Genital ulcers can be caused by infections such as herpes simplex virus, syphilis, chancroid, and lymphogranuloma venereum or by non-infectious causes. Clinical diagnosis of the cause is difficult so tests for syphilis, herpes simplex virus, and chancroid should be considered in all patients. Treatment depends on the suspected cause but herpes simplex virus is usually treated with oral acyclovir and syphilis with intramuscular penicillin G benzathine.

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505 50 Ps to Know All About Dengue Fever
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527 Herpes Zoster: Multiple Presentations in a Single Patient
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50 Ps to Know All About Dengue Fever
1. Pathogenesis is an endothermic dysfunction.
2. Plasma leakage is the cause of severe dengue.
3. Pregnancy is an indication for admission.
4. Paani (water) resuscitation is the treatment.
5. Pulse, if rises by 20, is a bad sign.
6. Pressure: If systolic blood pressure falls by 20, this is a red flag.
7. Pulse pressure <20, is a red flag.
8. Paracetamol is the drug of choice for fever.
9. Patti: If fever does not respond to paracetamol do tap water patti.
10. Pigment volume concentration (PCV), if rises by 20%, is a red flag.
11. Platelets count is not reliable and no transfusion if no active bleeding.
12. Piss: Make sure that the patient pisses (urinates) every three hours.
13. Papaya leaves have no scientific role.
14. Peeli haldi (yellow turmeric) can reduce plasma leakage.
15. Pancreatitis can occur in dengue.
16. Peelia (jaundice) can occur due to dengue but invariably is mild. Serum glutamic oxaloacetic (SGOT) will be
higher than serum glutamic pyruvic transaminase (SGPT).
17. Pot, if filled with fresh stagnant water, can grow dengue.
18. Potty: Dengue can present with loose motions.
19. Pasina: Dengue fever may be high with sweating.
20. Pediatric age: Dengue is more serious in children.
21. Pain in the head: There can be severe pain in the head (retro-orbital area) in dengue.
22. Pantoprazole with domperidone may be required to stop vomiting.
23. Palang: Extreme weakness in dengue may require rest.
24. Paisa: Do not waste paisa (money) on unnecessary treatments.
25. Positive: Always think positive and do not be afraid of mortality.
26. Panic: Do not panic; dengue is not all that dangerous.
27. Pareshani: Do not trouble hospitals for unnecessary admissions.
28. People: Multiple people may get dengue in one family.
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
505

6. from the desk of THE group editor-in-chief
29. Protect people from dengue by taking precautions.
30. Precautions: Take anti-mosquito precautions.
31. Prognosis is bad in second dengue.
32. Post-febrile period is the dangerous period.
33. Prayers may have a role in terminal cases of dengue.
34. Pradesh: Keep your pradesh free of dengue mosquitoes.
35. Patience: Be patient in dengue.
36. Picture: A picture of how a dengue patient looks should be in every house.
37. Population: Dengue affects 10% of the population in any epidemic.
38. Pagalpan: Dengue can cause encephalitis.
39. Pleural effusion: Dengue can cause pleural effusion.
40. Pericardial effusion: Dengue can cause pericardial effusion.
41. Patila: Do not keep empty patila (vessels) on the roof of your house.
42. Purify atmosphere with yagna smoke to kill mosquitoes.
43. Prem: Dengue is not a sexually transmitted illness.
44. Past-dengue illness history should be taken.
45. Plot: Workers working in construction sites are at risk.
46. Pehnava: Wearing full-sleeved clothes can prevent dengue.
47. Pajama: Wear full pajama in the day-time.
48. Passengers can carry mosquito to far-off places via car or train.
49. Posture is normal in dengue unlike in chikungunya, where the person comes with flexed posture.
50. Prepare: The government should be prepared in advance to prevent dengue fever.
■■■■
506
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013

7. American Family Physician
Diagnosis and Management of Genital Ulcers
MICHELLE A. ROETT, MEJEBI T. MAYOR, KELECHI A. UDUHIRI
Abstract
Herpes simplex virus infection and syphilis are the most common causes of genital ulcers in the United States. Other infectious
causes include chancroid, lymphogranuloma venereum, granuloma inguinale (donovanosis), secondary bacterial infections,
and fungi. Noninfectious etiologies, including sexual trauma, psoriasis, Behçet syndrome, and fixed drug eruptions, can also
lead to genital ulcers. Although initial treatment of genital ulcers is generally based on clinical presentation, the following tests
should be considered in all patients: serologic tests for syphilis and darkfield microscopy or direct fluorescent antibody testing
for Treponema pallidum, culture or polymerase chain reaction test for herpes simplex virus, and culture for Haemophilus ducreyi
in settings with a high prevalence of chancroid. No pathogen is identified in up to 25 percent of patients with genital ulcers.
The first episode of herpes simplex virus infection is usually treated with seven to 10 days of oral acyclovir (five days for
recurrent episodes). Famciclovir and valacyclovir are alternative therapies. One dose of intramuscular penicillin G benzathine
is recommended to treat genital ulcers caused by primary syphilis. Treatment options for chancroid include a single dose of
intramuscular ceftriaxone or oral azithromycin, ciprofloxacin, or erythromycin. Lymphogranuloma venereum and donovanosis
are treated with 21 days of oral doxycycline. Treatment of noninfectious causes of genital ulcers varies by etiology, and ranges
from topical wound care for ulcers caused by sexual trauma to consideration of subcutaneous pegylated interferon alfa-2a for
ulcers caused by Behçet syndrome.
Keywords: Herpes simplex, syphilis, genital ulcers, sexual trauma, oral acyclovir, penicillin G benzathine, doxycycline
G
enital ulcers may be caused by infectious or
noninfectious etiologies (Table 1).1-3 Sexually
transmitted infections (STIs) characterized
by genital ulcers include genital herpes simplex
virus (HSV) infection, syphilis (Treponema pallidum),
chancroid (Haemophilus ducreyi), granuloma inguinale
(donovanosis; Calymmatobacterium granulomatis), and
lymphogranuloma venereum (Chlamydia trachomatis
serotypes L1, L2, and L3). Secondary bacterial infections
or fungi can also cause genital ulcers. Noninfectious
etiologies include psoriasis, sexual trauma, Behçet
syndrome, Wegener granulomatosis, and fixed drug
eruptions.1,4 In the United States, most young, sexually
active patients who present with genital ulcers have
HSV infection or syphilis.1,4 Lymphogranuloma
MICHELLE A. ROETT, MD, MPH, FAAFP, is an associate professor in the Department
of Family Medicine at Georgetown University Medical Center, Washington, DC. She
is also associate program director at the Georgetown University/Providence Hospital
Family Medicine Residency Program and medical director at Fort Lincoln Family Medicine
Center, Colmar Manor, Md.
MEJEBI T. MAYOR, MD, JD, FACOG, is chair of the Department of Obstetrics and
Gynecology at Providence Hospital. She is also an assistant professor in the Department
of Obstetrics and Gynecology at Howard University,Washington, DC.
KELECHI A. UDUHIRI, MD, MPH, MS, is medical director of Health Care for the Homeless,
Baltimore, Md., and is a faculty member with the Franklin Square Hospital Family Medicine
Residency Program in Baltimore.
Source: Adapted from Am Fam Physician. 2012;85(3):254-262.
venereum, donovanosis, secondary bacterial infections,
fungi, and noninfectious etiologies are rare.
Epidemiology
The global incidence of genital ulcer disease is estimated
to be more than 20 million cases annually.4 HSV types 1
and 2 are the most common causes of genital ulcers in
the United States, followed by syphilis and chancroid.5
One in five women and one in nine men 14 to 49 years
of age has genital HSV type 2 infection.6
In 2009, the rate of syphilis was highest in men and
women 20 to 24 years of age (20.7 and 5.6 cases per
Table 1. Differential Diagnosis of Genital Ulcers
Infectious (most common)*
Noninfectious
(less common)
Genital herpes simplex virus
Behçet syndrome
Syphilis
Fixed drug eruption
Chancroid
Psoriasis
Lymphogranuloma venereum
Sexual trauma
Granuloma inguinale (donovanosis) Wegener granulomatosis
Fungal infection (e.g., Candida)
Secondary bacterial infection
*Listed in order of frequency.
Information from references 1 through 3.
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
507

8. American Family Physician
Table 2. Risk Factors for Genital Ulcers
History of inflammatory disease (e.g., psoriasis) and exposure
to trauma or medications such as nonsteroidal anti-inflammatory
drugs, antimalarials, angiotensin-converting enzyme inhibitors,
beta blockers, lithium, salicylates, or corticosteroids
Lack of male circumcision
Multiple sex partners, lifetime or current
Nonrecognition of ulcers in prodrome stage
Serodiscordant sex partners (i.e., one partner with herpes
simplex virus and one without)
Unprotected sexual contact
Unprotected skin-to-skin contact with ulcers
Information from references 1 through 3, 5, and 6.
100,000 persons, respectively). However, syphilis rates
increased in persons 15 to 19 years of age between 2002
and 2009 (1.3 versus 6.0 cases per 100,000 males and 1.5
versus 3.3 cases per 100,000 females).7,8 In 2006, most
cases of primary and secondary syphilis occurred in
men who have sex with men.7,8
Chancroid usually occurs in discrete outbreaks, but the
disease may be endemic in some regions. The incidence
of chancroid has been declining in the United States,
with only 28 cases reported to state health departments
in 2009.9 However, H. ducreyi infection is challenging
to confirm, likely leading to underreporting.9
Approximately 10 percent of patients with chancroid
are coinfected with syphilis or HSV; these are even
more common coinfections for patients who acquired
chancroid outside the United States.5
Lymphogranuloma venereum primarily occurs in men
who have sex with men.10 Behçet syndrome is most
common in young adults in the Eastern Mediterranean
and in men in the Far East, whereas women are
predominantly affected in the United States.2
Diagnostic Evaluation
The diagnosis of genital ulcer disease is based on
the presence of one or more mucocutaneous ulcers
involving the genitalia, perineum, or anus.5 Diagnosing
the specific cause of genital ulcers is based on history,
physical examination, and laboratory findings.
History and Physical Examination
Risk factors for infectious causes of genital ulcers
are similar to those for STIs, whereas risk factors for
noninfectious causes vary (Table 21-3,5,6). For instance,
patients with psoriasis are at greater risk of genital
ulcers after exposure to trauma or medications such as
508
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
nonsteroidal anti-inflammatory drugs, antimalarials,
angiotensin-converting enzyme inhibitors, beta
blockers, lithium, salicylates, or corticosteroids.1 Behçet
syndrome is associated with the human leukocyte
antigen-B51/B5 allele (57.2 percent of patients with
the allele have the condition).11 History and physical
examination findings associated with genital ulcers are
summarized in Table 3.1,3,5,12-16
Genital HSV infection usually begins as multiple
vesicular lesions, sometimes painless, that are located
inside the foreskin, labia, vagina, or rectum. Vesicles
may rupture spontaneously, becoming painful,
shallow ulcers (Figure 1).17 Prodromal symptoms may
occur in 20 percent of HSV cases before ulceration.
The prodrome may include a mild tingling sensation
up to 48 hours before ulceration, or shooting pain in
the buttocks, legs, or hips up to five days before.12
Asymptomatic viral shedding may occur in more than
60 percent of patients with HSV infection.18 First-time
infections may also feature constitutional symptoms
and regional lymphadenopathy.3
Primary syphilis usually begins with a single, painless,
well-demarcated ulcer (chancre) with a clean base
and indurated border19 (Figure 2). When the patient
seeks treatment for signs or symptoms, the solitary
chancre of primary infection may still be visible, or
it may have progressed to secondary infection (e.g.,
rash, lymphadenopathy) or tertiary infection (e.g.,
gummatous lesions).
Chancroid ulcers are usually nonindurated and painful
with a serpiginous border and friable base (Figure 3).
The ulcers occur on the prepuce and frenulum of the
penis in men or on the vulva or cervix in women.
Perineal lesions are common in women or in men
who have sex with men. Painful, unilateral, inguinal
adenitis occurs in one-half of patients with chancroid
and may develop into buboes.19,20 Fluctuant buboes
may rupture spontaneously if not aspirated or incised
and drained. Complications of chancroid include
phimosis in men and further ulceration caused by
secondary bacterial infection.20 Extragenital lesions on
the inner thighs and fingers have been reported but are
relatively rare.20
Lymphogranuloma venereum infection is characterized
by a small, shallow, painless genital or rectal papule that
may ulcerate at the site of infection after an incubation
period of three to 30 days. These ulcers may be selflimited and remain primarily undetected within the
urethra, vagina, or rectum. However, if left untreated,
the condition may be complicated by secondary

9. American Family Physician
Table 3. Summary of the Diagnosis and Treatment of Genital Ulcers
Etiology
Clinical presentation
Diagnosis
Treatment options
Usually multiple vesicular
lesions that rupture and
become painful, shallow
ulcers (Figure 1)
Definitive: herpes simplex virus identified
on culture or polymerase chain reaction
testing of ulcer scraping or vesicle fluid
aspirate
First episode
Constitutional symptoms,
lymphadenopathy in firsttime infections
Presumptive: typical lesions and any of the
following factors
Infectious*
Herpes simplex
virus infection
Previously known outbreak
Positive Tzanck smear of ulcer scraping
Exclusion of other causes of ulcers
Fourfold increase in acute and
convalescent antibody titer results
(in a first-time infection)
Acyclovir, 400 mg orally three times
daily for seven to 10 days, or 200 mg
orally five times daily for seven to 10
days
Famciclovir, 250 mg orally three
times daily for seven to 10 days
Valacyclovir, 1,000 mg orally twice
daily for seven to 10 days
Recurrent episode
Acyclovir, 400 mg orally three times
daily for five days, 800 mg orally twice
daily for five days, 800 mg orally three
times daily for two days, or 200 mg orally
five times daily for five days
Famciclovir, 1,000 mg twice daily for
one day, 500 mg orally once then 250
mg twice daily for two days, or 125 mg
orally twice daily for five days
Valacyclovir, 500 mg orally twice daily
for three days or 1,000 mg orally once
daily for five days
Suppressive therapy
Acyclovir, 400 mg orally twice daily or
200 mg orally three to five times daily
Famciclovir, 250 mg orally twice daily
Valacyclovir, 1,000 mg orally once daily
Valacyclovir, 500 mg orally once daily,
if fewer than 10 outbreaks per year
Syphilis (primary)
Single, painless, welldemarcated ulcer (chancre)
with a clean base and
indurated border (Figure 2)
Treponema pallidum identified on darkfield Penicillin G benzathine, 2.4 million
microscopy or direct fluorescent antibody units intramuscularly in a single dose
testing of a chancre or lymph node aspirate
or
Mild or minimally tender Positive result on serologic nontreponemal
inguinal lymphadenopathy testing (i.e., Venereal Disease Research
Laboratories or rapid plasma reagin)
that is confirmed with a positive result on
serologic treponemal testing (i.e., fluorescent
treponemal antibody absorption or T. pallidum
passive agglutination)
Chancroid
Nonindurated, painful with
serpiginous border and
friable base; covered with
a necrotic, often purulent
exudate (Figure 3)
Tender, suppurative,
unilateral inguinal
lymphadenopathy or
adenitis
Gram stain suggestive of Haemophilus Needle aspiration of fluctuant buboes
ducreyi (gram-negative, slender rod or Azithromycin, 1 g orally in a single dose
coccobacillus in a “school of fish” pattern)
Ceftriaxone, 250 mg intramuscularly in
Definitive: H. ducreyi identified on culture
a single dose
Presumptive: painful genital ulcer or ulcers Ciprofloxacin, 500 mg orally twice daily
with regional lymphadenopathy and no for three days†
evidence of T. pallidum infection at least
seven days after ulcer onset, and testing Erythromycin, 500 mg orally four times
daily for seven days
negative for herpes simplex virus
continued...
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
509

10. American Family Physician
Table 3. Summary of the Diagnosis and Treatment of Genital Ulcers (continued)
Etiology
Clinical presentation
Diagnosis
Lymphogranuloma Small, shallow, painless, Definitive:
venereum
genital or rectal papule or
Chlamydia trachomatis serotype L1, L2, or L3
ulcer; no induration
culture, identified from clinical specimen
Unilateral, tender
or
inguinal or femoral
Immunofluorescence demonstrating inclusion
lymphadenopathy
bodies in leukocytes of an inguinal lymph node
Rectal bleeding, pain,
(bubo) aspirate
or discharge; ulcerative
or
proctitis; constipation or
Microimmunofluorescence positive for
tenesmus
lymphogranuloma venereum strain of C.
trachomatis
Treatment options
Doxycycline, 100 mg orally twice daily
for 21 days
Erythromycin base, 500 mg orally four
times daily for 21 days
Pregnant or lactating women:
erythromycin, 500 mg orally four
times daily for 21 days
Presumptive:
Clinical suspicion
Community prevalence
Exclusion of other causes of proctocolitis,
inguinal lymphadenopathy, or genital ulcers
Granuloma
inguinale
(donovanosis)
Persistent, painless,
beefy-red (highly
vascular) papules or
ulcers (Figure 4)
May be hypertrophic,
necrotic, or sclerotic
No lymphadenopathy
Definitive:
Treatment should continue until
Intracytoplasmic Donovan bodies on Wright lesions have healed
Doxycycline, 100 mg orally twice daily
stain
for at least 21 days
or
Positive result with Giemsa stain or biopsy of Azithromycin, 1 g orally once weekly
for at least 21 days
granulation tissue
Ciprofloxacin, 750 mg orally twice
daily for at least 21 days
May have subcutaneous
granulomas
Erythromycin base, 500 mg orally four
times daily for 21 days
Trimethoprim/sulfamethoxazole
double strength, 160/800 mg orally
twice daily for at least 21 days
Noninfectious
Behçet syndrome
Aphthous oral ulcers
(100 percent of cases);
genital ulcers (70 to 90
percent of cases)
Consider rheumatoid factor, antinuclear antibody Spontaneous regression is possible
testing
Pegylated interferon alfa-2a, 6
May have positive antibodies to carboxy-terminal million units subcutaneously three
times weekly for three months for
subunit of SIP1
Biopsy may show diffuse arteritis with venulitis mucocutaneous involvement
Diagnostic criteria: recurrent aphthous oral
ulcers (more than three per year) and any two
of the following
Recurrent genital ulcers
Eye lesions (e.g., uveitis)
Cutaneous lesions (e.g., erythema nodosum)
Positive pathergy test (2 mm erythema appears
24 to 48 hours after skin prick test)
Biopsy may show diffuse arteritis with venulitis
continued...
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11. American Family Physician
Table 3. Summary of the Diagnosis and Treatment of Genital Ulcers (continued)
Etiology
Clinical presentation
Diagnosis
Treatment options
Fixed drug
eruptions
Varied ulcerations that
Diagnosis of exclusion when ulcers resolve Self-limited
resolve with withdrawal of after drug withdrawals
Topical analgesics or anti-inflammatory
offending agent
agents, as needed
Consider treating exacerbation of underlying
inflammatory disease if applicable
*Listed in order of frequency.
†Contraindicated in pregnant or lactating women and in patients younger than 18 years.
Information from references 1, 3, 5, and 12 through 16.
bacterial infections or lymphatic obstruction, which
may progress to genital elephantiasis.10 In persons who
have receptive anal intercourse, lymphogranuloma
venereum may result in tenesmus; constipation; rectal
bleeding; pain or discharge; proctitis; anogenital
ulcerations; and unilateral, tender inguinal or femoral
lymphadenopathy.13,20,21
Granuloma inguinale, or donovanosis, is characterized
by persistent, painless, beefy-red papules or ulcers,
which may be hypertrophic, necrotic, or sclerotic
with an incubation period of eight to 12 weeks
(Figure 4).22 Patients with Behcet syndrome usually
have intermittent arthritis, recurrent oral and genital
ulcers, and possibly a family history of inflammatory
disorders.23 Up to 60 percent of genital ulcers associated
with Behçet syndrome lead to significant scarring.24
Laboratory Evaluation
Laboratory evaluation of an initial genital ulcer outbreak
should include culture or polymerase chain reaction
testing for HSV infection, HSV type-specific serology,
serologic testing for syphilis, and culture for H. ducreyi
in settings with a high prevalence of chancroid. For
the diagnosis of HSV infection, polymerase chain
reaction testing is 96 to 100 percent sensitive and
97 to 98 percent specific (positive likelihood ratio = 49,
negative likelihood ratio = 0.02), much more sensitive
than culture.25,26 Among adults who report that they
have never had genital herpes, the seroprevalence of
HSV type 2 antibodies is 21.6 percent, suggesting the
disease is underdiagnosed.27
Darkfield microscopy and direct fluorescent antibody
tests of exudate or tissue material are the definitive
methods for diagnosing primary syphilis.3,4,28
However, in patients presenting with genital ulcers, a
presumptive diagnosis of syphilis can be made with
a serologic nontreponemal test (i.e., Venereal Disease
Research Laboratories or rapid plasma reagin). But,
because of possible false-positive results, positive
nontreponemal test results should be confirmed
with serologic treponemal testing (i.e., fluorescent
treponemal antibody absorption or T. pallidum passive
agglutination).3,4,28 Nontreponemal titers typically
decline and may become nonreactive after treatment,
but most positive treponemal test results tend to remain
persistently active. If primary syphilis is treated, up to
25 percent of patients may have nonreactive treponemal
results in two to three years; however, treponemal
titers are not recommended to evaluate response to
treatment.3
Although a definitive diagnosis of chancroid requires
identification of H. ducreyi, testing with special culture
media is less than 80 percent sensitive and polymerase
chain reaction testing for H. ducreyi is not available in
the United States.4 A presumptive diagnosis is possible
with a painful genital ulcer, regional lymphadenopathy,
no evidence of T. pallidum infection, and negative HSV
test results.3
To
diagnose
lymphogranuloma
venereum,
genital swabs or bubo aspirate may be tested for
C. trachomatis serotypes L1, L2, and L3 by culture, direct
immunofluorescence, or nucleic acid amplification.3
Nucleic acid amplification tests for lymphogranuloma
venereum are not approved by the U.S. Food and
Drug Administration for rectal specimens. Health care
professionals may collect and send rectal specimens
to state health departments for referral to the Centers
for Disease Control and Prevention for testing and
validating diagnostic methods for lymphogranuloma
venereum.3
Even with appropriate laboratory testing, no pathogen
is identified in up to 25 percent of patients with genital
ulcers.4 Biopsy is rarely needed to diagnose the cause
of genital ulcers, but it may be considered if an ulcer
persists after treatment.3
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
511

12. American Family Physician
Treatment
The 2010 Centers for Disease Control and Prevention
guidelines for managing STIs provide treatment options
for patients with genital ulcer disease.3 Treatment of
HSV infection should be initiated before test results
are available because early treatment decreases
transmission and duration of ulcers. Patients should be
instructed to abstain from sexual activity during the
prodrome stage, while lesions are present, and for the
duration of treatment. Treatments for common causes
of genital ulcers are outlined in Table 3.1,3,5,12-16
The first episode of genital HSV infection may be treated
with acyclovir, 400 mg orally three times daily for seven
to 10 days (five days for recurrent episodes). Alternative
therapies include famciclovir or valacyclovir.3,29 Topical
antivirals are of limited benefit in the treatment of HSV
infection and are not recommended.3
Primary syphilis may be treated with intramuscular
penicillin G benzathine, 2.4 million units in a single
dose. The Centers for Disease Control and Prevention
guidelines recommend that patients allergic to
penicillin undergo desensitization.3
Treatment options for chancroid include intramuscular
ceftriaxone, 250 mg in a single dose, or oral
azithromycin, ciprofloxacin, or erythromycin. Treatment
is less effective for uncircumcised males and patients
coinfected with human immunodeficiency virus (HIV).
Sex partners should be treated for chancroid, regardless
of symptoms, if they have had sexual contact with the
patient within the previous 10 days.3
Patients with lymphogranuloma venereum or
donovanosis are treated with oral doxycycline,
100 mg twice daily for 21 days, and followed clinically.
Donovanosis may require continued antibiotics until
resolution of symptoms. Erythromycin is an alternative
therapy for lymphogranuloma venereum.3
Treatment of mucocutaneous ulcers in Behçet syndrome
is based on associated symptoms because ulcerations
may regress spontaneously. In a randomized trial,
subcutaneous pegylated interferon alfa-2a, 6 million
units three times weekly for three months, improved
duration and pain of oral ulcers and frequency of
genital ulcers.14 A Cochrane review of randomized
controlled trials found insufficient evidence for the use
of oral acyclovir, oral colchicine, or topical interferon to
treat ulcers caused by Behçet syndrome.30 In patients
with Behçet syndrome, topical or vaginal sucralfate (not
available in the United States) decreases the pain of oral
ulcers, but does not significantly decrease the average
frequency, healing time, or pain of genital ulcers.31
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Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
Treatment of extensive genital ulcers, regardless of
etiology, has traditionally included wound cleansing
and dressing. Although clinical trials are lacking,
local treatment may include topical or oral analgesics,
perineal baths, topical or oral anti-inflammatory agents,
or cool compresses with Burow solution.15 Topical
antimicrobials, such as benzoyl peroxide, dimethyl
sulfoxide, gentamicin, oxyquinoline (not available
in the United States), and silver sulfadiazine, may
be beneficial for extragenital ulcers, but evidence of
effectiveness is limited.16
Promptly treating genital ulcers is particularly
important for patients with HIV to reduce HIV
shedding and transmission. Genital ulcers increase
HIV viral load in semen, increasing the likelihood of
transmission to sex partners. Conversely, a patient with
genital ulcers is more likely to acquire HIV infection
with unprotected sexual contact.28,32,33
Prevention and Screening
The U.S. Preventive Services Task Force recommends
screening for syphilis in persons at increased risk,34 and
recommends against routinely screening for HSV in
asymptomatic patients.35 There are no current screening
recommendations for chancroid, lymphogranuloma
venereum, or donovanosis.
Patients with genital ulcers should be counseled on
reducing risk factors for STIs, including limiting the
number of sex partners, using a condom with each
sexual encounter, and regularly being screened for
STIs if recommended by evidence-based guidelines.
HIV testing should be performed in all patients with
previously negative HIV test results who have genital
ulcers caused by T. pallidum or H. ducreyi infection,
and should be strongly considered for those who have
genital ulcers caused by HSV infection.3
Avoiding sexual intercourse during outbreaks does not
prevent HSV transmission.36 Although condom use
can effectively prevent transmission, the infection can
be spread through skin-to-skin contact in genital areas
unprotected by a condom.37,38 The American College
of Obstetricians and Gynecologists recommends that
women who have partners with HSV infection be
offered type-specific serologic testing to assess their
risk, and these couples should be advised on condom
and dental dam use, including a warning about
incomplete protection.39
Chemoprophylaxis is available for severe or recurrent
outbreaks of genital HSV infection in the form of
daily suppressive medication. Suppressive therapy

13. American Family Physician
Figure 3. Chancroid ulcers are usually nonindurated with
serpiginous borders and friable base, often covered with
purulent exudate.
Figure 1. Genital herpes simplex virus. Painful, shallow
ulcers may manifest from ruptured vesicular lesions.
Figure 4. Genital ulcer with hypertrophic borders, caused
by donovanosis.
Figure 2. Primary syphilis begins as a single, well-demarcated
ulcer (chancre) with a clean base and indurated border.
reduces the frequency and severity of outbreaks,
reduces asymptomatic viral shedding by 90 percent,
and reduces the risk of transmission to a seronegative
partner.40 Options for suppressive therapy include
acyclovir, 400 mg twice daily; famciclovir, 250 mg
twice daily; or valacyclovir, 1,000 mg daily.29,41,42 If a
patient has fewer than 10 outbreaks per year, 500 mg
of oral valacyclovir daily is an appropriate option.3
Famciclovir is equally effective for suppression but
less effective for the prevention of viral shedding and
transmission to sex partners.43
The American College of Obstetricians and
Gynecologists recommends that pregnant patients
with HSV infection begin suppressive therapy at 34 to
36 weeks’ gestation to reduce the likelihood of lesions
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
513

14. American Family Physician
during labor.44 Suppressive therapy reduces the risk
of recurrence by 75 percent and the rate of cesarean
delivery because of HSV lesions by 40 percent.45
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4. Low N, Broutet N, Adu-Sarkodie Y, Barton P, Hossain
M, Hawkes S. Global control of sexually transmitted
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6. Centers for Disease Control and Prevention. CDC fact
sheet. Genital herpes. http://www.cdc.gov/std/herpes/
herpes-fact-sheet-lowres-2010.pdf. Accessed September
27, 2010.
7. U.S. Department of Health and Human Services, Centers
for Disease Control and Prevention. Sexually transmitted
disease surveillance 2009. http://www.cdc.gov/std/
stats09/surv2009-Complete.pdf. Accessed May 8, 2011.
8. Centers for Disease Control and Prevention. CDC fact
sheet. Syphilis. http://www.cdc.gov/std/syphilis/syphilisfact-sheet-press.pdf. Accessed September 27, 2010.
9. Centers for Disease Control and Prevention. Chancroid:
tracking the hidden epidemics. Trends in STDs in the
United States. 2000. http://www.cdc.gov/std/Trends2000/
chancroid.htm. Accessed September 14, 2011.
10. Centers for Disease Control and Prevention. CDC fact
sheet. LGV. http://www.cdc.gov/std/lgv/LGV-Fact-Sheet.
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11. de Menthon M, Lavalley MP, Maldini C, Guillevin
L, Mahr A. HLA-B51/B5 and the risk of Behçet’s
disease: a systematic review and meta-analysis of casecontrol genetic association studies. Arthritis Rheum.
2009;61(10):1287-1296.
12. Schiffer JT, Corey L. Herpes simplex virus. In: Mandell GL,
Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s
Principles and Practice of Infectious Diseases. 7th ed.
Philadelphia, Pa.: Churchill Livingstone; 2009:1943-1962.
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13. Burstein GR. Sexually transmitted infections. In: Kliegman
R, Nelson WE, eds. Nelson Textbook of Pediatrics. 19th
ed. Philadelphia, Pa.: Saunders; 2011:705-714.
14. Alpsoy E, Durusoy C, Yilmaz E, et al. Interferon alfa-2a
in the treatment of Behçet disease: a randomized placebocontrolled and double-blind study. Arch Dermatol.
2002;138(4):467-471.
15. Warts, herpes simplex and other viral infections. In:
Clinical Dermatology: A Color Guide to Diagnosis and
Therapy. Habif TP, ed. 5th ed. Edinburgh, Scotland:
Mosby; 2010:454-490.
16. O’Meara SM, Cullum NA, Majid M, Sheldon TA.
Systematic review of antimicrobial agents used for
chronic wounds. Br J Surg. 2001;88(1):4-21.
17. Sharma R, Dronen SC. Herpes simplex in emergency
medicine. Medscape Reference. http://emedicine.medscape.
com/article/783113-overview. Accessed September 13, 2011.
18. Wald A, Zeh J, Selke S, et al. Reactivation of genital
herpes simplex virus type 2 infection in asymptomatic
seropositive persons. N Engl J Med. 2000;342(12):844-850.
19. Kimberlin DW, Rouse DJ. Clinical practice. Genital herpes.
N Engl J Med. 2004;350(19):1970-1977.
20. Lewis DA. Chancroid: clinical manifestations, diagnosis,
and management. Sex Transm Infect. 2003;79(1):68-71.
21. Sethi G, Allason-Jones E, Richens J, et al. Lymphogranuloma
venereum presenting as genital ulceration and inguinal
syndrome in men who have sex with men in London,
UK [published correction appears in Sex Transm Infect.
2009;85(5):406]. Sex Transm Infect. 2009;85(3):165-170.
22. Velho PE, Souza EM, Belda Junior W. Donovanosis. Braz J
Infect Dis. 2008;12(6):521-525.
23. Klippel JH, Weyand CM. Wortmann R, eds. Primer on
the Rheumatic Diseases. 11th ed. Atlanta, Ga.: Arthritis
Foundation; 1997:89.
24. Mat MC, Goksugur N, Engin B, Yurdakul S, Yazici
H. The frequency of scarring after genital ulcers in
Behçet’s syndrome: a prospective study. Int J Dermatol.
2006;45(5):554-556.
25. Ashley RL. Sorting out the new HSV type specific
antibody tests. Sex Transm Infect. 2001;77(4):232-237.
26. Wald A, Huang ML, Carrell D, Selke S, Corey L.
Polymerase chain reaction for detection of herpes simplex
virus (HSV) DNA on mucosal surfaces: comparison with
HSV isolation in cell culture. J Infect Dis. 2003;188(9):
1345-1351.
27. Fleming DT, McQuillan GM, Johnson RE, et al. Herpes
simplex virus type 2 in the United States, 1976 to 1994.
N Engl J Med. 1997;337:1105-1111.
28. Bruisten SM, Cairo I, Fennema H, et al. Diagnosing genital
ulcer disease in a clinic for sexually transmitted diseases
in Amsterdam, The Netherlands. J Clin Microbiol.
2001;39(2):601-605.
29. Fife KH, Barbarash RA, Rudolph T, Degregorio B, Roth
R. Valaciclovir versus acyclovir in the treatment of first-

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episode genital herpes infection. Results of an international,
multicenter, double-blind, randomized clinical trial. The
Valaciclovir International Herpes Simplex Virus Study
Group. Sex Transm Dis. 1997;24(8):481-486.
30. Saenz A, Ausejo M, Shea B, Wells G, Welch V, Tugwell
P. Pharmacotherapy for Behcet’s syndrome. Cochrane
Database Syst Rev. 2000;(2):CD001084.
31. Alpsoy E, Er H, Durusoy C, Yilmaz E. The use of sucralfate
suspension in the treatment of oral and genital ulceration
of Behçet disease: a randomized, placebo-controlled,
double-blind study. Arch Dermatol. 1999;135(5):529-532.
32. Powers KA, Poole C, Pettifor AE, Cohen MS. Rethinking
the heterosexual infectivity of HIV-1: a systematic review
and meta-analysis. Lancet Infect Dis. 2008;8(9):553-563.
33. Krieger JN. Prostatitis, epididymitis, and orchitis: semen
as a vector for human immunodeficiency virus. In:
Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas,
and Bennett’s Principles and Practice of Infectious
Diseases. 7th ed. Philadelphia, Pa.: Churchill Livingstone;
2009:1521-1527.
34. U.S. Preventive Services Task Force. Screening
for syphilis infection. July 2004. http://www.
uspreventiveservicestaskforce.org/uspstf/uspssyph.htm.
Accessed September 13, 2011.
35. U.S. Preventive Services Task Force. Screening
for genital herpes. March 2005. http://www.
uspreventiveservicestaskforce.org/uspstf05/herpes/
herpesrs.htm. Accessed September 13, 2011.
36. Kim HN, Wald A, Harris J, Almekinder J, Heitman C, Corey
L. Does frequency of genital herpes recurrences predict
risk of transmission? Further analysis of the valacyclovir
transmission study. Sex Transm Dis. 2008;35(2):124-128.
37. Martin ET, Krantz E, Gottlieb SL, et al. A pooled analysis
of the effect of condoms in preventing HSV-2 acquisition
[published correction appears in Arch Intern Med.
2010;170(11):929]. Arch Intern Med. 2009;169(13):12331240.
38. Wald A, Langenberg AG, Link K, et al. Effect of condoms
on reducing the transmission of herpes simplex virus type
2 from men to women. JAMA. 2001;285(24):3100-3106.
39. American College of Obstetricians and Gynecologists.
Gynecologic herpes simplex virus infections. ACOG
Practice Bulletin no. 57. Washington, DC: American
College of Obstetricians and Gynecologists; 2004.
40. Corey L, Wald A, Patel R, et al.; Valacyclovir HSV
Transmission Study Group. Once-daily valacyclovir to
reduce the risk of transmission of genital herpes. N Engl J
Med. 2004;350(1):11-20.
41. Diaz-Mitoma F, Sibbald RG, Shafran SD, Boon R,
Saltzman RL. Oral famciclovir for the suppression of
recurrent genital herpes: a randomized controlled trial.
Collaborative Famciclovir Genital Herpes Research
Group. JAMA. 1998;280(10):887-892.
42. Bodsworth NJ, Crooks RJ, Borelli S, et al. Valaciclovir
versus aciclovir in patient initiated treatment of recurrent
genital herpes: a randomised, double blind clinical trial.
International Valaciclovir HSV Study Group. Genitourin
Med. 1997;73(2):110-116.
43. Wald A, Selke S, Warren T, et al. Comparative efficacy of
famciclovir and valacyclovir for suppression of recurrent
genital herpes and viral shedding. Sex Transm Dis.
2006;33:529-533.
44. Randolph AG, Hartshorn RM, Washington AE. Acyclovir
prophylaxis in late pregnancy to prevent neonatal herpes:
a cost-effectiveness analysis. Obstet Gynecol. 1996;88(4 pt
1):603-610.
45. Sheffield JS, Hollier LM, Hill JB, Stuart GS, Wendel
GD. Acyclovir prophylaxis to prevent herpes simplex
virus recurrence at delivery: a systematic review. Obstet
Gynecol. 2003;102(6):1396-1403.
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16. American Family Physician
Practice Guidelines
ACIP Releases Influenza Vaccination
Updates for 2013-2014
The Centers for Disease Control and Prevention’s
Advisory Committee on Immunization Practices (ACIP)
has updated its annual guidelines for routine influenza
vaccination in 2013-2014. Vaccination is recommended
for all persons six months or older who do not have
contraindications. No specific vaccine product is
preferable to another if more than one product is
appropriate for an individual patient. This year’s updates
include changes to the U.S. trivalent influenza vaccine
and the quadrivalent influenza vaccine, the availability
of new recently licensed vaccine alternatives for specific
populations, and a new vaccine option for adults with
egg allergy. Table 1 lists the influenza vaccines available
for 2013-2014; contraindications and precautions to the
influenza vaccine are presented in Table 2.
This season, the U.S. trivalent influenza vaccines include
an A/California/7/2009 (H1N1)–like virus, an H3N2 virus
antigenically like the cell-propagated prototype virus
A/Victoria/361/2011, and a B/Massachusetts/2/2012–like
virus. The quadrivalent vaccines include an additional
virus strain, which is a B/Brisbane/60/2008–like virus.
There are several newly licensed vaccine alternatives
expected to be available. A quadrivalent live attenuated
influenza vaccine (Flumist) is anticipated to replace
the trivalent formulation; it is appropriate for healthy,
nonpregnant persons two to 49 years of age. Three
quadrivalent inactivated influenza vaccines are available
in addition to their previous trivalent formulations;
Fluarix and Flulaval are indicated for persons three
years or older, and Fluzone is indicated for persons six
months or older. Finally, a trivalent cell culture–based
inactivated influenza vaccine (Flucelvax) is indicated
for persons 18 years or older, and a recombinant
hemagglutinin vaccine (Flublok) is available for persons
18 to 49 years of age.
Although this is the first season both the trivalent and
quadrivalent inactivated influenza vaccines are available,
the quantity of quadrivalent doses may be limited. The
quadrivalent dose provides broader protection against
circulating influenza B viruses during seasons when
the B virus in the trivalent vaccine is not an optimal
match. There is no preference between the trivalent and
quadrivalent inactivated vaccines; therefore, if only the
trivalent vaccine is available, it should be used so as
not to delay vaccination. Additionally, the high-dose
trivalent inactivated influenza vaccine (Fluzone High-
Table 1. Vaccines for the 2013-2014 Influenza Season
Vaccine
Dispensing method
Mercury content
(mcg per 0.5-mL
dose)
Ovalbumin
Approved
content (mcg
ages
per 0.5-mL dose)
Route of
administration
0.5-mL single-dose prefilled syringe
0
≤ 1.0
≥ 9 years*
Intramuscular†
5.0-mL multidose vial
24.5
≤ 1.0
≥ 9 years*
Intramuscular†
Fluarix
0.5-mL single-dose prefilled syringe
0
≤ 0.05
≥ 3 years
Intramuscular†
Flucelvax
0.5-mL single-dose prefilled syringe
0
Not included‡
≥ 18 years
Intramuscular†
Flulaval
5.0-mL multidose vial
< 25.0
≤ 0.3
≥ 3 years
Intramuscular†
Fluvirin
0.5-mL single-dose prefilled syringe
≤ 1.0
≤ 1.0
≥ 4 years
Intramuscular†
5.0-mL multidose vial
25.0
≤ 1.0
≥ 4 years
Intramuscular†
0.25-mL single-dose prefilled syringe
0
—§
6 to 35 months
Intramuscular†
0.5-mL single-dose prefilled syringe
0
—
≥ 36 months
Intramuscular†
0.5-mL single-dose vial
0
—
≥ 36 months
Intramuscular†
5.0-mL multidose vial
25.0
—
≥ 6 months
Intramuscular†
0.1-mL prefilled microinjection system
0
—
18 to 64 years
Inactivated influenza vaccine, trivalent, standard dose
Afluria
Fluzone
Fluzone
intradermal||
Intradermal¶
continued...
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Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013

17. American Family Physician
Table 1. Vaccines for the 2013-2014 Influenza Season (continued)
Vaccine
Dispensing method
Mercury
content (mcg
per 0.5-mL
dose)
Ovalbumin
content (mcg
per 0.5-mL
dose)
Approved
ages
Route of
administration
0
—
≥ 65 years
Intramuscular†
Inactivated influenza vaccine, trivalent, high dose
Fluzone High-Dose** 0.5-mL single-dose prefilled syringe
Inactivated influenza vaccine, quadrivalent, standard dose
Fluarix quadrivalent
0.5-mL single-dose prefilled syringe
0
≤ 0.05
≥ 3 years
Intramuscular†
Flulaval quadrivalent
5.0-mL multidose vial
< 25.0
≤ 0.3
≥ 3 years
Intramuscular†
0
—
6 to 35 months
Intramuscular†
0.5-mL single-dose prefilled syringe
0
—
≥ 36 months
Intramuscular†
0.5-mL single-dose vial
0
—
≥ 36 months
Intramuscular†
0
0
18 to 49 years
Intramuscular†
0 (per 0.2-mL
dose)
< 0.24 (per 0.2mL dose)
2 to 49 years‡‡
Intranasal
Fluzone quadrivalent 0.25-mL single-dose prefilled syringe
Recombinant influenza vaccine, trivalent
Flublok
0.5-mL single-dose vial
Live attenuated influenza vaccine, quadrivalent
Flumist
quadrivalent††
0.2-mL single-dose prefilled
intranasal sprayer
Note: Immunization providers should check U.S. Food and Drug Administration–approved prescribing information for 2013-2014 influenza vaccines for
the most complete and updated information, including (but not limited to) indications, contraindications, and precautions. Package inserts for U.S.licensed vaccines are available at http://www.fda.gov/BiologicsBloodVaccines/Vaccines/ApprovedProducts/ucm093833.htm.
*Age indication per package insert is 5 years or older; however, the Advisory Committee on Immunization Practices recommends that Afluria not be used
in children 6 months to 8 years of age because of increased risk of febrile reactions noted in this age group with 2010 Southern Hemisphere trivalent
inactivated vaccine. If no other age-appropriate, licensed inactivated seasonal influenza vaccine is available for a child 5 to 8 years of age who has a medical
condition that increases the child’s risk of influenza complications, Afluria can be used; however, health care professionals should discuss with the parents
or caregivers the benefits and risks of influenza vaccination with Afluria before administering this vaccine. Afluria may be used in persons 9 years or older.
†For adults and older children, the recommended site of vaccination is the deltoid muscle. The preferred site for infants and young children is the anterolateral
aspect of the thigh. Specific guidance regarding site and needle length for intramuscular administration may be found in the Advisory Committee on
Immunization Practices General Recommendations on Immunization (Centers for Disease Control and Prevention. General recommendations on immunization:
recommendations of the Advisory Committee on Immunization Practices, 2011. MMWR. 2011;60[RR-2].).
‡Information not included in package insert. The total egg protein is estimated to be less than 50 femtograms (5 × 1014 g) total egg protein (of which a
fraction is ovalbumin) per 0.5-mL dose of Flucelvax.
§Available on request from Sanofi Pasteur (1-800-822-2463 or MIS.Emails@sanofipasteur.com).
||Inactivated influenza vaccine, intradermal: a 0.1-mL dose contains 9 mcg of each vaccine antigen (27 mcg total).
¶The preferred site is over the deltoid muscle. Fluzone intradermal is administered using the delivery system included with the vaccine.
**Inactivated influenza vaccine, high dose: a 0.5-mL dose contains 60 mcg of each vaccine antigen (180 mcg total).
††It is anticipated that the quadrivalent formulation of Flumist will replace the trivalent formulation for the 2013-2014 season. Flumist is shipped refrigerated
and stored in the refrigerator at 35°F to 46°F (2°C to 8°C) after arrival in the vaccination clinic. The dose is 0.2 mL divided equally between each nostril.
Health care professionals should consult the medical record, when available, to identify children 2 to 4 years of age with asthma or recurrent wheezing that
might indicate asthma. In addition, to identify children who might be at greater risk of asthma and possibly at increased risk of wheezing after receiving live
attenuated influenza vaccine, parents or caregivers of children 2 to 4 years of age should be asked, “In the past 12 months, has a health care professional
ever told you that your child had wheezing or asthma?” Children whose parents or caregivers answer “yes” to this question and children who have asthma
or who had a wheezing episode noted in the medical record within the past 12 months should not receive Flumist.
‡‡Flumist is indicated for healthy, nonpregnant persons 2 to 49 years of age. Persons who care for severely immunosuppressed persons who require a
protective environment should not receive Flumist given the theoretical risk of transmission of the live attenuated vaccine virus.
Dose) is approved for persons 65 years or older. Three
prelicensure studies among persons in this age group
showed that, compared with the standard dose, the
high-dose vaccine elicited higher hemagglutination
inhibition antibody titers against the three virus strains
included in the seasonal influenza vaccine during the
study period. However, there is no recommendation
for using the high-dose vaccine vs. the standard-dose
vaccine in this population.
Persons 18 to 49 years of age who have an egg allergy of
any severity now have the option of receiving trivalent
recombinant influenza vaccine, an egg-free vaccine. In
persons who have no known history of egg exposure
but who have received allergy test results suggestive of
an egg allergy, consultation with a physician who has
expertise in allergy management is recommended before
vaccination. Figure 1 provides an algorithm for influenza
vaccination in persons who report an allergy to eggs.
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
517

18. American Family Physician
Table 2. Contraindications and Precautions* to the Use of 2013-2014 Influenza Vaccines
Inactivated, including trivalent, quadrivalent, and cell culture–based
History of severe allergic reaction to any component of the vaccine, including egg protein, or after previous dose of any influenza vaccine
Recombinant
History of severe allergic reaction to any component of the vaccine
Live attenuated
History of severe allergic reaction to any component of the vaccine, including egg protein, gentamicin, gelatin, and arginine, or after a
previous dose of any influenza vaccine
Concomitant aspirin therapy in children and adolescents
In addition, the Advisory Committee on Immunization Practices recommends against use in the following groups:
Children < 2 years
Persons with asthma
Persons with egg allergy
Adults ≥ 50 years
Children and adults who have chronic
pulmonary, cardiovascular (except isolated
hypertension), renal, hepatic, neurologic/
neuromuscular, hematologic, or metabolic
disorders
Close contacts and caregivers of severely
immunosuppressed persons who require
a protected environment
Children 2 to 4 years of age whose parents
or caregivers report that a health care
professional has told them during the past
12 months that their child had wheezing or
asthma, or whose medical record indicates Children and adults who have
a wheezing episode has occurred during the immunosuppression (including
past 12 months (Table 1)
immunosuppression caused
by medications or by human
immunodeficiency virus infection)
Pregnant women
Note: Immunization providers should check U.S. Food and Drug Administration–approved prescribing information for 2013-2014 influenza vaccines for
the most complete and updated information, including (but not limited to) indications, contraindications, and precautions. Package inserts for U.S.licensed vaccines are available at http://www.fda.gov/BiologicsBloodVaccines/Vaccines/ApprovedProducts/ucm093833.htm.
*Precautions should be taken in persons with moderate to severe illness with or without fever, and in persons with a history of Guillain-Barré syndrome
within six weeks of receipt of influenza vaccine.
Influenza Vaccination in Patients with Egg Allergy
Can the person eat lightly cooked egg (e.g., scrambled egg)
without reaction?*
No
After eating eggs or egg-containing foods, does the person
experience only hives?
Yes
Yes
No
Yes
After eating eggs or egg-containing foods, does the individual
experience other symptoms such as:
Cardiovascular changes (e.g., hypotension)
Respiratory distress (e.g., wheezing)
Gastrointestinal symptoms (e.g., nausea, vomiting)
Reaction requiring epinephrine
Reaction requiring emergency medical attention
Administer vaccine per usual protocol
Administer recombinant influenza vaccine, trivalent,
if patient is 18 to 49 years of age
or
Administer inactivated influenza vaccine
Observe for reaction for at least 30 minutes following
vaccination
Administer recombinant influenza vaccine, trivalent,
if patient is 18 to 49 years of age
or
Refer to a physician with expertise in management of
allergic conditions for further evaluation
*Persons with egg allergy might tolerate egg in baked products (e.g., bread or cake). Tolerance to egg-containing foods does not exclude the
possibility of egg allergy. For persons who have no known history of exposure to egg but who are suspected of being egg-allergic on the basis of
previously performed allergy testing, consultation with a physician who has expertise in the management of allergic conditions should be obtained
before vaccination. Alternatively, recombinant influenza vaccine, trivalent, may be administered if the recipient is 18 to 49 years of age.
Figure 1. Algorithm for influenza vaccination in persons who report egg allergy.
Source: Adapted from Am Fam Physician. 2013;88(8):543-550.
518
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013

19. American Family Physician
Photo Quiz
Acute Foot Rash in a Healthy Child During
Travel
During a trip to Brazil, a two-year-old girl presented
with sudden foot pain while playing in the dirt near
a tree. Her mother saw no glass, nails, or insects on
the ground where the child was playing. The sole of
the child’s left foot initially turned white in a linear
pattern. Three hours later, the foot was erythematous
with multiple petechiae (Figure 1). Swelling
progressed from the sole to the rest of the foot, and
then to the ankle with linear streaks. The child could
not put weight on the foot. Four hours after the
injury, she developed a fever of 103° F (39.4° C) and
was difficult to console. Oral and topical antibiotics
and acetaminophen were ineffective.
Question
Based on the patient’s history and physical examination,
which one of the following is the most likely diagnosis?
Figure 1.
A. Acute dermatitis.
B. Cellulitis.
C. Contusion.
D. Foreign body injury.
E. Insect bites.
SEE THE FOLLOWING PAGE FOR DISCUSSION.
Source: Adapted from Am Fam Physician. 2011;83(2):201-202.
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
519

20. American Family Physician
Summary Table
Condition
Characteristics
Acute dermatitis A transient but sometimes painful inflammatory
reaction of the skin; reactions vary from mild,
localized itching to more severe pain, swelling,
and inflammation; more severe systemic
reactions are rare but possible
Cellulitis
Diffuse inflammation of subcutaneous and
loose connective tissue caused by bacterial
infection; may lead to localized pain,
erythema, swelling, and warmth
Contusion
Mechanical injury resulting in hemorrhage
beneath unbroken skin; often associated
with blunt trauma; injury may evolve with time
Foreign body
injury
Localized trauma causing a wound; traumatic
injuries can range from minor to life threatening
Insect bite
Inflammation at the site of punctured skin;
usually appears within minutes to a few hours
after the bite
Discussion
The answer is A: Acute dermatitis from a caterpillar
sting.
Further investigation found lime green caterpillars
feeding on the leaves of the tree near where the child
was playing (Figure 2). Caterpillars usually camouflage
themselves on tree leaves.
The family returned to the United States nine days after
the injury, and the mother took the child to their family
physician. Physical examination revealed swelling,
purulent pockets, and multiple black caterpillar
hairs/spines on the bottom of the foot. The physician
discontinued the antibiotics and cleaned the area with
soapstone (localized debridement). The child was
able to walk on the foot after two days, and her fever
subsided.
Stinging caterpillars have specialized spines that contain
poison glands. If the spines penetrate the skin, toxins
spread on the surface of the skin, causing dermatitis.1,2
Reactions vary from mild, localized itching to more
severe pain, swelling, and inflammation. Occasionally,
a systemic response with diarrhea occurs. There have
been reports from around the world of reactions from
caterpillar stings, including dermatologic, pulmonary,
and other systemic reactions.2,3
Removal of the caterpillar spines through debridement
is the most effective means to counteract the toxic
process and clear the localized reaction. Stings from
some species of caterpillars can cause hemorrhagic
reactions and arthritis.4,5
520
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
Figure 2.
Cellulitis is a diffuse inflammation of subcutaneous and
loose connective tissue caused by bacterial infection.
It can lead to localized pain, erythema, swelling,
and warmth. Typical treatment involves appropriate
antibiotic therapy.6
Contusions are usually caused by mechanical injury
resulting in hemorrhage beneath unbroken skin. They
are often associated with blunt trauma, and the injury
may evolve over time.
Foreign body injuries are associated with localized
trauma that causes a wound. Traumatic injuries can
range from minor to life threatening. A typical reaction
to an insect bite is an inflammatory response at the site
of the punctured skin. It usually appears within minutes
to a few hours after the bite. Insects that commonly
bite humans include fleas, mosquitoes, ticks, bedbugs,
blackflies, and sand flies.6,7
REFERENCES
1. Stanton G. Stinging caterpillars out in late summer
and fall. http:// ipmnet.umd.edu/landscape/docs/
StingingCaterpillars-UMD.pdf. Accessed July 5, 2009.
2. Diaz JH. The evolving global epidemiology, syndromic
classification, management, and prevention of caterpillar
envenoming. Am J Trop Med Hyg. 2005;72(3):347-357.
3. Bessin R. Stinging caterpillars. http://www.ca.uky.edu/
entomology/entfacts/ef003.asp. Accessed July 5, 2009.
4. Secretaria de Estado da Saude do Parana. (Lonomia)
acidentes II. http://www.saude.pr.gov.br/modules/conteudo/
conteudo.php?conteudo= 389. Accessed July 5, 2009.
5. Lima C. Largatas que queimam. January 31, 2008. http://www.
olharvital. ufrj.br/2006/index.php?id_edicao=114&codigo=10.
Accessed July 5, 2009.
6. Ectoparasite infestations and arthropod and stings:
caterpillar stings and dermatitis. In: Kasper DL, Harrison
TR, eds. Harrison’s Principles of Internal Medicine. 16th
ed. New York, NY: McGraw-Hill; 2005:2607.
7. Lepidoptera: arthropods and leeches. In: Cecil RL,
Goldman L, Ausiello DA, eds. Cecil Textbook of Medicine.
22nd ed. Philadelphia, Pa.: Saunders; 2004:2128-2129.

21. CARDIOLOGY
Systolic and Diastolic Ratio and Rate Pressure
Product in Anemia
K Singh
Abstract
Anemia, a common clinical entity is associated with hyperdynamic circulation and may be involved in etiopathology of heart
failure. So, the current study was carried out in 30 patients in the age group 20-40 years with hemoglobin level < 6 g/dl and of
at least three month duration of anemia (using WHO definition) and compared with 30 age- and sex-matched healthy subjects.
Duration of systole and diastole was estimated by recording of electrocardiogram, apex-cardiogram and phonocardiogram
on polyrite with the paper speed of 50 mm/sec. Duration of cardiac cycle was reduced (18.22%) and heart rate was increased
(p < 0.001) in anemia compared to controls. On comparison of duration of systole and diastole, there was more decrement in
diastole (26.76%, p < 0.001) compare to systole (6.45%, p < 0.01) in anemia versus healthy subjects. Similarly, when fraction
occupied by systole and diastole in cardiac cycle were compared, the systolic fraction was increased, diastolic fraction in cardiac
cycle was reduced and systole/diastole ratio was increased (p < 0.001) in anemics compared to controls. Rate pressure product
and double product were elevated (p < 0.001) in anemia versus controls, imposing mechanical load on heart. So, it is concluded
that patients of severe anemia are at the brink of heart failure and should be treated promptly.
Keywords: Systole, diastole, cardiac cycle, anemia
S
ystole and diastole are the fundamental periods of
cardiac cycle. Intervals of cardiac cycle as measured
by echocardiography, apex-cardiography, i.e.,
isovolumic contraction time, isovolumic relaxation
time are used to assess ventricular function.1 Recently,
importance of duration of systole and diastole is
emphasized and it is advocated that they can be
used to assess cardiac functions as prognosis of
patients suffering from diastolic heart failure (DHF)
is as ominous as prognosis of patients suffering from
systolic heart failure (SHF).2
Anemia, a frequently encountered clinical entity, said
to be a risk factor for functional and cognitive disease3
imposes mechanical load on heart and may be involved
in pathogenesis and progression of heart failure,4
chronic angina5 and acute coronary syndrome.6
Moreover, it is associated with ventricular hypertrophy,
ischemia and increased heart rate.6 So, the current
study is planned to evaluate the duration of cardiac
Professor
Dept. of Physiology
Pt. BD Sharma, Postgraduate Institute of Medical Sciences (PGIMS), University of
Health Sciences Rohtak (UHSR), Rohtak, Haryana
Address for correspondence
Dr K Singh
6J-11, Medical Campus, Rohtak - 124 001, Haryana
E-mail: dr_rb_singh@rediffmail.com
cycle, ratio of systole/diastole (S/D ratio), rate pressure
product (RPP - since, it is an easy measurable index
of myocardial oxygen consumption and load on heart)7
and double product (DoP) in patients of anemia.
Methods
The study was carried out in 30 patients of anemia
(hemoglobin level was >6 g/dl for at least 3-month
duration)8 using World Health Organization (WHO)
definition of anemia - hemoglobin <13 g/dl for
men and <12 g/dl in women9 in the age group of
20-40 years (mean age 32.65 ± 1.62) with body mass
index (BMI) 22.9 ± 0.33 without clinical evidence
of cardiac decompensation, and 30 age- (mean
31.49 ± 3.34 years) and sex-matched healthy subjects
(hemoglobin level 11-14.02 g/dl) having BMI 22.2 ± 0.36.
Electrocardiogram (ECG), apex-cardiogram (ACG) and
phonocardiogram (PCG) were recorded with the paper
speed of 50 mm/sec on polyrite (INCO). Systole was
measured from onset of ventricular depolarization to
first high frequency vibration of aortic sound. Diastole
was measured from beginning of first high frequency
of second heart sound to the beginning of sudden
upstroke of ACG (Fig. 1). Duration of cardiac cycle,
proportion of cardiac cycle occupied by systole and
diastole, and S/D ratio were evaluated. Heart rate (HR)
was assessed from ECG (lead II). Blood pressure (BP)
was recorded manually by using sphygmomanometer.
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
521

22. CARDIOLOGY
RPP was calculated as SP × HR × 10-2, where SP is
systolic pressure and value obtained was expressed
as mmHg beats/min.7 Similarly, DoP was calculated
as MP x HR, where MP is mean pressure and it was
expressed in mmHg beats/min.10 Statistical analysis
was done by unpaired ‘t’ test. Values were expressed
as mean ± SD. A p value of < 0.05 was accepted as
significant.
Result
Duration of cardiac cycle was 884.76 ± 87.54 msec.
in normal healthy controls at the HR of 75.4 ± 12.5
beats/min in contrast to 723.5 ± 55.02 msec at the HR
of 92.08 ± 18.19 beats/min in anemia. This reduction
in duration of cardiac cycle (18.22%) was significant
(p < 0.001). Duration of systole and diastole was 372.06
± 29.41 versus 512.70 ± 110.14 msec, respectively in
controls compared to duration of systole and diastole
348.04 ± 39.46 versus 375.46 ± 107.40 msec, respectively
Electrocardiogram
Apex-cardiogram
Phonocardiogram
Systole Diastole
Figure 1. Simultaneous recording of ECG, ACG and PCG
in controls.
Electrocardiogram
Apex-cardiogram
Phonocardiogram
Figure 2. Simultaneous recording of ECG, ACG and PCG
in anemia.
522
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
in anemic patients. On comparison of systole and
diastole, there was more decrement in diastole (26.76%,
p < 0.001) compared to systole (6.45%, p < 0.001) in
anemic patients versus healthy controls (Fig. 2).
In healthy subjects systole and diastole constitute
42.05% and 57.94% fraction of cardiac cycle, respectively.
While in anemia systole and diastole constitute 48.1%
and 51.89% fraction of cardiac cycle, respectively,
indicating fraction of systole was increased and diastole
was reduced in anemia (Table 1). S/D ratio was lengthened
(p < 0.001) in anemia, i.e., 1.04 ± 0.23 versus 0.71 ± 0.06
in controls (Fig. 2). RPP and DoP were significantly
(p < 0.001) elevated in anemia compared to controls
(Table 1).
Discussion
Anemia is said to be involved in the pathogenesis of heart
failure (HF).4 It is hypothesized that relative duration of
systole and diastole are altered and S/D ratio increases
in HF.1 Duration of cardiac cycle in present study is
about 0.88 second at normal HR in controls, which is in
agreement with other authors.11 But in anemia, duration
of cardiac cycle is shortened, which may be explained
by hyperkinetic circulation. Reduction in duration of
diastole is more (26%) than systole (6.4%), may be due to
tachycardia. Tachycardia adversely affects the diastolic
function by several mechanisms, as it diminishes the left
ventricular filling, coronary perfusion time, increases
myocardial oxygen demand, raises myocardial oxygen
consumption and causes incomplete relaxation.12 It has
to be noted that although duration of systole as such is
reduced, proportion of cardiac cycle occupied by systole
is lengthened from 42.05% in controls to 48% in anemics.
In contrast proportion of cardiac cycle occupied by
diastole is more reduced in anemia, from 57.9% to 51%
in controls and anemics, respectively. All these changes
result in enhanced S/D ratio in anemia in current study,
which is consistent with the findings described by
other authors in patients of HF. Myocardial perfusion
occurs primarily in diastole. Myocardial blood flow
in patients of left ventricular hypertrophy (LVH)
(anemia can be associated with LVH) may depend
upon diastolic perfusion time and perfusion pressure.
Myocardial remodeling induced by renin-angiotensin
system activated due to decreased renal perfusion
and increased catecholamine secretion in anemia
predisposes the ischemic damage.13 Reduced oxygen
carrying capacity of blood, increase in circulation time
and HR with reduction in diastolic time may further
complicate coronary perfusion and still worsen the
cardiac function.1

23. CARDIOLOGY
Table 1. Comparison of Parameters in Control and in Anemia (Mean ± SD)
Parameters
Heart
rate
(beats/
min)
Systolic Diastolic
BP
BP
(mmHg) (mmHg)
Cardiac
cycle
length
(msec)
Duration
of
systole
(msec)
Duration
of
diastole
(msec)
Proportion of
systole and
diastole (%)
in cardiac
cycle
S/D
ratio
RPP
mmHg,
beats/
min
DoP
mmHg,
beats/
min
Controls
75.4 ±
12.5
120.80 ±
8.90
71.10 ±
9.20
884.76 ±
87.54
372.06 ±
29.41
512.70 ±
110.14
42.05 and
57.94
0.71 ±
0.06
91.06 ±
12.32
7609.56
± 190.5
Anemia
92.08**
± 18.19
111.04**
± 10.21
70.80 ±
9.27
723.5** ±
55.02
348.04*
± 39.46
375.46**
± 107.40
48.1 and
51.89
1.04** ±
0.23
Difference or
p value
<0.001
<0.001
NS
18.22%
6.45%
26.76%
<0.001
102.24** 9029.37**
± 15.21 ± 260.1
0.001
<0.001
P value * = <0.01, ** = <0.001.
BP = Blood pressure; S/D ratio = Systolic/Diastolic ratio; RPP = Rate pressure product; DoP = Double product.
But clinical signs and symptoms pointing to HF were
not evident in these patients.14 They were not taking
treatment of it inspite of enhanced RPP and DoP in
anemia indicating increase in O2 consumption and
load on the heart. Enhanced O2 consumption of cardiac
muscles in severe anemia is demonstrated by other
authors also.15 But it is difficult to explain the reason
for absence of features of HF, may be at this HR filling
of LV is adequate enough to maintain cardiac output.11
As it is also stated that DHF is referred to as HF with
normal left ventricular ejection fraction (LVEF), i.e.
HFNLVEF.12 Moreover, onsets of symptoms also depend
on the rapidity with which the anemia develops as well
as physical activity of patient.
So, our findings as lengthened systole, enhanced systolic
and diastolic ratio and reduction in duration of diastole
pointed out that patients of anemia are at the brink of
HF. So, while treating the patient of HF and coronary
artery disease, we should also have a look for anemia
as treatment of systole and diastole failure is different.
References
1. Friedberg MK, Silverman NH. Cardiac ventricular diastolic
and systolic duration in children with heart failure
secondary to idiopathic dilated cardiomyopathy. Am J
Cardiol 2006;97(1):101-5.
2. Aurigemma GP. Diastolic heart failure: a common and lethal
condition by any name. N Engl J Med 2006;355(3):308-10.
3. Denny SD, Kuchibhatla MN, Cohen HJ. Impact of anemia
on mortality, cognition, and function in communitydwelling elderly. Am J Med 2006;119(4):327-34.
4. de Silva R, Rigby AS, Witte KK, Nikitin NP, Tin L, Goode
K, et al. Anemia, renal dysfunction, and their interaction
in patients with chronic heart failure. Am J Cardiol
2006;98(3):391-8.
5. Sharma S, Gage BF, Deych E, Rich MW. Anemia: an
independent predictor of death and hospitalizations
among elderly patients with atrial fibrillation. Am Heart J
2009;157(6):1057-63.
6. Meneveau N, Schiele F, Seronde MF, Descotes-Genon V,
Oettinger J, Chopard R, et al; Reseau de Cardiologie de
Franche Comte. Anemia for risk assessment of patients with
acute coronary syndromes. Am J Cardiol 2009;103(4):442-7.
7. Gobel FL, Norstrom LA, Nelson RR, Jorgensen CR,
Wang Y. The rate-pressure product as an index of
myocardial oxygen consumption during exercise in
patients with angina pectoris. Circulation 1978;57(3):
549-56.
8. Agarwal V, Sachdev A, Lehl S, Basu S. Unusual
haematological alterations in rheumatoid arthritis. J
Postgrad Med 2004;50(1):60-1.
9. Felker GM, Gattis WA, Leimberger JD, Adams KF, Cuffe
MS, Gheorghiade M, et al. Usefulness of anemia as a
predictor of death and rehospitalization in patients with
decompensated heart failure. Am J Cardiol 2003;92(5):625-8.
10. Madanmohan, Udupa K, Bhavanani AB, Vijayalakshmi
P, Surendiran A. Effect of slow and fast pranayams on
reaction time and cardiorespiratory variables. Indian J
Physiol Pharmacol 2005;49(3):313-8.
11. Ganong WF. Heart as a pump. Chapter 29. In: Review of
Medical Physiology. 21st edition, A Lange Medical Book:
McGraw-Hill, New Delhi 2010;Chap. 31, Sec.VI, p.570.
12. Chopra HK. Diastolic heart failure: a clinical challenge
early recognition and timely intervention is the need of the
hour. Indian Heart J 2009;61(2):138-45.
13. Schrier RW, Abraham WT. Mechanism of disease:
Hormones and haemodynamics in heart failure. N Engl J
Med 1999;341:577-85.
14. Braunwald E. Heart failure and corpulmonale. Chapter
216. In: Harrison’s Principle of Internal Medicine. Vol. II,
6th edition, McGraw-Hill: New York 2005:p.1370.
15. Levy PS, Quigley RL, Gould SA. Acute dilutional anemia
and critical left anterior descending coronary artery
stenosis impairs end organ oxygen delivery. J Trauma
1996;41(3):416-23.
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
523

24. DENTISTRY
Probiotics: How Promising are they in Promoting
Periodontal Health?
R Hemalatha*, A Sivachandran**
Abstract
With the widespread emergence of bacterial resistance to antibiotics, the concept of probiotic therapy has been considered for
application in oral health. Dental caries, periodontal disease and halitosis are among the oral disorders that have been targeted.
More than 700 species of oral microbiota have been detected in the human mouth and the resident microbiota of an individual
may consist of 30-100 species. Studies suggest that lactobacilli as members of resident oral microflora could play an important
role in the microecological balance in the oral cavity.
Keywords: Probiotic therapy, dental caries, periodontal disease, halitosis, lactobacilli
T
he term ‘probiotics’, the antonym of the term
‘antibiotics’, was introduced in 1965 by Lilly
and Stillwell as substances produced by
microorganisms that promote the growth of other
microorganisms. First probiotic species to be introduced
in research was Lactobacillus acidophilus by Hull et al in
1984, followed by Bifidobacterium bifidum by Holcombh
et al in 1991.1,2 Probiotics most commonly belong to the
genera Lactobacillus and Bifidobacterium.
The term ‘probiotic’ is derived from the Greek
word, meaning ‘for life’.3 As defined by the Food
Agricultural Organization/World Health Organization
(FAO/WHO) probiotics are living organisms, principally
bacteria, that are safe for human consumption and,
when ingested in sufficient quantities, have beneficial
effects on human health, beyond the basic nutrition.4
Such nonpathogenic organisms (yeasts or bacteria,
particularly lactic acid bacteria) are present in food and
can have a favorable impact on host health.
Common Probiotic Strains
Essential Conditions for Microorganisms
to Exert Probiotic Properties
To exert probiotic properties in the oral cavity, it is
essential for the microorganisms that they:6
ÂÂ
Should resist the oral environmental conditions
and defense mechanisms
ÂÂ
Should adhere to the saliva-coated surfaces
ÂÂ
Should colonize and grow in the mouth
ÂÂ
Should inhibit oral pathogens
ÂÂ
Should be also safe for the host.
Periodontal pathogens
The main pathogenic
periodontitis are:
agents
associated
ÂÂ
Porphyromonas gingivalis
ÂÂ
Treponema denticola
ÂÂ
Tannerella forsythia
ÂÂ
with
Aggregatibacter actinomycetemcomitans.7
Lactobacillus species from which probiotic strains have
been isolated include L. acidophilus, L. johnsonii, L. casei,
L. rhamnosus, L. gasseri and L. reuteri. Bifidobacterium
strains include B. bifidum, B. longum and B. infantis.5
These bacteria have a variety of virulent characteristics
allowing them to colonize the subgingival sites, escape
the host’s defense system and cause tissue damage.7
*Reader
Karpaga Vinayaga Institute of Dental Sciences, Kanchipuram, Tamil Nadu
**Senior Lecturer
SRM Kattankulathur Dental College, Kanchipuram, Tamil Nadu
Address for correspondence
Dr A Sivachandran, Senior Lecturer
SRM Kattankulathur Dental College, Kanchipuram, Tamil Nadu
The treatment strategies conferred by probiotics
against periodontal diseases are mainly anticipated
to be either by inhibition of specificx pathogens or
by altering the host immune response through the
following multiple factors:6,8,9
524
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
Probiotics: Proposed Mechanism of Action
Against Periodontal Pathogens

25. DENTISTRY
ÂÂ
Inhibition of specific organisms
Inhibition of pathogen adhesion, colonization and
biofilm formation
Inhibition of pathogen growth by various substances
such as organic acids, hydrogen peroxide and
bacteriocins against oral pathogens
Effects on host response
Inhibition of collagenases and reduction of
inflammation-associated molecules
Induction of expression of cytoprotective proteins
on host cell surfaces
Modulation of proinflammatory pathways induced
by pathogens
Prevention of cytokine-induced apoptosis
ÂÂ
Modulation of host immune response
ÂÂ
ÂÂ
ÂÂ
ÂÂ
ÂÂ
ÂÂ
ÂÂ
Probiotics: Role in prevention of
periodontal disease
Various studies have reported the capacity of lactobacilli
to inhibit the growth of periodontopathogens,
including P. gingivalis, Prevotella intermedia and
A. actinomycetemcomitans.10,11
Krasse and colleagues12 assessed the beneficial effect
of L. reuteri against gingivitis. First, L. reuteri is known
for its secretion of two bacteriocins, reuterin and
reutericyclin, that inhibit the growth of a wide variety
of pathogens;13,14 second, L. reuteri has a strong capacity
to adhere to host tissues, thereby competing with
pathogenic bacteria.15
periodontitis.19 Hojo et al suggested that Bifidobacterium
inhibited some black-pigmented anaerobes by
competing for an essential growth factor vitamin K.20
Shimauchi et al demonstrated that the oral
administration of a tablet containing L. salivarius
WB21 decreased plaque index significantly and pocket
probing depth markedly in smokers and reduced
salivary lactoferrin at the end of 8-week trial.21
Twetman et al used L. reuteri-containing chewing gum in
42 healthy patients and assessed its effects on crevicular
fluid volume, cytokine (interleukin-1β, interleukin-6,
interleukin-10 and tumor necrosis factor-α [TNF-α])
levels and bleeding on probing. Crevicular fluid
volume, as well as TNF-α and interleukin-8 levels and
bleeding were significantly reduced.22
When the probiotic Streptococcus salivarius K12 was
added to this bacterial model, the amount of cytokine
release was greatly reduced after eight hours. This
strongly suggests that S. salivarius K12 was able to
dramatically downregulate the cytokine release from
the pathogenic bacteria.23
Probiotics and Halitosis
Kang and colleagues24 reported the capacity of various
strains of W. cibaria to inhibit the production of volatile
sulfur compounds by F. nucleatum. They concluded
that this beneficial effect resulted from the production
of hydrogen peroxide by W. cibaria, which inhibited the
proliferation of F. nucleatum.24
Staab et al observed reduction in activity of matrix
metalloprotein-3 (MMP-3) and elastase enzymes in
subjects with plaque-induced gingivitis after consuming
probiotic milk containing Lactobacillus casei species for a
period of eight weeks.16
Currently Available Probiotic Agents in
Periodontal Disease Management
Riccia et al studied the anti-inflammatory effects of
Lactobacillus brevis in a group of patients with chronic
periodontitis. Anti-inflammatory effects of L. brevis
could be attributed to its capacity to prevent the
production of nitric oxide and consequently the release
of prostaglandin E2(PGE2) and the activation of MMPs
induced by nitric oxide.17
ÂÂ
Probiotics in the form of tablets, lozenges, chewing
gums or toothpastes are available:
Another probiotic lozenge is avaliable, which
is a blend of two L. reuteri strains containing a
minimum of 1 × 108 colony forming units (CFU)
for each of the strains DSM 17938 and ATCC PTA
5289.26
Ishikawa et al observed in vitro inhibition of P. gingivalis,
P. intermedia and P. nigrescens by daily ingestion of
L. salivarius in tablet form.18
Van Essche et al have reported that B. bacteriovorus
attack, prey on and kill A. actinomycetemcomitans,
thus suggesting a potential scope for the role of
B. bacteriovorus in the prevention and treatment of
Lozenges: One of the first probiotic specifically
formulated to fight periodontal disease, contained
a patented combination of two strains of L. reuteri
selected for their synergistic properties in fighting
cariogenic bacteria and periodontopathogens. Each
dose of lozenge contained at least 2 × 108 living
cells of L. reuteri Prodentis.25
ÂÂ
Toothpastes: Toothpastes containing Dental-Lac,
a functional Lactobacillus paracasei probiotic are
available.25
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
525

26. DENTISTRY
ÂÂ
Tablets: A probiotic preparation, which is a
complex of five live lyophilized lactic acid bacteria
is available and is claimed to improve both clinical
and microbiologic parameters in gingivitis and
mild periodontitis patients.
Conclusion
Various studies have shown that the use of oral
probiotics is associated with improvement in
periodontal health. More research and clinical trials
will facilitate identification of the probiotics that are
best suited to oral use, as well as the most appropriate
vehicles: Food products (cheese, milk, yogourt) or
supplements (chewing gum, lozenges). The existence
of probiotics in the indigenous oral microflora of
humans needs exploration because these bacteria offer
the advantage of being perfectly adapted to the human
oral ecosystem.
References
1. Tanboga I, Caglar E, Kargul B. Campaign of probiotic
food consumption in Turkish children, oral perspectives
“Probiotics for your child”. Int J Pediatr Dent 2003;13:59-64.
2. Flichy-Fernández AJ, Alegre-Domingo T, PeñarrochaOltra D, Peñarrocha-Diago M. Probiotic treatment in the
oral cavity: an update. Med Oral Patol Oral Cir Bucal
2010;15(5):e677-80.
3. Hamilton-Miller JM, Gibson GR, Bruck W. Some insights
into the derivation and early uses of the word ‘probiotic’.
Br J Nutr 2003;90(4):845.
4. Report of a Joint FAO/WHO Expert consultation on
evaluation of health and nutritional properties of
probiotics in food including powder milk with live lactic
acid bacteria. FAO/WHO, October 2001.
5. Suvarna VC, Boby VU. Probiotics in human health: a
current assessment. Curr Science 2005;88:1744-88.
6. Stamatova I, Meurman JH. Probiotics and periodontal
disease. Periodontol 2000 2009;51:141-51.
7. Houle MA, Grenier D. Maladies parodontales: connaissances
actuelles. Current concepts in periodontal diseases.
Médecine et Maladies Infectieuses 2003;33(7): 331-40.
8. Mackay AD, Taylor MB, Kibbler CC, Hamilton-Miller JM.
Lactobacillus endocarditis caused by a probiotic organism.
Clin Microbiol Infect 1999;5(5):290-2.
9. Reid G, Jass J, Sebulsky MT, McCormick JK. Potential
uses of probiotics in clinical practice. Clin Microbiol Rev
2003;16(4):658-72.
10. Sookkhee S, Chulasiri M, Prachyabrued W. Lactic acid
bacteria from healthy oral cavity of Thai volunteers:
inhibition of oral pathogens. J Appl Microbiol
2001;90(2):172-9.
11. Kõll-Klais P, Mändar R, Leibur E, Marcotte H,
Hammarström L, Mikelsaar M. Oral lactobacilli in chronic
periodontitis and periodontal health: species composition
and antimicrobial activity. Oral Microbiol Immunol
2005;20(6):354-61.
526
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12. Krasse P, Carlsson B, Dahl C, Paulsson A, Nilsson A,
Sinkiewicz G. Decreased gum bleeding and reduced
gingivitis by the probiotic Lactobacillus reuteri.
Swed Dent J 2006;30(2):55-60.
13. Gänzle MG, Höltzel A, Walter J, Jung G, Hammes
WP. Characterization of reutericyclin produced by
Lactobacillus reuteri LTH2584. Appl Environ Microbiol
2000;66(10):4325-33.
14. Talarico TL, Casas IA, Chung TC, Dobrogosz WJ.
Production and isolation of reuterin, a growth inhibitor
produced by Lactobacillus reuteri. Antimicrob Agents
Chemother 1988;32(12):1854-8.
15. Mukai T, Asasaka T, Sato E, Mori K, Matsumoto M,
Ohori H. Inhibition of binding of Helicobacter pylori to
the glycolipid receptors by probiotic Lactobacillus reuteri.
FEMS Immunol Med Microbiol 2002;32(2):105-10.
16. Staab B, Eick S, Knöfler G, Jentsch H. The influence of a
probiotic milk drink on the development of gingivitis: a
pilot study. J Clin Periodontol 2009;36(10):850-6.
17. Riccia DN, Bizzini F, Perilli MG, Polimeni A, Trinchieri
V, Amicosante G, et al. Anti-inflammatory effects of
Lactobacillus brevis (CD2) on periodontal disease. Oral Dis
2007;13(4):376-85.
18. Ishikawa H, AibaY, Nakanishi M, Oh-Hashi Y, Koga Y.
Suppression of periodontal pathogenic bacteria by the
administration of Lactobacillus salivarius T12711. J Jap Soc
Periodontol 2003;45:105-12.
19. Van Essche M, Quirynen M, Sliepen I, Van Eldere
J, Teughels W. Bdellovibrio bacteriovorus attacks
Aggregatibacter actinomycetemcomitans. J Dent Res
2009;88(2):182-6.
20. Hojo K, Mizoguchi C, Taketomo N, Ohshima T, Gomi K,
Arai T, et al. Distribution of salivary Lactobacillus and
Bifidobacterium species in periodontal health and disease.
Biosci Biotechnol Biochem 2007;71(1):152-7.
21. Shimauchi H, Mayanagi G, Nakaya S, Minamibuchi
M, Ito Y, Yamaki K, et al. Improvement of periodontal
condition by probiotics with Lactobacillus salivarius WB21:
a randomized, double-blind, placebo-controlled study.
J Clin Periodontol 2008;35(10):897-905.
22. Twetman S, Derawi B, Keller M, Ekstrand K, YucelLindberg T, Stecksen-Blicks C. Short-term effect of
chewing gums containing probiotic Lactobacillus reuteri
on the levels of inflammatory mediators in gingival
crevicular fluid. Acta Odontol Scand 2009;67(1):19-24.
23. Streptococcus salivarius K12 and M18 Probiotics reduce
Periodontal Pathogen-induced inflammation.
24. Kang MS, Kim BG, Chung J, Lee HC, Oh JS. Inhibitory
effect of Weissella cibaria isolates on the production
of volatile sulphur compounds. J Clin Periodontol
2006;33(3):226-32.
25. Wilson M. Manipulation of the indigenous microbiota.
In: Microbial Inhabitants of Humans. Wilson M (Eds.),
Cambridge University Press: New York 2005:p.395 -416.
26. Vivekananda MR, Vandana KL, Bhat KG. Effect of the
probiotic Lactobacilli reuteri (Prodentis) in the management
of periodontal disease: a preliminary randomized clinical
trial. J Oral Microbiol 2010;2.

27. DERMATOLOGY
Herpes Zoster: Multiple Presentations in a Single
Patient
SONIA JAIN
Abstract
Herpes zoster is a common viral opportunistic infection in human immunodeficiency virus (HIV)-infected patients with low
CD4 count and high viral load. This is consistent with previous observations that HIV-infected individuals on highly active
antiretroviral therapy (HAART) may not fully recover from the varicella zoster virus-specific cell-mediated immune (CMI)
responses. Herpes zoster is an acute posterior ganglion radiculitis and results from reactivation of the varicella zoster virus that
remains quiescent in the neurons. It can occur in any age, irrespective of the immune status. Here we report the case of an elderly
male who was seropositive for HIV and had an atypical presentation with disseminated and multidermatomal herpes zoster.
Keywords: Multidermatomal, herpes zoster, human immunodeficiency virus
D
espite three decades of concerted effort, human
immunodeficiency virus (HIV) epidemic
poses a tremendous public health challenge
in developed and developing countries.1,2 Varicella
zoster virus (VZV) is a neurotropic virus belonging to
alpha herpesvirus group. Primary infection occurs as
varicella (chicken pox) after which the virus remains
latent in ganglionic neurons along the entire neuraxis.
Factors like increasing age, immunosuppression, organ
transplant, malignancy or acquired immunodeficiency
syndrome (AIDS) cause reactivation of VZV to produce
herpes zoster.3 There is high incidence of zoster in HIVpositive adults4,5 and children,6 where it follows a more
protracted course. VZV reactivation produces multiple
ocular and neural disorders, estimated to occur in
upto 11% of HIV-positive cases.7 Multidermatomal
and disseminated herpes zoster frequently occurs in
patients with lymphoreticular malignancy or HIV
infection.8
Case Report
We report a case of a 65-year-old married man
who presented to us with multiple vesiculobullous,
hemorrhagic lesions associated with burning sensation
over his left upper back of arm, forearm and medial
three fingers of hand (Figs. 1-3). He also had large
eschar (gangrenous) with hyperpigmentation and
Professor
Dept. of Skin and VD
Mahatma Gandhi Institute of Medical Sciences
Sewagram, Wardha, Maharashtra
Figure 1. Multiple vesiculobullous hemorrhagic lesions over
left arm and medial three fingers of hand.
hemorrhagic crust over the back (periscapular area)
(Fig. 4). The lesions were distributed along C 6, 7, 8
and T 1, 2, 3 dermatomes. Within three four days
he developed multiple fluid-filled lesions over face,
abdomen, back and upper and lower extremities,
suggestive of disseminated herpes zoster (Fig. 5). He
was found to be reactive for both HIV-1 and HIV-2
antibodies by Comb AIDS and Triline diagnostic kits.
The tests are based on the principles of immunodot and
immunochromatographic assays, respectively. Blood,
and urine tests along with a chest X-ray were normal.
Tzanck smear showed presence of acantholytic cells.
He was treated with oral acyclovir and analgesics and
he responded well. He was referred to the government
hospital for further management.
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
527

30. DERMATOLOGY
Figure 2. Multiple vesiculobullous hemorrhagic lesions over
left forearm.
Figure 3. Multiple vesiculobullous hemorrhagic lesions over
left upper back of the arm.
Figure 4. Large eschar with hyperpigmentation and
hemorrhagic crust over the back.
Figure 5. Multiple fluid-filled lesions over abdominal
area.
Discussion
Conclusion
The presentation of HIV has changed over the past
15 years. Cutaneous markers like extensive seborrheic
dermatitis, psoriasis, multidermatomal herpes zoster,
oral hairy leukoplakia and molluscum contagiosum are
all pointers toward immunosuppression. Such patients
should be thoroughly screened for the primary infection
leading to immunosuppression, especially HIV.
Disseminated cutaneous zoster is defined as having
more than 20 vesicles in other than the area of primary
and adjacent dermatomes. In a study by Abdul Latheef
et al, 90% HIV patients had localized lesions as in
normal patients and only 10% had dissemination, bulla
formation and necrosis. Disseminated herpes zoster
can occur in the immunocompromised elderly patient
and HIV may sometimes be overlooked. HIV-infected
patients with low CD4 cell counts have impaired VZVspecific cell-mediated immunity and thus they remain
at a higher risk for developing multidermatomal herpes
zoster.9,10 Intravenous acyclovir administered for three
days is an effective treatment for cutaneous herpes
zoster in patients with HIV infection.11
We report this case because of its rarity and multiple clinical
presentations in one patient having multidermatomal,
disseminated, hemorrhagic and gangrenous pattern
of herpes zoster in an immunocompromised host.
Timely diagnosis, adequate therapy and prevention of
untoward complications should be our primary aim of
treatment.
530
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
REFERENCES
1. Hall HI, Song R, Rhodes P, Prejean J, An Q, Lee LM, et
al; HIV Incidence Surveillance Group. Estimation of
HIV incidence in the United States. JAMA 2008;300(5):
520-29.
2. Coenen T, Lundgren J, Lazarus JV, Matic S. Optimal HIV
testing and earlier care: the way forward in Europe. HIV
Med 2008;9 Suppl 2:1-5.
3. Birlea M, Arendt G, Orhan E, Schmid DS, Bellini WJ,
Schmidt C, et al. Subclinical reactivation of varicella
zoster virus in all stages of HIV infection. J Neurol Sci
2011;304(1-2):22-4.
Cont’d on page 534...

31. DERMATOLOGY
Lichen Sclerosus et Atrophicus in a Young Girl
YS Marfatia*, SoNIA JAIN**
Abstract
Lichen sclerosus et atrophicus is a chronic inflammatory dermatosis that results in white plaques and epidermal atrophy. The
condition has both genital and extragenital presentations. Here we describe the case of a 12-year-old girl who presented to us
with white plaques over her genitals and no manifestation of extragenital disease.
Keywords: Lichen sclerosus et atrophicus, lichen albus, white spot disease
L
ichen sclerosus is a chronic inflammatory
dermatosis that most commonly affects the
anogenital region and leads to intractable
pruritus and soreness. The condition is more common
in females1 as in the present case also the patient
is a young girl who presented with complaints of
white plaques with itching over the genitals since her
prepubertal years. The condition involves the risk of
malignant transformation more so over the genital
lesions but the precise incidence has not been defined.
Pathophysiologically, the condition is associated
with the presence of autoantibodies to glycoprotein
extracellular matrix protein 1 (ECM-1).2 Several risk
factors have also been proposed including autoimmune
diseases, infections and genetic predisposition.3 There
is evidence of its association with thyroid disease.4
Figure 1. Photograph showing labial atrophy.
CASE SUMMARY
A 12-year-old young girl presented to us with
depigmented patches over the genitals, which had
an insidious onset and were gradually progressive
over a period of one year (Fig. 1). She had moderate
itching over the site and she had seen many doctors
for her complaints but had no relief. On dermatological
examination, labia majora showed atrophy along
with depigmentation of the labia minora (Fig. 2). The
*Professor and Head
Dept. of Skin and VD, Baroda Medical College
SSG Hospital, Raopura, Vadodara, Gujarat
**Professor
Dept. of Skin and VD
MGIMS, Sewagram, Wardha, Maharashtra
Address for correspondence
Dr Sonia Jain
A-14, Dhanvantri Nagar
MGIMS, Sewagram, Wardha, Maharashtra
E-mail: soniapjain@rediffmail.com
Figure 2. Photograph showing depigmented patch over
the labia.
depigmented patches extended from the fourchette to
the vestibule and she had no oral or cutaneous lesions
elsewhere. There was no history of sexual abuse or any
high-risk behavior and none of the family members
Indian Journal of Clinical Practice, Vol. 24, No. 6, November 2013
531