aimed at curing
the infection and preventing complications. The US Centers of Disease Control and Prevention
recommends that individuals who have had sexual contact
with a person who has LGV within 60 days before onset of the patient’s symptoms should be
examined, tested for urethral or cervical chlamydial infection, and treated with a standard chlamydia
regimen (azithromycin 1 g perioral once daily or doxycycline 100 mg perioral twice daily for 7 days).
Pregnant and lactating women should be treated with erythromycin. Fluctuant buboes should be
aspirated through healthy adjacent skin and surgical incision is usually contraindicated due to a high
risk of complications. As with other GVUD, LGV increases the risk for acquiring HIV.

Syphilis is caused by the bacterium Treponema pallidum and is acquired either via sexual contact or
transmitted vertically from mother to baby. Acquired syphilis can be divided into primary, secondary,
latent, and tertiary stages. The primary lesion or chancre usually presents as an indurated, solitary,
painless lesion, however, the lesion may be atypical and may be soft, painful and there may be
multiple lesions. A painful chancre may also result from coinfection with chancroid or genital herpes.
Secondary syphilis represents the systemic stage of the infection and presents with a generalized rash
affecting the palms and soles, generalized lymphadenopathy, and orogenital mucosal lesions such as
condylomata lata (Figure 5). Latent syphilis is diagnosed by the presence of positive serologic tests in
the absence of clinical evidence of syphilis, and if acquired within the first 2 years is classified as early
latent and after 2 years as late latent. Tertiary syphilis is usually a slowly progressive, destructive
inflammatory process that can affect any organ in the body to produce clinical illness 5 to 30 or more
years after the initial infection. It is subdivided into neurosyphilis, ocular syphilis, cardiovascular
syphilis, and gummatous syphilis.

The diagnosis is stage dependent and requires a combination of clinical and laboratory criteria.
Laboratory diagnosis is made by identification of treponemes using dark field microscopy or via direct
fluorescent antibody stain, staining of the treponemes in a histologic specimen, and by serologic tests.

The vast majority of congenital syphilis cases are believed to arise in utero. The fetus can be infected
during any stage of syphilitic infection in the mother, but it is most likely to occur during the
spirochetemia associated with untreated primary and secondary syphilis, and less frequently during
early latency. Fetal syphilis can occur during the first trimester, however, the risk to the fetus increases
significantly during the second and third trimesters.

There is a strong link between syphilis and HIV infection. Syphilis chancre may transmit HIV by
several mechanisms including:

1) a breach of the epithelial barrier creates a portal of entry or exit for HIV

2) the entry of macrophages and lymphocytes provides receptors for propagation of HIV

3) cytokine production by macrophages enhances HIV replication

4) T pallidum induces the expression of CCR5 on macrophages, and increases transmission of
macrophage trophic HIV-1

Penicillin remains the cornerstone of therapy and the type and duration varies with the stage of
disease. Penicillin is the drug of choice in patients with HIV disease and those that are allergic to
penicillin require desensitization and penicillin therapy for all stages of syphilis.

In patients with HIV, the presentation of GVUD may be more severe and atypical. Table 2 shows some
selected characteristics of GVUD in HIV-infected patients.
PREP Pearls

Genital vesiculoulcerative diseases (GVUD) are sexually transmitted diseases that have a
major impact on morbidity and mortality in many countries. These diseases include: genital
herpes, granuloma inguinale (Donovanosis), granuloma venereum (chancroid),
lymphogranuloma venereum (LGV), and syphilis.

Patients may be coinfected with one or more of these diseases at the same time

Infection with GVUD increases a person’s risk for acquiring HIV infection. Patients with HIV
infection who develop GVUD may have severe, prolonged courses of disease with atypical
presentations.

American Board of Pediatrics Content

Specification(s)

Know the epidemiology and risk for transmission of pathogens causing vesiculoulcerative genital
lesions between sexual partners, and from mother to newborn, regardless of symptoms

Understand the likely clinical course and prognosis of vesiculoulcerative genital lesions, and
the association of these lesions with other infectious pathogens, including HIV

Suggested
Readings

Ballard RC. Klebsiella granulomatis (Donovanosis, granuloma inguinale). In: Bennett JE, Dolin R,
Blaser MJ, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 8th
ed. Philadelphia, PA: Saunders Elsevier; 2015:2664-2666.

Hope-Rapp E, Anyfantakis V, Fouéré S, et al. Etiology of genital ulcer disease. A prospective

study of 278 cases seen in an STD clinic in Paris. Sex Transm Dis. 2010;37(3):153-158. doi:
http://dx.doi.org/10.1097/OLQ.0b013e3181bf5a98

Karthikeyan K. Recent advances in management of genital ulcer disease and anogenital warts.
Dermatol Ther. 2008;21(3):196-204. doi: http://dx.doi.org/10.1111/j.1529-8019.2008.00191.x

Lewis DA. Chancroid: clinical manifestations, diagnosis, and management. Sex Transm Infect.
2003;79(1):68-71. doi: http://dx.doi.org/10.1136/sti.79.1.68

Figure 1. Genital
herpes

Reprinted with permission from the American Academy of Pediatrics. Herpes Simplex.
In: Kimberlin DW, Brady MT, Jackson MA, Long SS, eds. Red Book: 2015 Report of the
Committee on Infectious Disease. 3 0th ed. Elk Grove Village, IL: American Academy of
Pediatrics; 2015:432-445. Courtesy of Larry Frenkel, MD. Available at:
http://redbook.solutions.aap.org/chapter.aspx?sectionId=88187163&bookId=1484&resu
ltClick =1#91036880

Figure 2. Granuloma inguinale

(Donovanosis)
Reprinted with permission from Satter EK. Granuloma Inguinale
(Donovanosis). Medscape. A vailable at:
http://emedicine.medscape.com/article/1052617- overview

Figure 3. Granuloma venereum

(Chancroid)
Reprinted with permission from Nguyen AD. Chancroid in
Emergency Medicine. Medscape. A vailable at:
http://emedicine.medscape.com/article/781520-overview

Figure 4. Lymphogranuloma venereum

(LGV).

Reprinted with permission from Jo EK, Jang JY, Choi SA, Kim YS, Bae DH, Choi HJ,
Lee JH. A case of lymphogranuloma venereum in woman. Korean J Obstet Gynecol.
2011;54(9):566-569. http://dx.doi.org/10.5468/KJOG.2011.54.9.566

Figure 5.
Syphilis
Reprinted with permission from Chandrasekar PH. Syphilis. Medscape.
Available at: http://emedicine.medscape.com/article/229461-overview
Table 1. Causes of Genital Vesiculoulcerative Diseases.

Sexually transmitted disease Causative organism Treatment regimens

xycycline 100 mg PO BID for at least 3 weeks until all lesions
Genital herpes Herpes simplex viruses
healed, Alternative regimens: Azithromycin 1 gram
1&2
once per week for at least 3 weeks until
Primary episode: Acyclovir PO TID for 7-10 days OR
healed, Alternative regimens: Azithromycin 1 gram
Acyclovir PO five times a day for 7-10 days OR Famciclovir
once per week for at least 3 weeks until
250 mg PO TID for 7-10 days OR Valacyclovir 1 gram PO
BID for 7-10 days Episodic treatment: Acyclovir 400 mg all lesions healed, OR Ciprofloxacin 750 mg PO BID for at least
PO TID for 5 days OR Acyclovir 800 mg PO BID for 5 days healed, OR Erythromycin base 500 mg PO QID for at least 3 we
OR Acyclovir 800 mg PO TID for 2 days OR Famciclovir lesions healed, OR Trimethoprim-sulfamethoxazole one double
125 mg PO BID for 5 days OR Famciclovir 1000 mg PO
(160mg.800m
BID for 1 day OR Valacyclovir 500 mg PO BID for 3 days
completely he
OR Valacyclovir 1000 mg PO once a day for 5 days Daily
suppressive therapy for persons infected with HIV nuloma venereum
Acyclovir 400 to 800 mg PO BID to TID OR Famciclovir 500 in 1 gram PO in a single dose, OR
mg PO BID OR Valacyclovir 500 mg PO BID
hancroid
Granuloma inguinale
ftriaxone 250 mg IM in a single dose, OR
(Donovanosis
rofloxacin 500 mg PO BID for 3 days, OR
)
thromycin base 500 mg PO TID for 7 days

mphogranuloma
ereum (LGV)

Doxycycline 100 mg PO BID for at least 3 weeks until all lesions

ocycline 300 mg PO loading dose followed by 200 mg PO
Doxycycline 100 mg PO BID for 21 days Alternative xycycline 100 mg PO BID for 21 days Alternative
regimen: Erythromycin base 500 mg PO QID for 21 days imen: Erythromycin base 500 mg PO QID for 21 days
Minocycline 300 mg PO loading dose followed by 200 mg POocycline 300 mg PO loading dose followed by 200 mg PO
Doxycycline 100 mg PO BID for 21 days Alternative BID for 21 da
regimen: Erythromycin base 500 mg PO QID for 21 days

reatment for primary syphilis and early latent disease:

Syphilis Treponema pallidum T
Benzathine penicillin G 2.4 million units IM in a single dose
Treatment for late latent syphilis or latent syphilis of
unknown duration:: Benzathine penicillin G 3 doses of 2.4 million units IM each at 1
week intervals
Syphilis – Continued . . . Treponema pallidum – io units IM each at 1
Continued . . . week intervals Neurosyphilis or syphilitic eye disease (uveit
Treatment for tertiary syphilis (gumma and cardiovascular
disease): Benzathine penicillin G 3 doses of 2.4
neuroretinitis, and optic neuritis): Aqueous crystalline penicillin G 18 to 24 million units per day,
administered as 3-4 million units IV every 4 hours or continuous
infusion for 10-14 days OR Procaine penicillin 2.4 million unit IM
once daily plus probenecid
500 mg PO QID both for 10-14 days. Congenital syphilis: Aqueous crystalline penicillin G 100,000-150,000
units/kg/day
administered as 50,000 units/kg/dose IV q 12 hours during the
first 7 days of life and every 8 hours thereafter for a total of 10
days OR Procaine penicillin G 50,000 units/kg/dose IM in a
single daily
dose for 10 days Penicillin allergic patients with primary or secondary

syphilis: Doxcycycline 100 mg PO BID for 14 days OR Tetracycline 500 mg PO QID for 14 days Courtesy of TQ

Tan, MD
Table 2. Some Characteristics of Genital Vesiculoulcerative Diseases in HIV-infected
Patients.
Disease Clinical Features Course Treatment Genital Herpes Lesions increased in number
and size and are more painful. The lesions may be progressive, multifocal and coalescing in the
mucocutaneous and anogenital areas. Lesions may be hyperkeratotic, very large, hemorrhagic
and echthymatous. Ulcers present may
commonly at other sites including on the buttock and lower back Presentation of disease may
be atypical with necrotizing lymphadenitis, urinary retention, intestinal obstruction, transverse
myelitis, esophagitis, hepatitis, pneumonitis, and disseminated disease.
Disease is of increased
severity with slow healing of lesions and increase occurrence of recurrent outbreaks
Acute: Acyclovir 400 mg PO TID for 5-10
days Acyclovir 200 mg PO 5 times a day
for 5-10 days Famciclovir 500 mg PO BID for 5-10
days Valacyclovir 1 gram PO BID for 5-10
days Suppressive: Acyclovir 400-800 mg PO BID to TID Famciclovir 500 mg PO BID
Valacyclovir 500 mg PO BID Severe: Acyclovir 5 mg/kg/dose IV q 8 hours
for 7 days Resistant or systemic infection: Foscarnet 40 mg/kg/dose IV q 8
hours Cidofovir 3-5 mg/kg/dose IV q 2
weeks
Granuloma inguinale
(Donovanosis)
Ulcers persist for a very long duration and are slow to heal with a greater incidence of genital
tissue destruction. Ulcers may present more
commonly in extra-genital sites.
Disease is of increased severity. Ulcers may be very slow to heal and treatment failure is more
common.
Timethoprim sulfamethoxazole –
one double strength tablet BID for 3 weeks or until lesions heal Doxycycline 100 mg PO BID for
3
weeks or until lesions heal Alternative regimens: Ciprofloxacin 750 mg BID for 3
weeks or until lesions heal Erythromycin 500 mg QUID for 3
weeks or until lesions heal Azithromycin 1 gram PO once a
week for at least 3 weeks Consider adding gentamicin 1
mg/kg IV q 8 hours for at least 3 weeks if ulcers are very slow to heal
Granuloma venereum
(chancroid)
Ulcers last for longer period
of time and there are greater numbers of ulcers that may be necrotizing. Also may have
mutlilocular buboes. Higher risk of lesions
appearing at atypical sites
Disease has increased
severity with slow healing of the ulcers and higher incidence of treatment failure
Erythromycin 500 mg QID for 7
days Azithromycin 1 gram PO X1
(recommended only with good follow up) Ceftriaxone 250 mg IM as single dose (recommended
only with good follow up)
especially on legs
and digits.
Ciprofloxacin 500 mg PO BIDsease is prolonged Doxycycline 100 mg PO BID for
for 3
day sease is prolonged Doxycycline 100 mg PO BID for
s
nereum
Lymphogranulo
GV)
ma
y systemically ill with rapidly
h developing polymorphic,
and ulcerating, heaped up
crusted lesions sparing
the palms and soles. Late
or tertiary syphilis
weeks Aspiration or incision and drainage presents with
weeks Aspiration or incision and drainage neurosyphilis, ocular
of buboes Alternative regimen: Erythromycin 500 mg PO QID for 3 syphilis, syphilitic
weeks Aspiration or incision and drainage aortitis and
encephalitis
of
tertiary syphilis
buboes
and
Syphilis Primary disease presents neurosyphilis.
Rapid progression Treatment same as for those
to that are not HIV-infected,
Treatment same as for those however, higher rates of
that are not HIV-infected, treatment failure and relapse
however, higher rates of inspite adequate therapy
treatment failure and relapse Treatment same as for those
inspite adequate therapy that are not HIV-infected,
Treatment same as for those however, higher rates of
that are not HIV-infected, treatment failure and relapse
however, higher rates of inspite adequate therapy
treatment failure and relapse
inspite adequate therapy
with multiple and extensive
chancres that are very
painful. Lesions may be
persistent and gummatous
and higher incidence of
extra-genital chancres.
There may be rapid
progression to
neurosyphilis which may
have unusual
presentations. Secondary
disease may be
severe and extensive and
rapidly progressive to late
or tertiary disease.
Patients may be very
Courtesy of TQ Tan, MD

February

Question: 5

During rounds in the intensive care unit, the charge nurse reminds the team to discuss central line
number of days for each patient. The attending initiates a discussion of central line infection prevention
care bundles.

Of the following, the preferred method to prevent a catheter-related blood stream infection in patients
with a history of multiple catheter-related infections is

A. daily cleansing of the patient with chlorhexidine 2 %

B. heparin anticoagulation
C. use of minocycline/rifampin-impregnated lines

D. vancomycin locks

Reset

February

Question: 5

Of the following, the preferred method to prevent a catheter-related blood stream infection in patients
with a history of multiple catheter-related infections is

A. daily cleansing of the patient with chlorhexidine 2 %

B. heparin anticoagulation

C. use of minocycline/rifampin-impregnated lines

D. vancomycin locks
About 80,000 catheter-related blood stream infections (CRBSI) occur in intensive care units
annually. There are several well-established measures in place to help prevent the incidence of
CRBSI. Key components of a preventive “care bundle” include staff education, prompt removal of
catheters when no longer needed, and strict sterile technique and hand hygiene during insertion
and manipulation. In patients with multiple catheter-related infections despite adherence to
established preventive protocols, studies have demonstrated the effectiveness of vancomycin
locks, use of chlorhexidine/silver sulfadiazine, and minocycline/rifampin impregnated lines.
However, per the 2011 Infectious Diseases Society of America (IDSA) guidelines for the prevention
of intravascular catheter- related infections for prevention of CRBSI, the use of chlorhexidine/silver
or minocycline/rifampin received a category IA recommendation (strongly recommended for
implementation and is strongly supported by well-designed experimental, clinical, or epidemiologic
studies), while the use of vancomycin or ethanol locks received a weaker category II (suggested for
implementation and supported by suggestive clinical or
Correct Answer : C

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January

Assessment Review & Tools ​

Figure 2a. ​Child in the

Assessment Review & Tools ​

Inclusion conjunctivitis is a bilateral follicular conjunctivitis caused by ​Chlamydia trachomatous​,

Hyperacute bacterial conjunctivitis is usually caused by ​Neisseria gonorrhoeae ​and leads to

Epidemic keratoconjunctivitis (EKC) is a more severe type of conjunctivitis commonly caused by

Epidemic keratoconjunctivitis is highly contagious; nosocomial outbreaks from contaminated

In addition to adenovirus-associated epidemic keratoconjunctivitis, other causes of viral

Bartonella henselae ​is a common cause of Parinaud oculoglandular syndrome, a unilateral

Infectious conjunctivitis must be distinguished from noninfectious causes; allergic conjunctivitis

​Course Status ​Links may open in separate window

Copyright © 2017. American Academy of Pediatrics. All rights reserved.

Follicular conjunctivitis is often seen in viral, allergic, and chlamydial conjunctivitis.

Viral conjunctivitis is commonly associated with mild-to-moderate discharge and early

LaMattina K, Thompson L. Pediatric conjunctivitis. ​Disease-a-Month. ​2014;60(6):231-238.

Initiate 3 or more antiretroviral drugs.

• ​Moderate HIV-related symptoms ​(AII)

Reprinted with permission from the ​American Academy of Pediatrics. Human

Assessment Review & Tools ​

​Course Status ​Links may open in separate window

Copyright © 2017. American Academy of Pediatrics. All rights reserved.

American Academy of Pediatrics. In: Kimberlin DW, Brady MT,

Assessment Review & Tools ​

Assessment Review & Tools ​

Assessment Review & Too

Complications that may be associated with SSTIs include lymphadenitis, myositis/necrotizing

A. causing an allergic reaction

B. causing a chemical reaction

C. contaminated with a mold

D. contaminated with coagulase-negative staphylococci

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A. causing an allergic reaction

B. causing a chemical reaction

C. contaminated with a mold

D. contaminated with coagulase-negative staphylococci

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Pityriasis versicolor is caused by ​Pityrosporum orbiculare​, previously known as ​Malassezia furfur​,

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Pityrosporum orbiculare, ​previously known as Malassezia furfur, is the cause of

Gupta AK, Kogan N, Batra R. Pityriasis versicolor: a review of pharmacological treatment

Hu SW, Bigby M. Pityriasis versicolor: a systemic review of interventions. ​Arch Dermatol.

Of the following, the MOST appropriate treatment for this infection is

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Of the following, the MOST appropriate treatment for this infection is

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Education for prevention of recurrent cutaneous fungal infections should occur

American Board of Pediatrics Content

Gemella, Leuconostoc, ​and ​Pediococcus ​organisms are catalase-negative,

Gemella, Leuconostoc, ​and ​Pediococcus ​species are catalase-negative, Gram-positive

American Board of Pediatrics Content

Understand the clinical significance of infections with Pediococcus, Leuconostoc, or

Figure. ​Identification of gram-positive cocci by catalase result. ​Courtesy of K

Of the following, the MOST appropriate control measure to advise would be to

within 3 to 5 days of the exposure

age in the classroom

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Reprinted with permission from the American Academy of Pediatrics.

Reprinted with permission from the American Academy of

Of the following, the MOST appropriate control measure to advise would be to

within 3 to 5 days of the exposure

age in the classroom

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Correct Answer: A ​Average Correct: 75.56%

1. Documentation of receipt of age-appropriate varicella vaccination 2.

Varicella vaccination of susceptible healthy individuals administered within 3 to 5 days after

Varicella-zoster immune globulin (VariZIG) may be useful in preventing or ameliorating

American Board of Pediatrics Content

Make recommendations to a child-care center for control of varicella-zoster infection

A. cerebrospinal fluid, serum, and urine histoplasma antigen

D. tuberculin skin test and interferon-γ release assay

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3) cytokine production by macrophages enhances HIV replication

American Board of Pediatrics Content

Hope-Rapp E, Anyfantakis V, Fouéré S, et al. Etiology of genital ulcer disease. A prospective

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Figure 2a. Child in the

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Inclusion conjunctivitis is a bilateral follicular conjunctivitis caused by Chlamydia trachomatous,

Hyperacute bacterial conjunctivitis is usually caused by Neisseria gonorrhoeae and leads to

Bartonella henselae is a common cause of Parinaud oculoglandular syndrome, a unilateral

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LaMattina K, Thompson L. Pediatric conjunctivitis. Disease-a-Month. 2014;60(6):231-238.

• Moderate HIV-related symptoms (AII)

Reprinted with permission from the American Academy of Pediatrics. Human

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Pityriasis versicolor is caused by Pityrosporum orbiculare, previously known as Malassezia furfur,

Course Status Links may open in separate window

Pityrosporum orbiculare, previously known as Malassezia furfur, is the cause of

Hu SW, Bigby M. Pityriasis versicolor: a systemic review of interventions. Arch Dermatol.

Assessment Review & Tools

Assessment Review & Tools

Gemella, Leuconostoc, and Pediococcus organisms are catalase-negative,

Gemella, Leuconostoc, and Pediococcus species are catalase-negative, Gram-positive

Figure. Identification of gram-positive cocci by catalase result. Courtesy of K

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Correct Answer: A Average Correct: 75.56%

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Figure 2. Granuloma inguinale

Figure 3. Granuloma venereum

Figure 4. Lymphogranuloma venereum

reatment for primary syphilis and early latent disease: