Infectious disease Archer USMLE Step3 Review Lectures

Infectious Diseases
Archer online USMLE reviews
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Archer Slides are intended for use with Archer USMLE step 3 video
lectures. Hence, most slides are very brief summaries of the concepts
which will be addressed in a detailed way with focus on High-yield
concepts in the Video lectures.

 Penicillins
 Monobactams – Aztreonam
 Carbapenems – primaxin, ertapenem
 Cephalosporins
 Macrolides
 Quinolones
 Aminoglycosides
 Tetracyclines
 Glycoproteins – vancomycin
 Linezolid

Anti-Pseudomonal Antibiotics
GOOD ACTIVITY :
 Piperacillin/ tazobactam
 Cefepime
 Ceftazidime
 Imipenem/ cilastatin (Primaxin)
Fair Activity
 Aminoglycosides
 Quinolones

Skin and Soft Tissue
Infections
Impetigo
Cellulitis
Necrotizing Fasciitis

Impetigo
 Infection of superficial layers of epidermis
 Nonbullous impetigo starts as a single erythematous
macule that rapidly evolves into a vesicle or pustule, and
ruptures leaving a crusted yellow exudate over the
erosion.
 Bullous impetigo begins as a rapid onset of blisters that
enlarge and rupture. ( cause mostly s.aureus, also
MRSA)
 Common bugs : gram +ves - S.aureus and GABHS (
S.pyogenes)
 Rx – Topical mupirocin for mild cases, Cephalexin p.o
for severe cases

Cellultis
 Inflammation of skin and underlying
subcutaneous tissues – can be infectious or non
infectious.
 Commonest causes – group A streptococci
(S.pyogenes) and S.aureus
 Rx – usually a cephalosporin such a cephalexin
can be used. If allergic to penicillin, use
clindamycin
 If MRSA is suspected, use oral drugs for mild/
moderate cellulitis such as Bactrim, Doxycycline,
Clindamycin or quinolone. For severe MRSA
cellulitis, use Vancomycin or Tigecycline IV. If
resistant to Vanco, use Linezolid

MRSA – Risk factors
Emperically, treat patients with moderate to severe
cellulitis with risk factors for MRSA infection:
 Recent antibiotic use
 Recent hospitalization
 Hemodialysis
 IV drug use
 Diabetes
 Previous MRSA infection or colonization

Recurrent MRSA
 In patients with recurrent MRSA soft tissue
infections, consider NASAL CARRIAGE
 Culture the nares of patients with recurrent
infection who are suspected of carrying
MRSA.
 Treat nasal carriers with mupirocin to the
nares twice a day for 7 days

Cellultis from Bites
 Pasteurella multocida – etiology in cat bites and
rarely, dog bites. Rx – Amoxicillin/clavulanate.
Tmp/smx in penicillin allergic patient.
 Eikenella cordans – human bites. Rx –
Amoxicllin/ clavulanate or Ampicillin/sulbactam.
TMP/SMX plus clindamycin in penicillin-allergic
patient
 Capnocytophaga tonsurans – cellulitis,
disseminated infection seen in asplenic patients
after Dog bites ( meningitis, endocarditis, renal
failure).

Bites
 Risk of wound infection:
 2-30% in dog bites
 15-50% in cat bites ( since cat bites are more likely
to be puncture wounds, risk of infection is high)
 9-50% of human bites
 Risk of infection is particularly high in
( high grade wounds):
 puncture wounds
 hand injuries
 full-thickness wounds
 wounds involving joints, tendons, ligaments, or
fractures.

Bites – Antibiotic Prophylaxis
 In case of cat and dog bites, there is no necessity for giving
prophylactic antibiotics if it is a low grade non-infected bite. Cleansing
with sterile/ tap water and debridement are sufficient.
 However, remember that cat bite that is a true puncture wound will
need antibiotic prophylaxis as even when they are small they can
cause a deep puncture and carry 50% risk of infection. So, if it is a
minor scrape or nip , there is no necessity for antibiotics but if there is
a puncture, antibiotic should be given. ( Dog bites have less risk of
infection)
 If it is a high grade non infected wound, antibiotic prophylaxis should
be given to prevent cellulitis ( i.e; if the wound involves the hands, feet,
cartilaginous structures, or is deeper than the epidermal
layer(puncture).)
 Human bites have the highest risk of getting infected. However,
antibiotic prophylaxis is recommended only in high grade wounds.

Bites – Wound Closure
 Primary closure with sutures
 not recommended for non-facial bite wounds, deep
punctures, bites to the hand, clinically infected wounds and
wounds greater than 6 hours old 9 due to high risk of
infection) . Delayed closure is appropriate in this conditions.
 Facial wounds may need sutures to prevent scarring and
improve cosmetic outcome. owever, the risk of such closure
is uncertain, but in most cases this is safe if the person has
presented early and the wound has been thoroughly cleaned.
 Delayed primary closure (after 3-5 days)
 Recommended for bites to the hand, bites with extensive
crush injury, wounds needing a considerable amount of
debridement, and wounds more than 6 hours old.

Human Bites – HIV Transmission
 HIV transmission has been reported only very rarely
after a human bite.
 Exposure to saliva alone is not regarded as a risk factor
for transmission of HIV (or hepatitis). So, CDC does not
recommend routine prophylaxis in human bites.
 Transmission risk in human bites is significant when :
 If the biter has HIV, his saliva is mixed with his blood and the bite caused a
breach in the skin of the victim.
 If the Victim has HIV, the blood drawn from him should come in to contact
with mucous membranes of the biter ( Victim to biter transmission) .
 CDC (2005) recommends postexposure prophylaxis with
active antiretroviral therapy (HAART) ( 28 day course)
ONLY in either of the above two scenarios

Human Bites – Closed Fist Injury
Closed-fist injuries:
 Consult a hand surgeon
 Requires exploration under anesthesia for joint
space violation or tendon injury.
 Patients with tendon injury or joint space violation
or underlying fractures should be admitted for
inpatient treatment.
 Management :
 Thorough cleansing and antibiotics. This is a high grade wound.
Antibiotic should be started even when there is no evidence of
infection.
 If discharged, close follow up is needed as outpatient.
 In a infected closed fist injury, patients should be admitted for IV
antibiotic therapy ( ampicillin/ sulbactam). Surgical debridement is
needed. ( Remember that these infected close fist wounds need
aggressive care because of poor vascular supply to the tendons
and because of the deep nature of this infection.)

Tetanus Prophylaxis
Tetanus prone wounds:
 Age > 6 hours
 Configuration : avulsion, stellate
 Depth > 1cm ( puncture wounds)
 If devitalized tissue is present
 If contaminants ( dirt, saliva i.e; bites) are
present.

Tetanus Prophylaxis
 If hx of tetanus immunization is unknown or < 3
doses  give Td+TIG for a dirty tetanus prone
wound. Td alone for a clean, non tetanus prone
wound.
 If hx of Tetanus immunization is present and if
the patient has already received 3 or more
doses  no TIG needed. In case of dirty wound,
Give Td only if it is greater than 24 hour old or if
greater than 5 years since last booster ( bites
are dirty). In case of clean wound, give Td
booster if greater than 10 years since last
booster.

Rabies Post-Exposure Prophylaxis
 All wounds must be thoroughly cleansed with soap and
water.
 In case of Dogs and cats  if the animal is healthy and
available for 10 day observation, do not start prophylaxis
until animal develops symptoms. If animal develops
symps, start HRIG+HDCV ( if patient is not previously
vaccinated). If pt is previously vaccinated, give HDCV
alone ( don’t give HRIG)
 If animal is known rabid or suspected rabid, immediate
vaccination.
 If animal is a skunk, bat or a fox  considered as rabid
always!  Immediate vaccination eg: even if the bat was
found flying in the room

Necrotizing Fascitis
- Infection of the fascial planes resulting in the death of the affected tissues.
- Skin color – blue-black (Black necrotic eschar may be seen at the borders
of the affected areas). Crepitance at the site, Fever, malaise and
leukocytosis can be seen
- Common bugs – Group A strep, S.aureus, C.Perfringens Rx – Aggressive
debridement + Clindamycin.
- Rare causes – Vibrio vulnificus ( clue : necrotizing fasciitis after immersion
in warm salt water) Rx - Tetracycline
- Diagnosis – mainly clinical, however in early cases CT may be obtained.
Finding of gas or inflammatory stranding on CT is very suspicious of
necrotizing fasciitis.
Differentiate simple cellulitis from skin changes associated with a deeper
infection, such as necrotizing fasciitis or gas gangrene, in patients with:
 A rapid increase in lesion size
 Evolution of bullous lesions
 Reddish-purple coloring of the skin
 Systemic toxicity (Hypotension, altered mental status)
 Pain out of proportion to the clinical findings (extreme local tenderness)

Toxic Shock Syndrome
 Caused by an exotoxin that acts as a
superantigen
 Fever, Nausea, vomiting, diarrhea, Shock and
Skin rash characterized by exfoliation.
 The initial lesion might be cellulitis or necrotizing
fasciitis
 Causes : S.aureus, Group A Streptococci
 Rx – shock appropriately
 Drug of choice : clindamycin as it blocks toxin
production.

Ecthyma Gangrenosum
 Caused by P.aeruginosa/ can be associated
with pseudomonas septicemia ( obtain blood
cultures and local cultures).
 Usually affects critically ill and
immunocompromised hosts – AIDS, Steroid use,
Cancer, Chemotherapy.
 Characteristic lesions  hemorrhagic pustules
or infracted-appearing areas with surrounding
erythema that evolve into necrotic ulcers
surrounded by erythema
 Rx with antipseudomonal antibiotic

Clinical Stages
 Primary Syphilis : a solitary, painless chancre that develops at the site of
infection three weeks after exposure  Screen with Dark Field microscopy of skin
lesion.
 Secondary Syphilis: Without treatment, blood-borne spread of T. pallidum over
the next several weeks to months results in secondary syphilis  c/f are fever,
lymphadenopathy, diffuse rash ( including palms and soles) , and genital or
perineal condyloma latum  If lesions present  Screen with dark filed
microscopy. If no lesion, screen with Non Treponemal tests and confirm with
Treponemal Specific tests
 Latent syphilis : Skin lesions resolve, and patients are asymptomatic. However,
serologic tests are positive for T. pallidum. Diagnosis – Screen with Non
Treponemal and confirm with Treponemal Specific tests
 Tertiary or late syphilis: develops years after the initial infection and can involve
any organ system. Complications are neurosyphilis and Aortic Aneurysms). 
Diagnosis – Screen with Treponemal Specific tests.
 Neurosyphilis: A type of late syphilis. ( TABES DORSALIS)  Seizures, ataxia,
aphasia, paresis, hyperreflexia, personality changes, cognitive disturbance,
visual changes, hearing loss, neuropathy ( Vibration/ Position lost) , loss of bowel
or bladder function.  Dx is by CSF examination.

Secondary Syphilis
 Maculopapular rash in
secondary syphilis
 Note involvement of
palms and soles
 Pruritic

Diagnosis
 Dark Field Microscopy
 Non-treponemal tests
 Treponemal Specific Tests

What is the next step in diagnosis ?
 A. VDRL
 B. RPR
 C. FTABS
 D. Cultures
 E. Dark field
microscopy of the
scraping
ANS. ???

Dark Field microscopy
 Most specific technique for diagnosing syphilis
when an active chancre or condyloma latum is
present ( Lesion must be present – so usually
good for primary/ secondary syphilis if lesion is
present)
 T. pallidum is identified by its characteristic
corkscrew appearance  its accuracy depends
on operator experience, number of treponemes
in the lesion and the presence of non-
pathological treponemes in oral/ anal lesions.
 Given the difficulties of dark-field microscopy,
negative examinations on three different days
are necessary before a lesion is considered
negative for T. pallidum.

Non Treponemal Tests VDRL, RPR
 Principle: Syphilitic infection leads to the production of nonspecific
antibodies that react to cardiolipin  the basis of traditional non-
treponemal tests such as the VDRL test and rapid plasma reagin test.
 Mainly used as screening tests  Sensitivity, however, is very low in Early
Primary syphilis and during late syphilis  during these periods, 1/3 of pts
may be non reactive. So, if suspicion is very high despite a negative
screening test, go ahead with treponemal specific test ( FTA-Abs)
 False Positives are common in pregnancy, autoimmune diseases and
infections
 False negative reactions can occur too : large amounts of antibody block
the antibody-antigen reaction, causing a false-negative test in the undiluted
sample ( Prozone phenomenon – similar to hook effect)
 Use in Monitoring treatment adequacy : In many cases nontreponemal tests
become nonreactive after adequate syphilis treatment – so, use VDRL/ RPR
for follow-up after treatment. However, remember that even with sufficient
treatment, patients sometimes have a persistent low-level positive
nontreponemal test (referred to as a serofast reaction). However, this drop
in titers can help in follow up
 Remember  Titers are not interchangeable between different test types.
Hence, the same nontreponemal test should be used for follow-up
evaluations.( If used RPR for screening, use the same for follow up)

Treponemal Tests
 Treponemal-specific tests detect antibodies to antigenic
components of T. pallidum.
 Used primarily to confirm the diagnosis of syphilis in patients with
a reactive nontreponemal test. ( So, if you have a positive RPR, the
next step is FTA-Abs or TPHA)
 Treponemal-specific tests : EIA for anti-treponemal IgG, the T.
pallidum hemagglutination (TPHA) test, the microhemagglutination
test with T. pallidum antigen, the fluorescent treponemal antibody-
absorption test (FTA-abs), and the enzyme-linked immunosorbent
assay.
 Treponemal tests have sensitivities and specificities equal to or
higher than those for nontreponemal tests. However, treponemal-
specific tests are more difficult and expensive to perform, which
limits their usefulness as screening tests.
 False-positive results can occur, especially when the FTA-abs test
is used in patients with systemic lupus erythematosus or Lyme
disease.

Treponemal Tests
 Can they be used for follow-up? 
Unlike nontreponemal tests, which
show a decline in titers or become
nonreactive with effective treatment,
treponemal-specific tests usually
remain reactive for life  Therefore,
treponemal-specific test titers are not
useful for assessing treatment efficacy.

Genital Lesions – Differential Diagnosis
Disorder or disease Characteristics of genital lesion Etiology
Primary syphilis: chancre Solitary, painless ulcer with indurated
border
Treponema
pallidum
Secondary syphilis:
condyloma latum
Slightly raised or flat, round or oval
papules covered by gray exudate
T. pallidum
Genital herpes Cluster of shallow, small, painful ulcers
on a red base
Herpes
simplex
virus
Chancroid Painful ulcers with sharp, undermined
borders + tender lymphadenopathy
Haemophilu
s
ducreyi
Venereal warts Soft, usually painless skin-colored or
red papules
Human
papillom
avirus
Lymphogranuloma
venereum: primary
stage
Painless papule, shallow erosion, or
ulcer; may be multiple or single
( Bubos or unilateral massive inguinal
nodes will be helpful in
differentiating it from syphilitic
Chlamydia
trachom
atis

Treatment
 Primary Syphilis : Diagnosed by dark-field microscopy of a
suspected lesion or by serologic testing. Either technique can
have a false-negative result early in the course of the disease.
Thus, if clinical suspicion is high, treatment for syphilis should
be initiated.
 Clinical Manifestation : Chancre
 Treatment: -Penicillin G benzathine, 2.4 million units IM (single
dose)
 Alternatives in nonpregnant patients with penicillin allergy:
doxycycline (Vibramycin), 100 mg orally twice daily for 2 weeks
or tetracycline, 500 mg orally four times daily for 2 weeks.
ceftriaxone (Rocephin), 1 g once daily IM/IV for 10 days; or
azithromycin (Zithromax), 2 g orally (single dose)
 Follow-up : At six and 12 months after treatment, reexamine
and repeat serologic testing. Treatment failure is defined as
recurrent or persistent symptoms or a sustained fourfold
increase in nontreponemal test titers despite appropriate
treatment.
 Patients with treatment failure should be tested for HIV
infection and evaluated for neurosyphilis with a cerebrospinal
fluid (CSF) examination.

Treatment
 Secondary Syphilis : The diagnosis of
secondary syphilis is confirmed by
nontreponemal and treponemal-specific
tests.
 Treatment employs the same antibiotic
regimens used for primary syphilis. Follow-
up is the same as that for primary syphilis.
Definition of treatment failure is the same.

Treatment
 Latent Syphilis : early/ late Latent
 CNS involvement may be asymptomatic. Therefore, the
possibility of neurosyphilis should be considered in patients
with early or late latent syphilis.
 Early latent syphilis Rx the same way as primary and secondary
syphilis.
 Late latent syphilis  RX with 2.4 million units of penicillin G
benzathine IM once a week for three weeks. Alternative regimens
in nonpregnant patients with penicillin allergy include
doxycycline 100 mg po twice daily for four weeks, or tetracycline
500 mg po four times daily for four weeks.
 Follow- up: After treatment of early or late latent syphilis,
quantitative nontreponemal titers should be measured at six, 12,
and 24 months.
 Neurosyphilis should be strongly considered in patients who
show a fourfold increase in titers, patients who have an initially
high titer (1:32 or greater) that fails to decline at least fourfold,
patients who have HIV infection, and patients who develop signs
or symptoms of neurosyphilis.

NeuroSyphilis
 Occurs in up to 10% of patients with untreated syphilis.
 Neurosyphilis  consider in patients with signs or symptoms of neurologic
involvement at any stage of T. pallidum infection and in all patients with late
latent or tertiary syphilis, although asymptomatic neurosyphilis is the most
common presentation.
 Neurologic involvement  strongly suspect and evaluate in patients who
previously have been treated for neurosyphilis, patients who have not responded
to treatment for primary, secondary, or latent syphilis, and patients who have HIV
infection/ other immunocompromised states.  in pts with HIV, newly diagnosed
of Syphilis, next step is always LUMBAR PUNCTURE TO R/O NEUROSYPHILIS
 Diagnosis : Lumbar puncture. CSF should be tested for white blood cell count
and protein level, and for reactivity on a VDRL test  Although a positive CSF
VDRL test result is specific for neurosyphilis, a negative result does not exclude
the possibility of this infection, because sensitivity is less than 100 percent. A
CSF white blood cell count greater than 10 per mm3 (10 3 106 per L) or a CSF
protein level greater than 50 mg per dL (0.50 g per L) indicates possible
neurosyphilis.
 Treponemal-specific testing (e.g., TPHA) has high negative-predictive value  is
helpful only when the result is negative (i.e., it rules out neurosyphilis). Because
IgG can cross the blood-brain barrier, a positive test may falsely imply CNS
involvement. ( so not used for diagnosis)

Neurosyphilis
 C/F : seizures, ataxia, aphasia, paresis, hyperreflexia,
personality and cognitive changes, visual changes, hearing
loss, neuropathy, and loss of bowel and bladder functions.
 Penicillin is the only drug that has proved effective in the
treatment of neurosyphilis. If pen-allergic , desensitize and
treat.
 Follow-up : following treatment, follow-up depends on the
initial CSF findings. If pleocytosis was present, the CSF should
be reexamined every six months until the white blood cell
count is normal. Retreatment should be considered if the CSF
white blood cell count does not decline after six months or
completely normalize after two years.
 The CSF also can be reexamined to look for serial decreases in
antibodies on the VDRL test or serial decreases in protein
levels. It is expected that CSF parameters will normalize within
two years. Failure to normalize may warrant retreatment. Most
treatment failures occur in immunocompromised patients

Genital Herpes
A recurrent, lifelong disease with no cure
 Two types of HSV (i.e., HSV-1 and HSV-2) are
distinguished by antigenic differences in their envelope
proteins  HSV-1 normally is associated with oral
infections and HSV-2 with genital infections, but either
type can infect a person anywhere on the skin.

Risk Factors for Genital HSV
 Advent of sexual activity at or before 17
years of age
 History of sexually transmitted diseases
 History of undiagnosed genital lesions or
discharge
 Human immunodeficiency virus infection
 Multiple sex partners
 Multiple lifetime sex partners  strongest
predictor for genital Herpes
 Partner diagnosed with genital HSV infection

Clinical Features
 Prodrome: lasts 2-24 hrs  characterized by localized or regional pain,
tingling, and burning  may have constitutional symptoms such as headache,
fever, inguinal lymphadenopathy, anorexia, and malaise.
 As the disease progresses, papules, vesicles on an erythematous base, and
erosions appear over hours to days.
 Patterns of HSV-1 and HSV-2 infection appear identical: vesicles usually are
uniform in size, and the tense center umbilicates to form a depressed center.
These lesions usually crust and then re-epithelialize and heal without scarring.
 In women, ulcers can occur on the introitus, urethral meatus, labia, and
perineum. In men, ulcers often appear on the shaft or glans of the penis. In
both men and women, lesions may appear on the perianal area, thighs, or
buttocks.
 Recurrent HSV outbreaks usually are milder than the initial episode: there
typically are fewer grouped lesions and viral shedding occurs at a lower
concentration and for a shorter duration (i.e. about 3 days).
 Recurrence rates for HSV-2 vary greatly, but the median is four recurrences
per year.
 Patients who experience more severe primary infections (i.e., lasting 35 days
or more) have recurrent episodes twice as often.
 Recurrences are spontaneous, but various factors such as fever; nerve or
tissue damage; physical or emotional stress; exposure to heat, cold, and
ultraviolet light; immunosuppression; menses; concurrent infection; fatigue;
and sexual intercourse have been associated with recurrences

Prevention
 Most genital herpes is spread asymptomatically  In the U.S., 22% of persons age
14 years or older are infected with HSV-2, and almost 90% do not know they are
infected  Most transmission occurs from persons who have no recognized lesions
and who do not know they are infected
 As many as one third of new genital herpes cases may be caused by HSV-1, which
is usually transmitted by oral sex; however, only 5% to 10% of recurrent genital
herpes is due to HSV-1 infection
 The use of condoms has been shown to reduce transmission rates of HSV-2
significantly in susceptible women but not in men.
 Using condoms during 25 percent or more instances of sexual intercourse was
associated with reduced rates of HSV transmission, which suggests that even
occasional condom use can protect women from acquisition of HSV-2.
 To be effective, the condom must completely cover lesions on an infected man.
 Inform patients that asymptomatic shedding is common and that condoms should be
used routinely, even when no lesions are recognized

Diagnosis
 Clinical exam/ high risk history
 Swab test : swab from HSV lesions taken for culture or PCR
1. Viral Culture : Not very sensitive but it is the preferred method for identifying HSV infection,
when pts present with lesions. Also, very helpful in differentiating HSV-1 from HSV-2
2.POLYMERASE CHAIN REACTION TESTING for HSV DNA : greater sensitivity than the
traditional viral culture (sensitivity > 95%, compared with 75% for culture) High cost is
its limitation  hence, used only for the diagnosis of HSV encephalitis because the
results are more rapid than viral culture
3. SEROLOGIC TESTING
 HSV antibodies form during the first several weeks after infection and remain
indefinitely.
 Fifty to 90 percent of adults have antibodies to HSV, but only about 30 percent have
antibodies specific to HSV-2.
 Type-specific serologic assays can be used to confirm HSV infection in persons with a
questionable history or in those who have unrecognized or subclinical infections.
 Serologic testing also is helpful in the presence of a false-negative culture, which is
common in patients with recurrent infection or healing lesions. Because HSV-2 infection
is almost exclusively sexually acquired, HSV-2 antibodies are consistent with an
anogenital infection. However, HSV-1 antibodies may be present in anogenital and
orolabial infections; they cannot be used to differentiate between infections.
 If HSV antibodies are present, testing for other causes of genital ulcers (e.g., syphilis,
chancroid) should be considered, especially in high-risk populations..

Screening
 Consider offering type-specific serologic testing for HSV-
2 to:
 Persons with undiagnosed past or present genital symptoms or
lesions, especially if recurrent
 Patients who have a current or past partner with genital herpes
 Patients who have been diagnosed by clinical exam only and
want confirmation of their diagnosis or typing of their infection
 Patients requesting a full STD screen
 Persons who are HIV positive
 Be aware that the false-positive rate can be high in
populations with a low prevalence of infection;
confirmation of the initial serology with another assay
can be used to increase the specificity.
 Universal screening for HSV antibodies is not
recommended

Management Hospitalization is indicated for patients with genital
Herpes if they also have
 Symptoms of meningitis: Severe headache, Stiff neck,
Photophobia
 Symptoms of autonomic nervous system dysfunction:
Urinary retention, Constipation , Dysesthesias of the
perineal, sacral, or lower back regions
 Symptoms of transverse myelitis: Leg weakness ,
Decreased deep tendon reflexes , Autonomic nervous
system dysfunction
 If meningitis is suspected, send CSF for PCR to detect
HSV DNA.
 Next step: Begin therapy with intravenous acyclovir, 5 to
10 mg/kg every 8 hours. ( do not wait for PCR results
to come back if pt has genital lesions suspicious of
HSV and has above indications for aggressive
therapy)
 When symptoms improve, switch to oral therapy for a
total of 10 to 14 days of treatment

Treatment
 FIRST CLINICAL EPISODE  must be treated with anti HSV
agents ( Acyclovir/ Famciclovir/ valacyclovir) as soon as
possible. Studies have shown prompt Rx for initial episode
reduced constitutional symptoms by three days, local pain by
two days, viral shedding by seven days, time until all lesions
were crusted by three days, and time until all lesions were
healed by six days.  Counsel patients about the high
frequency of recurrences, the inevitability of asymptomatic
shedding, and the risk of transmission even after initial therapy.

Rx – Recurrent herpes
 Recurrences :
 For mild, infrequent recurrences  Episodic therapy is the best. To be efective, it is
very important that treatment is started early during prodromal phase or within 1 day of
lesion onset. So, counsel pts to recognize the recurrences early and self-initiate the
treatment ASAP. Provide prescriptions in advance.
 The goal of episodic therapy is to reduce symptoms and to reduce infectivity during the
episodes. This therapy does not prevent future recurrences or asymptomatic shedding
between the episodes.
 Topical Acyclovir is not effective.
 For Frequent recurrences  six or more episodes per year  START LONG TERM
SUPPRESSIVE THERAPY ( ACYCLOVIR/ FAMACYCLOVIR/ VALACYCLOVIR)
 Inform patients that continuous suppressive therapy decreases, but does not
eliminate, transmission:
 Instruct patients taking suppressive therapy to continue to use
condoms, although they are only 50% effective in reducing
transmission
 Explain to patients that treatment is not curative and will not affect the
severity or frequency of recurrences when stopped
 Inform patients that long-term, continuous treatment is safe and does
not require laboratory-test monitoring

Treatment
 Immunocompromised pts : Genital herpes
Rx in HIV pts is similar to that without HIV
 But recognize that immunosuppressed patients
often develop extensive genital lesions that may
not respond to routine courses of antiviral therapy
 So, be sure to treat aggressively and early.
 Treat early lesions that are not extensive with
usual doses of oral medications  If no
improvement occurs, or if initial involvement is
extensive, try higher doses of oral medications.
 If still not responding  Treat with high-dose
intravenous acyclovir or foscarnet, or topical
trifluridine, foscarnet, or cidofovir; note that
prolonged treatment may be required.

Preventing Mother-Infant Transmission
 Advise pregnant women to avoid acquiring genital herpes infection,
especially late in pregnancy, in order to prevent exposing the infant to
herpetic lesions during birth:
 In general, recommend abstinence or only protected coital activity in
late pregnancy (week 34 onward)
 Advise patients that both HSV-1 and HSV-2 can cause neonatal herpes
 Inform women that if they acquire HSV 1 or 2 during the third trimester,
there is a 30% to 50% chance of transmitting HSV to their neonate
 Ask pregnant women regarding h/o genita or orolabial herpes. However,
remember 90% of those infected with HSV would deny a history of
genital herpes, making history taking of limited value
 Advise pregnant women with no history of orolabial herpes or genital
HSV-1 infection to avoid vaginal intercourse with a partner who has or
may have genital HSV-1 infection and to avoid cunnilingus in the third
trimester with partners who may have orolabial herpes, even if no
lesions are present at the time of sexual contact
 Inform women who do experience their first episode of genital herpes
late in pregnancy that:
 They are at high risk of perinatal transmission
 Mother and child should be managed by a specialist
 Cesarean section is generally recommended
 Acyclovir treatment should usually be given
 Exposed infants often are monitored with surveillance cultures
and treated with acyclovir

Preventing Mother-Infant Transmission
 Identify women who are at risk for reactivation of HSV-2 at time of delivery:
 Consider type-specific antibody testing for some pregnant women (or
women who plan to become pregnant) and their partners to determine
the risk of acquiring HSV-1 or HSV-2, but do not obtain periodic viral
cultures from pregnant patients with a history of recurrent genital herpes
if no lesions are present
 Inform women with a history of recurrent genital herpes that they have a
low risk (<1%) for perinatal transmission:
 If during labor they have no symptoms of genital herpes or its
prodrome and if a careful clinical examination shows no genital
lesions in the entire area innervated by the sacral ganglia, they
may deliver vaginally
 If herpetic lesions are present, cesarean section is usually
recommended
 Culture lesions during pregnancy, especially those present during labor,
to determine whether they contain herpes virus
 Administer intravenous acyclovir to all pregnant women with severe HSV
infection or disseminated infection, pneumonitis, hepatitis, or CNS infection.
Give oral acyclovir to pregnant women with an uncomplicated first episode
of genital herpes or severe recurrences of genital herpes.
 Consider suppressive antiviral therapy (acyclovir, 400 mg tid or
valacyclovir, 500 mg bid) beginning at 36 weeks' gestation for women
with first-episode genital herpes during pregnancy and for pregnant
women with frequent recurrent episodes.

Prevention
Most commonly acquired STD, affecting 50% to 75% of sexually
active men and women.
 Abstinence is the most effective strategy to prevent HPV
infection. Maintain monogamy. Condoms do not
efficiently protect against HPV.
 HPV can spread by skin-skin contact without exchange
of body fluids.
 Treating HPV-related genital warts MAY reduce
infectivity but will not eliminate it.
 Counsel pregnant women with HPV infection about the
risk of peripartum transmission of HPV infection, pointing
out that:
 Infection with HPV types 6 and 11 can result in
respiratory papillomatosis in infants and children
 The role of cesarean section in reducing
peripartum transmission of HPV is unknown 
SO, NOT RECOMMENDED

Screening
 Screening modalities
 Papanicolaou test (Pap)
 Liquid-based cytology
 For women > 30 years of age, combined cytology (either Pap or
liquid-based) and HPV DNA testing.
 Start to Screen ( pap smear) for HPV-related cervical lesions (e.g., cervical
cancer, LSIL, HSIL) in sexually active women 3 years after onset of sexual
intercourse or at the age of 21, whichever is earlier.
 HIV associated with increased risk of cervical cancer/ dysplasia  Perform
cervical cytology screening in HIV-seropositive women twice in the first
year after HIV diagnosis, then annually if the results are normal.
 Perform cervical cytology screening in women under age 30 on an annual
basis.
 If three consecutive cytologies are normal , consider increasing the
interval between cervical cytology screening in women > 30 years of age
without a history of either CIN-2 or CIN-3, immune compromise, HIV
infection, or in utero exposure to diethylstilbestrol to every 2 to 3 years.
 Consider HPV DNA testing in addition to cervical cytology screening in
women < 30 years of age.
 Do not screen women who are negative by both HPV DNA testing and
cytology before 3 years.
 Repeat HPV DNA testing and cervical cytology testing at 6 to 12 months in
women whose results are negative by cytology but who are high-risk HPV
DNA positive.

Stop Screening!
 Discontinue routine cervical cytology
screening (pap) in women who have had a
hysterectomy for benign disease.
 Consider discontinuing routine cervical
cytology screening in women at age 65 or 70
who have had adequate recent cervical
cytology screening and have no other risk
factors for cervical cancer.

Diagnosis
 History, physical exam
 the morphologic characteristics of cutaneous or
genital warts.
 Hx of smoking – increases risk of cervcal ca
 Symptoms – Pruritis, burning, vaginal bleeding/
post coital bleeding.
 Consider differential diagnosis:
 Benign lesions mimicking warts : Pearly penile papules (
surrounding corona) , Achrocordon ( skin tag), Vulvar
lymphangiomata, Vestibular papillae in females and
sebaceous glands
 Other infectious etiologies : molluscum contagiosum (
immunocompromised pts), HSV, condyloma lata.
 Malignancies : Squamous cell ca, Bowens disease,
malignant melanoma

Ans. Vestibular Papillae
•For more pictures on benign lesions mimicking warts, please refer Dermatology
Slides.
• Vestibular Papillae are common benign lesions that are often mistaken as genital
warts and cause unnecessary concern to the patients. So, questions like these are
often high yield on the USMLE.
• Vestibular papillae are flesh-colored, soft pearly papules found on the inner aspects
of labia minora. They are usually symmetrically distributed on either side of the
vulva and can be easily separated from each other on examination.
•On the other hand, genital warts are not confined to the vestibule. The cauliflower
or filiform projections of genital warts tend to fuse at the base and cannot be
seperated easily.
• Acetic acid test : When 5% acetic acid is applied to condyloma acuminatum, a
whitening occurs. There is usually no whitening with Vestibular papillae.
•Vestibular papillomatosis is a normal vulvar anatomical condition. It is a female
counterpart of male pearly penile papules. A correct diagnosis is important and
prevents unnecessary stress to the patient.

Diagnosis
 Biopsy not routinely done. Consider it for
excluding intraepithelial lesions/ cancer/
dysplasia in:
 Atypical appearing lesions
 Vaginal/ Cervical warts
 Uncertain diagnosis
 Progression of disease during treatment
 Frequent recurrence
 Warts that are pigmented, indurated, ulcerated, or
fixed to underlying tissue
 Warts >1 cm
 Suspected neoplasia (e.g., blue or black
discoloration)
 Occurrence in immunocompromised patients

Treatment Options – Drug therapy
Mechanisms of action – drug therapy
 Patient-applied therapies include podophyllotoxin and imiquimod
 Provider-applied therapies include podophyllin resin and TCA
 Imiquimod (Aldara) : Cell-mediated immune response modifier;
induces interferon production
 Interferon: Antiviral, antiproliferative, and immunomodulatory
activity
 Podofilox (Condylox)solution or gel : Cytotoxic, antimitotic; major
biologically active component of podophyllin resin
 Podophyllin resin: Cytotoxic, antimitotic (causes tissue necrosis)
 Trichloroacetic acid : Protein coagulation of wart tissue
Surgical therapy
 Cryotherapy: Destruction by thermal-induced cytolysis
 Excision
 Electrosurgery
 Laser surgery
RECURRENCES ARE COMMON EVEN AFTER SURGERY OR DRUG
THERAPY

Treatment
 The choice of therapy is based on the
number, size, site, and morphology of
lesions, as well as patient preference,
treatment cost, convenience, adverse
effects, and provider experience.
 Consider gynecology consult in pts with
cervical/ vaginal warts – r/o CIN/ cancer

Treatment in Pregnancy
 TCA has been used in pregnant patients without adverse effects.
 Podophyllin, podofilox, and fluorouracil should not be used in
pregnant patients because of possible teratogenicity.
 Imiquimod is not approved for use in pregnant women, although
treatment with this agent can be considered after informed consent
has been obtained.
 Surgical excision, cryotherapy, and electrocautery are appropriate
treatment options during pregnancy if treatment is necessary.
 The goal of treatment in pregnant women primarily is to minimize
neonatal exposure to the virus by reducing the number of lesions
present during delivery.  Anogenital warts and laryngeal
papillomatosis are potential complications in infected children. (
children born to mother with anogenital warts)

Molluscum Contagiosum
-Umbilicated pearly papules
-Look for clues – “Central depression”
-May be filled with pus like material
-Rx is Liquid Nitrogen

Screening
 Test all pregnant women for gonorrhea at the first prenatal
visit if they are at risk for acquisition (defined as report of
new or multiple sex partners) or if they live in an area with
high prevalence.
 Screen for gonorrhea and chlamydia in all patients by the
third trimester
 Screen young women (under age 25) at risk for STD
acquisition if they are seeking care in a clinic with high
gonorrhea prevalence
 Screen men who have sex with men on an annual basis or
more frequently depending on risk behavior.
 Use any approved test, including culture, nucleic acid probe
( cervical probe for N.gonorrheae) , and nucleic acid
amplification methods, for screening

Clinical Features - Men
 Suspect gonorrhea as a likely cause of urethritis in a man with purulent or
mucopurulent urethral discharge.
 Could be a possible infectious cause of epididymitis, particularly in sexually
active men under age 35. ( In older men, likely cause is E.coli)
 A possible cause of proctitis (esply among men who have sex with men).
 Recognize that pharyngeal infection with N. gonorrhoeae is usually
asymptomatic but occasionally causes mild sore or “scratchy” throat.
 Consider gonorrhea in the differential diagnosis of conjunctivitis, especially
if it is associated with copious, purulent conjunctival discharge.
 Disseminated Gonococcal infection can occur in men and, if considered,
should prompt examination of mid- to large-sized joints and major tendon
sheaths and their insertions for tenderness and inflammation.
 Be aware that N. gonorrhoeae is an unusual cause of endocarditis and
meningitis

Clinical Features - Women
 Consider gonorrhea as a cause of mucopurulent cervicitis (defined by the
presence of mucopurulent discharge or easily induced endocervical
bleeding) or PID.
 Be aware that while N. gonorrhoeae is a major cause of mucopurulent
cervicitis (along with C. trachomatis), infection of the cervix most frequently
causes neither signs nor symptoms.
 Evaluate sexually active women with mucopurulent cervicitis or a
laboratory-confirmed diagnosis of gonorrhea for the presence of PID.
( pelvic exam  discharge, cervical motion tenderness, adnexal
tenderness; fever; elevated ESR/ CRP – aid in diagnosis  maintain high
index of suspicion for PID and treat in view of high incidence of infertility
and morbidity)
 Consider gonorrhea as a possible cause of proctitis in women who have
been exposed through receptive anal sex.
 Recognize that pharyngeal infection with N. gonorrhoeae is usually
asymptomatic but occasionally causes mild sore or “scratchy” throat.
 DGI occurs more commonly in women than in men

Diagnosis – Best tests
 In men with urethral discharge  perform a Gram stain
smear of urethral secretions.
 In women with mucopurulent cervicitis or PID  obtain
DNA Probe or nucleic acid amplification of discharge and
urine ( not gram stain)
 Obtain urine for nucleic acid amplification tests at least 1
hour after last void, and be sure that it contains the initial
15 to 20 mL of the urine stream (“first catch”).
 Proctitis or Pharyngitis  get cultures ( not gram
stain)
 If DGI (rash, arthritis) is suspected, obtain blood cultures
and also cultures from mucosal sites exposed during
sex (e.g., cervix, urethra, oropharynx, and rectum), even
if no signs or symptoms are evident at these sites.

Diagnosis
 In sexually active patients with acute,
monoarticular, nontraumatic arthritis, perform
bacterial culture and Gram stain of aspirate from
affected joints.
 N. gonorrhoeae is a rare cause of bacterial
meningitis; the overwhelming majority of
meningitis cases presenting with gram-negative
intracellular diplococci in the cerebrospinal fluid
are due to N. meningitidis.

Diagnosis
 Test for other common STDs
 Chlamydia
 HIV
 Syphilis
 When gonorrhea is suspected in the setting of urethritis, cervicitis, or
proctitis, also consider infection with C. trachomatis, which can
cause presentations identical to gonorrhea.
 In men whose urethritis does not respond to antibiotic treatment for
gonorrhea and chlamydia, consider less common causes of
urethritis, including T. vaginalis.
 Among women with pelvic pain, also consider noninfectious
etiologies, including ovarian cyst, ectopic pregnancy, endometriosis,
ovulation, and gastrointestinal causes
 In case of DGI, D/D includes other causes of acute, nontraumatic,
oligoarticular arthritis in young adults, including Reiter's syndrome,
Lyme disease, and various viral infections.

Hospitalization
Indicated only if
 Patients with DGI if they are moderately severely or
severely ill (including temperature >38.0°C [100.4°F] or
inability to take oral antibiotics).
 All patients with documented or suspected gonococcal
endocarditis or meningitis
 Hospitalize women with PID in any of the following
circumstances:
 If surgical emergencies, such as appendicitis, cannot be
excluded
 Pregnancy
 Failure to respond to previously administered oral or
outpatient parenteral antibiotics
 Inability to take oral therapy ( VOMITING/ NAUSEA)
 Severe illness (nausea and vomiting, high fever, hemodynamic
instability)
 Presence of tubo-ovarian abscess
 IMMUNOCOMPROMISED STATES

Treatment
 Quinolones are no longer recommended for Rx
of gonorrhea in the USA due to increasing
resistance.
 Treat patients with gonococcal cervicitis for
chlamydial infection as well, even if laboratory
confirmation of the latter is not obtained ( vice
versa is not needed)
 In sexually active men under age 35, treat
epididymitis empirically with an antibiotic
regimen active against both N. gonorrhoeae and
C. trachomatis  Ceftriaxone + doxycycline
 Always treat sexual partners.

Treatment – uncomplicated gonorrhea
 For uncomplicated cervicitis due to gonorrhea :
Ceftriaxone 125 mg IM. Also effective for rectal
gonorrhea.(proctitis)
 For endometritis/ uncomplicated PID  Ceftriaxone 250
mg IM.
 Cefixime  Oral single dose Rx for uncomplicated
gonorrhea ( 400mg single dose)
 For gonococcal pharyngitis  use 1gm single dose
ceftriaxone  cure rates for pharyngeal gonorrhea
lesser when compared to other sites
 Provide concomitant Rx to chlamydia  Doxycycline
100mg po bid x 7 days is first line Rx in non pregnant pts
or alternative is Azythromycin 1gm single dose ( also
preferred in pregnant pts). Also, Amoxicillin 500 po tid x
7 days alternative Rx for Chlamydia in Pregnancy

Treatment – Uncomplicated Gonorrhea
 Penicillin Allergic Patients : due to cross
reactivity with cephalosporins, use
spectinomycin therapy as a choice.
 Alternatively, use Azithromycin 2gm po dose in
penicillin allergy pts ( double the dose required
for chlamydia)
 Neonates : Treat all newborns prophylactically
for gonococcal conjunctivitis with topical silver
nitrate solution, tetracycline ointment, or
erythromycin ointment.

Treatment - DGI
 For Disseminated Gonococcal infection 
 Hospitalize the patient
 Obtain blood, cervical and pharyngeal cultures
 Start IV therapy with Ceftriaxone 1gm/d until
clinical improvement occurs and then switch to oral
antibiotics to complete total 7 days of Therapy
 Oral choices : Cefixime 400/d, cefpodoxime 400
bid

COUNSEL
 Counsel persons with gonorrhea to
abstain from sexual contact for at least 1
week after treatment and until all sex
partners have been treated 
OTHERWISE, RE-INFECTION CAN
OCCUR!

HIV infection
High-yield topics

Acute Retroviral Syndrome
 Occurs within 4 to 28 days after infection corresponding
to exponential increase in HIV viral load. Occurs in 50-
90% of patients
 Diagnosis often missed due to confusion with other
illnesses
 Most common complaints : low grade fever, headache
and malaise. Symptoms last 1-4 weeks and involves
lymphadenopathy, anorexia, weightloss and a
maculopapular rash that may extend to palms and soles.
Pharyngeal erythema, oral ulcerations and oro-
pharyngeal candidiasis are common.
 Severe cases include meningo-encephalitis, neuropathy,
radiculopathy and Guillianne-barre syndrome
 A similar type illness can occur in 5% pts who
discontinued HAART owing to exponential increase in
HIV viral load

Acute Retroviral Syndrome
 D/D :
 Infectious mononucleosis ( EBV/ CMV)
 Secondary syphilis
 Acute early hepatitis B or A
 Influenza
 Acute Toxoplasmosis
 Roseola
 Acute HSV infection
 Still disease
 Diagnosis : one of the two criteria sets below
1. symptoms consistent with Acute retroviral syndrome + Negative HIV ELISA in past
6 months + Positive HIV ELISA at current testing (or)
2. symptoms consistent with Acute retroviral syndrome + Negative HIV ELISA at
current testing + High HIV RNA titer at current testing ( usually > 100,000 copies/
ml)
 Once Acute Retroviral syndrome is diagnosed  screen pt for
Syphilis, chlamydia, gonorrhea, HSV and HPV.
 Baseline Genotype testing recommended to r/o resistant mutations,
regardless of whether or not you are starting PT on HAART
 As per current guidelines, HAART is optional in Rx of Acute
retroviral illness

When to start HAART?
 When to start depends on symptoms, CD4
counts, and to a lesser extent, viral load. Current
(March 2004) North American guidelines state
that treatment should be:
 Considered at CD4 counts below 350 cells/mm3,
 Definitely started before CD4 counts fall below 200,
and
 definitely started if there are serious symptoms or
AIDS-related illnesses irrespective of CD4 count
 Also consider HAART if viral load > 50,000 by RT
PCR

Question
 A 27-year-old man with HIV presents to your clinic to establish
care. He believes he acquired his infection from a blood
transfusion he received in sub-Saharan Africa while serving in
the Peace Corps 3 years ago. He is currently asymptomatic and
has a strong social support network. His examination is
unremarkable. During the clinic visit, he asks about starting
medical therapy for his HIV. His CD4+ T cell count is 450/mm3,
and his HIV RNA level is 20,000 copies/ml.
 Which of the following is an indication to initiate HAART?
 1. CD4+ T cell count of less than 500/mm3
2. HIV RNA level of 50,000 copies/ml and a normal CD4+ T cell
count
3. Oral thrush
4. HIV RNA level of 75,000 copies/ml and CD4+ T cell percentage of
28%

Preventing Mother-Child
Transmission
 Use of Cesarean section
 Use of HAART therapy during pregnancy
and labor
 No breast feeding ( formula feeding only)

Prophylaxis in HIV
 Prophylaxis against Pneumocystis jiroveci (PCP) when CD4 count is
<200 cells/µL with trimethoprim/sulfamethoxazole, one double-
strength tablet daily or every other day. In pts allergic to Bactrim,
atovaquone.
 If CD4 count < 100, do IgG serology for Toxoplasmosis. If +ve
serology, give trimethoprim/sulfamethoxazole.
 In patients with positive PPD skin tests (>5 mm induration in an HIV-
infected patient), evaluate and treat for either active or latent
tuberculosis.
 When CD4 count is <50 cells/µL, begin prophylaxis against
Mycobacterium avium complex with azithromycin, 1200 mg/week
 Recognize that patients with refractory, frequent, or severe mucosal
candidiasis may require long-term systemic antifungal therapy ( oral
diflucan).

Vaccinations in HIV
 Administer annual influenza vaccination to
all HIV-infected patients.
 Administer pneumococcal vaccine to all
HIV-infected patients (and strongly
consider repeating at intervals of 5 to 10
years).
 Administer vaccination to patients who are
at risk for hepatitis A and B.

Progressive Multifocal
Leucoencephalopathy
Cause : Papova virus JC
c/f : Dementia a common presenting symptom. Other
c/f - hemiparesis, aphasia, dysarthria
Dx : MRI/ CT. If +ve for white matter lesions, next step
is CSF analysis for JC virus by PCR
Rx – HAART

Toxoplasmosis
Screen all patients with HIV with CD4 less than 100. screening test
toxoplasma IgG
Screen all patients undergoing organ transplantation
C/F – encephalitis, pneumonitis, myocarditis in
immunocompromised. Mononucleosis like syndrome and
chorioretinitis in immunocempetant
If Suspected Toxoplasmosis  get IgM and IgG serologies. If
neurological symptoms  get CT/MRI. If patients are seronegative
for Toxoplasma or if lesions don’t respond to toxoplasma Rx in 2
weeks  r/o Lymphoma. Get a stereotactic brain biopsy
Rx  Sufladiazine + pyremethamine + folate ( Start emperic Rx in
patients with ring enhancing lesions in brain and +ve IgG serology for
toxoplasma and CD4 less than 200). If CD4 goes higher than 200,
may d/c therapy

Cryptococcal Meningitis
AIDS with CD4 less than 50
Headache, fever, delirium are present
Diagnosis : LP, India ink and Cryptococcal
antigen in serum and CSF
Rx: Amphotericin + Fluconozole
Increased CSF pressure is associated with
increased mortality  do a daily therapeutic
lumbar punctures to keep CSF pressures < 20

Prevention
Advise Patients to avoid exposure to
vector ticks in endemic areas and to
promptly remove attached ticks.
 Wear protective clothing
 Use insect repellant containing
diethyltoluamide (DEET) or a tick-killing spray
containing permethrin, the latter to be applied
to clothing, not skin

Lymes
 Acute, localized Lyme disease:
 Erythema migrans and other symptoms (e.g., fever, fatigue, headache,
arthralgias, myalgias) occuring within 30 days of possible tick exposure
( this is sufficient to diagnose Lyme disease)
 Acute, disseminated Lyme disease :
 Multiple, secondary erythema migrans lesions, Acute carditis (heart
block) , CNS Disease (e.g., cranial neuropathy, radiculoneuropathy,
lymphocytic meningitis) and brief episodes of monoarticular or
oligoarticular inflammatory arthritis occuring within weeks to months
after tick exposure
 Late Lyme disease:
 Occuring within months to years after possible tick exposure
 Chronic (>1 year) inflammatory monoarthritis or oligoarthritis
 Nervous system complications : peripheral neuropathy or
encephalomyelitis

Diagnosis and Rx
 Erythema migrans in an endemic area is
sufficient for diagnosis  do not get serology (
can be negative in acute disease - ). Start
therapy as next step – oral doxycycline or
amoxicillin or cefuroxime.
 Disseminated Lymes  Get serologic testing.
Use 2 step approach – first ELISA. If ELISA
indeterminate, get western blot.
 Arthritis, Carditis ( except third degree block,
cranial nerve palsy without meningitis  Rx
similar to erythema migrans
 Third degree block or Meningitis/
neuroborreliosis  Rx with ceftriaxone IV

Q
 A 30 y/o pregnant woman has a one week
history of a slowly enlarging red lesion on her
right thigh. She reports having gone on a
camping trip about 3 weeks ago and now
recalls that she removed a tick from the site of
the lesion. An ELISA test is negative for
Lymes. What is the next step?
A. Re-assurance
B. Ampicillin
C. Doxycycline
D. Western blot testing
E. Medical termination of pregnancy

Ans. B
 Acute lymes – serology is often –ve. No
need to do western blot – give rx wioth
ampicillin
 Doxycycline is contraindicated in
pregnancy.

Other
 RMSF  Rash starting on ankles and
wrists few days after fever. 
Doxycycline. If pregnant, cholramphenicol
 Ehrilichiosis  central distribution of rash,
no involvement of periphery. Dx 
inclusions in leucocytes

Meningitis
Refer Neurology Lecture

Meningitis
 Symptoms : Fever, Photophobia, Headache,
Neck stiffness, vomiting, seizures
 Use physical exam findings to confirm a
diagnosis of meningitis.
 Look for:
 Fever
 Nuchal rigidity
 Brudzinski's sign
 Kernig's sign
 Signs of encephalitis, such as weakness and change
in mental status

Meningitis
 Do lumbar puncture to obtain CSF for:
 Protein, glucose, and cell count determinations
 Gram stain and bacterial culture
 PCR testing for enterovirus and HSV if bacterial Gram stain and culture
results are negative and cell counts suggest viral meningitis
 Obtain CT scan before lumbar puncture in patients with: ( HIPFAN)
 Immunucompromised state (I)
 History of CNS disease (H)
 New onset seizures (N)
 Papilledema (P)
 Altered level of consciousness ( suggests encephalitis)(A)
 Focal neurologic signs (F)
Be aware that delay in initiating appropriate antibiotics while awaiting
results of CT scan in patients with bacterial meningitis may result in an
adverse clinical outcome.

Meningitis – Empiric Rx
 Base empiric antibiotic therapy on:
 Patient's age
 CSF gram-stain result
 Potential bacterial pathogens
 Knowledge of local resistance patterns for those
pathogens
Thereafter, base targeted antibiotic therapy on
culture results and susceptibility data.
Administer dexamethasone 15 to 20 minutes
before the first antimicrobial dose in adult
patients with suspected meningitis.

Meningitis – Emperical therapy
Predisposing Factor
AGE
Common Bacterial
Pathogens
Antimicrobial Rx
<1 month Streptococcus
agalactiae, Escherichia
coli, Listeria
monocytogenes,
Klebsiella species
Ampicillin plus
cefotaxime or ampicillin
plus an aminoglycoside
1 - 23 months Streptococcus
pneumoniae, Neisseria
meningitidis, S.
agalactiae, Haemophilus
influenzae, E. coli
Vancomycin plus a third-
generation
cephalosporin
2- 50 years N . meningitidis, S.
pneumoniae
generation
cephalosporin
>50 years S. pneumoniae, N.
meningitidis, L.
monocytogenes, aerobic
gram-negative bacilli
Vancomycin plus
ampicillin plus a third-
generation
cephalosporin

Meningitis – Emperical therapy
Predisposing Factor
HEAD TRAUMA
Common Bacterial Pathogens Antimicrobial Rx
Basilar skull fracture S. pneumoniae, H.
influenzae, group A -
hemolytic streptococci
generation cephalosporin
Penetrating trauma Staphylococcus aureus,
coagulase-negative
staphylococci (especially
Staphylococcus epidermidis),
aerobic gram-negative bacilli
(including Pseudomonas
aeruginosa)
Vancomycin plus cefepime,
vancomycin plus ceftazidime,
or vancomycin plus
meropenem  YOU ARE
Adding an antipseudomonal
antibiotic.
Postneurosurgery Aerobic gram-negative bacilli
(including P. aeruginosa), S .
aureus, coagulase-negative
staphylococci (especially S.
epidermidis)
Vancomycin plus cefepime,
vancomycin plus ceftazidime,
or vancomycin plus
meropenem
CSF shunt Coagulase-negative
staphylococci (especially S.
epidermidis), S. aureus,
aerobic gram-negative bacilli
(including P. aeruginosa),
Propionibacterium acnes
Vancomycin plus cefepime,c
vancomycin plus
ceftazidime,c or vancomycin
plus meropenem

Catheter Related
Infections
Indwelling catheters  suspect candida. R/o
endophthalmitis in candida sepsis, get
Ophthal consult
If catheter site looks infected  remove
catheter. Do not use same site.

Febrile Neutropenia
 Absolute neutropenia - < 500
 Consider Neupogen
 Start Gram - ve emperic therapy with
cefepime or imipenem.
 If very critically ill or MRSA risk, add
vancomycin
 If no response in 48 hours, add antifungals

Neutropenic Precautions
 Remove any offending drugs or agents.
 Use careful oral hygiene to prevent
infections of the mucosa and teeth.
 Avoid rectal temperature
measurements and rectal
examinations.
 Use good skin care for wounds and
abrasions

Influenza
 Vaccination
 Drugs used in Influenza

Anti-flu drugs
 ZANAMAVIR
 OSTELTAMAVIR ( Tamiflu)
  These drugs are effective only if given in
48hrs of onset of flu symptoms.
  Zanamavir can cause bronchoconstriction 
caution in asthmatics ( keep a bronchodilator
inhaler handy)
  Osteltamavir causes nausea and vomiting.

Immune Reconstitution
Syndrome

Infectious disease Archer USMLE Step3 Review Lectures

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Infectious disease Archer USMLE Step3 Review Lectures