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USMLE Step 2 CK
l Internal Medicine
Clinical Presentation. The most important feature of any person presenting with possible
food poisoning is the presence or absence of blood in the stool. Blood is most commonly
associated with invasive enteric pathogens, such as Salmonella, Shigella, Yersinia, invasive E.
coli, and Campylobacter. The time between the development of the diarrhea from the inges-
tion of the food is not as important as the presence of blood. Incubation times are helpful
only if you have a group outbreak and you can pinpoint a common source of contamination.
In other words, the last thing you eat is not necessarily the thing that was contaminated. The
invasive enteric pathogen may be causing infection in the absence of blood, however, and the
absence of blood does not exclude them. Campylobacter is rarely associated with GuillainBarré syndrome.
Ingestion of ciguatera toxin causes symptoms within 2–6 hours, which includes paresthesias, numbness, nausea, vomiting, and abdominal cramps. In severe cases symptoms can be
neurologic (weakness, reversal of hot-cold sensations), and cardiovascular (hypotension).
Neurologic symptoms can be severe, progressive, and debilitating. There is no specific
therapy to reverse ciguatera poisoning. The most commonly implicated fish are barracuda,
red snapper, and grouper.
E. coli 0157:H7 and Shigella are associated with hemolytic uremic syndrome (HUS).
Bacillus cereus and Staphlococcus predominantly present with vomiting within 1–6 hours of
their ingestion because they contain a preformed toxin. They can give diarrhea later.
Giardia, Cryptosporidium, Cyclospora, and most other protozoans do not give bloody diarrhea.
The major protozoan associated with blood in the stool is Entamoeba histolytica.
Viruses can give voluminous watery diarrhea but do not result in bloody diarrhea.
Scombroid is a type of poisoning that occurs after ingesting scombroid fish (tuna, mackerel,
mahi mahi), which may contain a large amount of histamine. When ingested, scombroid can
give symptoms within a few minutes: rash, diarrhea, vomiting, and wheezing, along with a
burning sensation in the mouth, dizziness, and paresthesias.
Diagnosis. When there is no blood present in the stool, the best initial method of determining the etiology of the diarrhea is to test the stool for the presence of WBCs with methylene
blue testing. WBCs will tell you that you have an invasive pathogen but will not distinguish
the specific type. Culture is necessary to determine the specific type.
Giardia and Cryptosporidia are detected by direct examination of the stool for the parasites, as
well as for their eggs. A special modified AFB stain is necessary to detect Cryptosporidia. Stool
ELISA is also used for Giardia.
Treatment. Therapy is determined by the severity of disease. Mild infections with the invasive
pathogens and viruses usually require only oral fluid and electrolyte replacement. More severe
infections, such as those producing high fever, abdominal pain, tachycardia, and hypotension,
require IV fluids and oral antibiotics. You rarely, if ever, have the luxury of a specific etiology
identified when the initial therapeutic decision must be made. The best initial empiric antibiotic therapy of an invasive pathogen is with a fluoroquinolone such as ciprofloxacin.
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Organism-specific therapy is as follows:
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• CampylobacterErythromycin
• GiardiaMetronidazole
• CryptosporidiumControl of underlying HIV disease with antiretrovirals, nitazoxanide
• Nitazoxanide is the first truly useful therapy for cryptosporidiosis.
• ScombroidAntihistamines such as diphenhydramine
ACUTE VIRAL HEPATIC INFECTIONS
An 18-year-old woman comes to the emergency department because of several
days of nausea, vomiting, and fever. She uses no medications. She reports
unprotected sex. Her stool is light in color. On physical examination she is
jaundiced.
Definition. Viral hepatitis is an infection of the liver caused by hepatitis A, B, C, D, or E.
• Hepatitis A and E are transmitted by contaminated food and water. They are orally
ingested and have an asymptomatic incubation period of several weeks, with an average of 2−6 weeks. They cause symptomatic disease for several days to weeks, have no
chronic form, and do not lead to either cirrhosis or hepatocellular carcinoma.
• Hepatitis B, C, and D are transmitted by the parenteral route. They can be acquired perinatally or through sexual contact, blood transfusion, needlestick, and needle sharing.
• Hepatitis G has been identified in a small number of patients through screening of the
blood supply but has not yet been associated with clinical disease.
• Hepatitis B and C can lead to a chronic form, which can cause cirrhosis and hepatocellular carcinoma. Four million people in the United States are infected with hepatitis C.
Hepatitis C is the most common disease leading to the need for liver transplantation in
the United States.
Chapter 7
l Infectious Diseases
All forms can occasionally present with fulminant hepatic necrosis and acute liver failure.
Clinical Presentation. The most common presentation of acute hepatitis of any cause is
jaundice, dark urine, light-colored stool, fatigue, malaise, weight loss, and a tender liver. On
physical examination the liver may be enlarged. You cannot distinguish the precise viral etiology of the hepatitis by initial presentation alone. In fact, drug-induced hepatitis, such as
that from isoniazid or massive alcohol use, may present with the same symptoms. Hepatitis
B and C can also give symptoms similar to serum sickness, such as joint pain, rash, vasculitis,
and glomerulonephritis. They also lead to cryoglobulinemia. Hepatitis B has been associated
with the development of polyarteritis nodosa (PAN). Hepatitis E has been associated with a
more severe presentation in pregnant women.
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USMLE Step 2 CK
Table 7-3. Comparative Features: Hepatitis A, B, C, E, and Delta
Feature Hepatitis A Hepatitis B Hepatitis C Delta Hepatitis E
l Internal Medicine
Incubation period
(wk)
Transmission Fecal-oral Sexual >
Severity Mild Occasionally
Fulminant
hepatitis
Symptoms Fever, malaise,
Carrier state None Yes Yes Yes None
Chronicity (%) 0 5−10 80
Associated
with blood
transfusion (%)
2−6 (avg. 4) 4−26 (avg. 13) 2−20 4−8
Parenteral >
parenteral
severe
Rare Very rare (1% of
icteric patients
As with A, but
headache,
anorexia,
vomiting, dark
urine, jaundice
Very rare 5−10 Almost negligible
10−20%
with serum
sickness-like
(joint pain,
rash)
sexual
Usually
subclinical
Extremely rare Co-infection
Only 20% acutely
symptomatic
2% to routine
screening
Parenteral, sexual Fecal-oral
Co-infection
with B
occasional
As with A As with A
5
Occurs, but
frequency
unknown
Mild, except
Rare
0
Rare
in pregnant
women
Serology Anti-HAV
IgM fraction
IgG fraction
Postexposure
prophylaxis
Association with
cirrhosis
Association
with primary
hepatocellular
carcinoma
Immunoglobin
Hep A vaccine
No Ye s Ye s Ye s No
No Ye s Ye s Ye s No
HBsAg, HBsAb
HBeAg
Anti-HBs
Anti-HBc
Anti-HBe
HBIg/Hep B
vaccine
Antibody to
hepatitis C
PCR-RNA
None effective None Unknown
Anti-delta
IgM fraction
IgG fraction
Anti-Hep E
IgM
IgG
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Diagnosis. All forms of viral and drug-induced hepatitis will produce elevated total and
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direct bilirubin levels.
• Viral hepatitis will produce both elevated ALT and AST, but ALT is usually greater
than the AST.
• With drug- and alcohol-induced hepatitis, AST is usually more elevated than the ALT.
• Alkaline phosphatase and GGTP are less often elevated because these enzymes usually
indicate damage to the bile canalicular system or obstruction of the biliary system.
• If there is very severe damage to the liver, prothrombin time and albumin levels will be
abnormal.
Chapter 7
l Infectious Diseases
Hepatitis A, C, D, and E are diagnosed as acute by the presence of the IgM antibody to each of
these specific viruses. IgG antibody to hepatitis A, C, D, and E indicates old, resolved disease.
• Hepatitis C activity can be followed with PCR-RNA viral load level. However, do not
use PCR to establish the initial diagnosis.
• Hepatitis B is diagnosed as acute with the presence of the hepatitis B surface antigen,
which is the first viral marker to elevate. The hepatitis B e antigen and IgM core antibody also help establish acute infection.
– The e antigen indicates high levels of viral replication and is a marker for greatly
increased infectivity.
– Resolution of the infection is definitively indicated by the loss of surface antigen
activity and the development of hepatitis B surface antibody.
– Hepatitis B core antibody of the IgG type and hepatitis e antibody also indicate that
the acute infection is about to resolve and may be the only marker present in the
period of 2-6 weeks between the loss of surface antigen activity and development
of the surface antibody.
Treatment. There is no effective therapy for acute hepatitis B. Chronic hepatitis B can be treated
with either interferon, entecavir, adefovir, or lamivudine.
With the approval of the newest hepatitis C drugs, the goal of HCV treatment is to cure the
virus, which can be done with a combination of drugs. The specific medications used and the
duration of treatment depend on a number of factors:
• HCV genotype
• Viral load
• Past treatment experience
• Degree of liver damage
• Ability to tolerate the prescribed treatment
• Whether patient is waiting for a liver transplant or is transplant recipient
Note
Entecavir, adefovir, tenofovir,
and telbivudine can be used
in place of lamivudine for the
treatment of hepatitis B.
There are a number of approved therapies to treat HCV, such as sofosbuvir/ledipasvir
(Harvoni), simeprevir (Olysio), sofosbuvir (Sovaldi) and Viekira Pak (ombitasvir, paritaprevir
and ritonavir tablets co-packaged with dasabuvir tablets that may be prescribed with or without
ribavirin). Sofosbuvir and simeprivir may be prescribed together with or without ribavirin, or
each may be separately combined with ribavirin and in some cases peginterferon as well.
Sofosbuvir/ledipasvir, the current preferred HCV treatment, is 2 drugs formulated in to one
daily pill. For genotype 1 success rates of sofosbuvir/ledipasvir are around 94–99%, while
treatment duration is 8–12 weeks. Both are direct-acting antivirals (DAAs) which means they
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USMLE Step 2 CK
l Internal Medicine
directly interfere with hepatitis C virus replication. Sofosbuvir is a polymerase inhibitor while
ledipasvir, an NS5A inhibitor. Patients who have never been treated for HCV—whether they
have cirrhosis or not—take sofosbuvir/ledipasvir for 12 weeks. Treatment-naïve patients without
cirrhosis whose pre-treatment viral load (HCV RNA) is <6 million IU/mL may be considered
for 8 weeks of treatment.
When hepatitis C treatment is working, the virus will become undetectable within 4-12 weeks
and will remain that way throughout treatment. Patients are considered cured when they have
achieved what is known as a sustained virologic response (SVR), or continuation of this undetectable status, 12-24 weeks after completing therapy.
After a needlestick from a hepatitis B surface-antigen−positive patient, the person stuck
should receive hepatitis B immunoglobulin (HBIg) and hepatitis B vaccine. If the person
stuck already has protective levels of surface antibody to hepatitis B present in the blood, then
no further therapy is indicated. There is no effective postexposure prophylaxis to hepatitis
C, and there is no vaccine. All healthcare workers, IV drug users, and others at risk should
be vaccinated for hepatitis B. All newborn children are vaccinated against hepatitis B and A.
Hepatitis A vaccine should be given to those traveling to countries that may have contaminated food and water, those with chronic liver disease, and those with high risk sexual behavior.
GENITAL AND SEXUALLY TRANSMITTED INFECTIONS
Urethritis
A 31-year-old man is in your clinic today with several days of urinary frequency,
urgency, and burning.
Definition. Inflammation of the urethra.
Etiology
• Gonococcal urethritis caused by Neisseria gonorrhoeae
• Nongonococcal urethritis caused by either Chlamydia trachomatis (50%), Ureaplasma
urealyticum (20%), Mycoplasma hominis (5%), Trichomonas (1%), herpes simplex
Clinical Findings. Purulent urethral discharge; dysuria, urgency, and frequency in urination.
Diagnosis. Smear can show the Gram-negative, coffee bean−shaped diplococci intracellularly.
Serology (fluorescent antibodies) for chlamydia by swabbing the urethra, or by ligase chain
reaction test of voided urine. Culture for gonorrhea is the most specific test for gonorrhea.
Treatment. Single-dose ceftriaxone intramusculary and single-dose azithromycin orally is
now the treatment of choice. An alternative regimen with doxycycline for 7 days can also be
used. Gonorrhea can also be treated with single-dose cefixime. This is the same treatment as
that for cervicitis. Ciprofloxacin should not be used as first-line therapy for gonorrhea.
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Chapter 7
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Pelvic Inflammatory Disease
Definition. Infections involving the fallopian tubes, uterus, ovaries, or ligaments of the uterus.
Etiology. N. gonorrhoeae, Chlamydia, Mycoplasma, anaerobic bacteria, or Gram-negative bac-
teria. Intrauterine devices predispose to PID.
Clinical Findings. Lower abdominal and pelvic pain on palpation of the cervix, uterus, or
adnexa; fever, leukocytosis, and discharge are common. Cervical motion tenderness is key.
Discharge from the cervix may be present.
Diagnosis. Culture on Thayer-Martin for gonococcus and Gram stain of discharge, increased
ESR. Laparoscopy is the only definitive test. If there is fluid in the retrouterine cul-de-sac, a
culdocentesis will rarely be performed. A pregnancy test should be done. Ultrasonography
of the pelvis may also be helpful to exclude other pathology, such as an ovarian cyst or tuboovarian abscess. Clinical presentation is the main method (CMT/adnexal tenderness).
Treatment. Doxycycline and cefoxitin (or cefotetan) for inpatient therapy. Outpatient therapy
is with single-dose ceftriaxone intramuscularly and doxycycline orally for two weeks. The
main reason to treat in hospital is a high WBC or high fever. Outpatient therapy can also be
with 2 weeks of oral ofloxacin and metronidazole as a second-line agent.
l Infectious Diseases
Complications. Infertility and ectopic pregnancy.
Syphilis
A 43-year-old man comes to the clinic with several days of an ulcerated genital
lesion. He also has some surrounding adenopathy.
Definition. A systemic contagious disease caused by a spirochete; characterized by periods of
active manifestations and by periods of symptomless latency.
Etiology. Treponema pallidum.
Clinical Findings. Syphilis can be classified as being congenital or acquired.
Congenital
• Early: symptomatic; seen in infants up to age 2
• Late: symptomatic, Hutchinson teeth, scars of interstitial keratitis, bony abnormali-
ties (saber shins)
Acquired
• Early infectious syphilis
– Primary stage: Chancre that appears within the third week and disappears within
10–90 days; also, regional lymphadenopathy is painless, rubbery, discrete, and nontender to palpation. Primary chancres are usually found on the penis, anus, rectum
in men, and vulva, cervix, and perineum in women (may be found in other places
such as lips, tongue, etc.).
– Secondary stage: Cutaneous rashes appear 6–12 weeks after infection, usually
found symmetrically and more marked on the flexor and volar surfaces of the
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USMLE Step 2 CK
l Internal Medicine
body (pinkish or pale red in white persons; pigmented spots, copper-colored macules in blacks). Lymphadenopathy, papules that develop at mucocutaneous junctions and moist areas, are termed condylomata lata (extremely infectious), and
alopecia can be seen.
• Latent stage: Asymptomatic; may persist for life, and one-third of patients develop
late or tertiary syphilis.
• Late or tertiary syphilis: Most commonly neurologic
Note
Use the FTA to exclude
neurosyphilis in CSF.
Centers for Disease Control and Prevention, M. Rein, VD
Figure 7-5. Syphilis, Primary Chancre
These patients are symptomatic but not contagious. Benign tertiary develops 3–20 years after
the initial infection, and the typical lesion is the gumma (a chronic granulomatous reaction),
found in any tissue or organ. It will heal spontaneously and leave a scar. Cardiovascular syphilis and neurosyphilis are the other manifestations of tertiary syphilis. The Argyll Robertson
pupil (usually only with neurosyphilis) is a small irregular pupil that reacts normally to
accommodation but not to light. Tabes dorsalis (locomotor ataxia) results in pain, ataxia,
sensory changes, and loss of tendon reflexes. Neurosyphilis is rare and is essentially the only
significant manifestation of tertiary syphilis likely to be seen. The FTA on CSF is far more
sensitive for neurosyphilis than a VDRL.
236
Centers for Disease Control and Prevention
Figure 7-6. Syphilis, Secondary Palms
Chapter 7
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Diagnosis
• Screening tests are the VDRL and RPR; specific tests are the FTA-ABS, MHA-TP, and
Darkfield exam of chancre.
• False–positives VDRL with EBV, collagen vascular disease, TB, subacute bacterial
endocarditis
Treatment. Penicillin is the drug of choice for all stages of syphilis. A reaction called JarischHerxheimer can occur in >50% of patients (general malaise, fever, headache, sweating rigors,
and temporary exacerbations of the syphilitic lesions 6–12 hours after initial treatment).
• Primary, secondary, and latent syphilis are treated with 2.4 million units of intramuscular
benzathine penicillin given once a week. Primary and secondary syphilis receive one week
of therapy. Late latent syphilis is treated with 3 weeks of therapy and diagnosed when the
VDRL or RPR titers are elevated >1:8 without symptoms.
• Tertiary syphilis is treated with penicillin 10−20 million units/day IV for 10 days.
• Penicillin-allergic patients receive doxycycline for primary and secondary syphilis, but
must be desensitized in tertiary syphilis. Pregnant patients must also undergo desensitization.
Chancroid
Definition. An acute, localized, contagious disease characterized by painful genital ulcers and
suppuration of the inguinal lymph nodes.
l Infectious Diseases
Centers for Disease Control and Prevention
Figure 7-7. Chancroid Lesion
Etiology. Haemophilus ducreyi (Gram-negative bacillus).
Clinical Findings. Small, soft, painful papules that become shallow ulcers with ragged edges.
They vary in size and coalesce. Inguinal lymph nodes become very tender and enlarged.
237
USMLE Step 2 CK
l Internal Medicine
Diagnosis. Made on clinical findings; usually Gram stain initially with culture to confirm;
PCR testing is useful.
Treatment. Azithromycin single dose or ceftriaxone intramuscularly (single dose).
Erythromycin for 7 days or cipro for 3 days are alternatives.
Lymphogranuloma Venereum
Definition. A contagious, sexually transmitted disease having a transitory primary lesion followed by suppurative lymphangitis.
Etiology. Chlamydia trachomatis.
Clinical Findings. A small, transient, nonindurated lesion that ulcerates and heals quickly;
unilateral enlargement of inguinal lymph nodes (tender); multiple draining sinuses (buboes)
develop (purulent or bloodstained); scar formation occurs, sinuses persist or recur; fever, malaise, joint pains, and headaches are common.
Diagnosis is made by clinical examination, history, and a high or rising titer of complement
fixing antibodies. Isolate chlamydia from pus in buboes.
Treatment. Doxycycline (or erythromycin as an alternative).
Wikimedia, Herbert L. Fred, MD, and Hendrik A. van Dijk
Figure 7-8. Lymphogranuloma Venereum
Granuloma Inguinale
Definition. A chronic granulomatous condition, probably spread by sexual contact.
Etiology. Donovania granulomatis, Calymmatobacterium granulomatis.
238
Clinical Findings. A painless, red nodule that develops into an elevated granulomatous mass.
In males, usually found on the penis, scrotum, groin, and thighs; in females on the vulva,
vagina, and perineum. In homosexual males, the anus and buttocks are common areas.
Healing is slow, and there is scar formation. Looks like condyloma lata or carcinoma.
Diagnosis
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• Clinically and by performing a Giemsa or Wright stain (Donovan bodies) or smear of
lesion
• Punch biopsy
Treatment. Doxycycline ceftriaxone or TMP/SMZ. Erythromycin as an alternative.
Chapter 7
l Infectious Diseases
phil.cdc.gov
Figure 7-9. Lesions of Granuloma Inguinale Due to
Calymmatobacterium Granulomatis Infection
Genital Herpes
Etiology. Herpes virus, Type II, although Type I can be seen in genital herpes.
Clinical Findings. Vesicles develop on the skin or mucous membranes; they become eroded and
painful and present with circular ulcers with a red areola. Itching and soreness usually precede
them. The ulcers are scarring; there can be inguinal lymphadenopathy. Lesions are commonly
seen in the penis in males and on the labia, clitoris, perineum, vagina, and cervix in females.
Diagnosis. Tzanck test and culture.
Treatment. Oral acyclovir, famciclovir, or valacyclovir. Must explain to the patient the relaps-
ing nature of the disease. Those with frequent recurrence should be given chronic suppressive therapy.
Genital Warts
Definition. Also known as condylomata acuminata or venereal warts.
Etiology. Papilloma virus.
Clinical Findings. Genital warts commonly found on warm, moist surfaces in the genital
areas. They appear as soft, moist, minute, pink, or red swellings that grow rapidly and become
pedunculated. Their cauliflower appearance makes them unique in appearance.
Clinical Pearl
Transmission of genital herpes
commonly occurs during an
asymptomatic phase, when a
person who is shedding the
virus inoculates virus onto a
mucosal surface of the sexual
partner.
Note
Refer to the discussion of
mulluscom contagiosum in
Dermatology chapter.
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