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10 Cards in this Set

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A 24-year-old man with AIDS is brought to the clinic by his partner after losing consciousness the previous evening. The event was witnessed by the man's partner and he reports that the patient exhibited a 3-minute episode of convulsive extremity jerking. After the episode the patient found he had lost bladder function and had bitten his tongue. Included in the evaluation of this episode is a magnetic resonance imaging of the brain, which shows a classic asymmetric target sign interpreted as representing concentric ring-enhancing abscesses with similarly enhancing eccentric nodules in the abscess cavity.

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Amphotericin B
B. Clotrimazole
C. Prednisone
D. Trimethoprim-sulfamethoxazole
E. Flucytosine
F. Pentamidine
G. Zidovudine
H. Ganciclovir
I. Pyrimethamine
J. Enfuvirtide
Option I (Pyrimethamine) is correct. This patient most likely is suffering from AIDS-associated toxoplasma encephalitis. The asymmetric target sign is virtually pathognomonic for central nervous system toxoplasmosis. Pyrimethamine is a folic acid antagonist that selectively inhibits plasmodial dihydrofolate reductase.
A 29-year-old woman with AIDS presents to the emergency department complaining of shortness of breath. This symptom began 2 days ago and is accompanied by a dry, productive cough. Vital signs are temperature: 38.3°C (100.9°F), blood pressure: 115/70 mm Hg, heart rate: 105 beats/min, and respiratory rate: 22 breaths/min. The CD4 cell levels are 50 cells/mm3. Chest X-rays show bilateral, perihilar, diffuse, fine, granular reticular interstitial opacifications. No pleural effusions are present. A high-resolution chest computed tomography shows ground-glass attenuation in the regions of opacification. Bronchioalveolar lavage and subsequent examination of the fluid verify the most likely diagnosis. After the patient is managed at maximum dosage for the first-line medication for treatment of her acute condition, she continues to have shortness of breath and a partial pressure of oxygen, arterial (PaO2) of 65 mm Hg.

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Amphotericin B
B. Clotrimazole
C. Prednisone
D. Trimethoprim-sulfamethoxazole
E. Flucytosine
F. Pentamidine
G. Zidovudine
H. Ganciclovir
I. Pyrimethamine
J. Enfuvirtide
Option C (Prednisone) is correct. Glucocorticoids are effective as adjuvant treatment with pentamidine in the treatment of Pneumocystis carinii pneumonia (PCP). They decrease the incidence of respiratory failure in AIDS patients with moderate to severe PCP pneumonia and are generally prescribed if PaO2 less than 70 mm Hg.
A 63-year-old man presents to the emergency department with the sudden onset of a swollen, red, hot, painful joint. Arthrocentesis reveals the following:
Appearance Yellow, turbid
Total Leukocyte Count 11,000/mm3
Polymorphonuclear leukocytes 85%
Monocytes 15%
Viscosity Reduced
Gram stain Gram-positive cocci
Crystals Absent

What is the most appropriate next step in therapy?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Ceftriaxone
B. Doxycycline
C. Nafcillin
D. Spectinomycin
E. Surgical drainage
Option C (Nafcillin) is correct. The results of arthrocentesis suggest septic arthritis with Staphylococcus aureus. This is the most common organism in community-acquired septic arthritis, particularly in the elderly.

Option A (Ceftriaxone) is incorrect. This is the most appropriate therapy when gonococcal septic arthritis is diagnosed. Gonococcal septic arthritis presents with a papular rash on the extremities, and a tenosynovitis and migratory polyarthropathy.

Option B (Doxycycline) is incorrect. Doxycycline should be administered when gonococcal arthritis is diagnosed in order to treat Chlamydia.

Option D (Spectinomycin) is incorrect. Spectinomycin is an alternative to ceftriaxone for gonococcal septic arthritis.

Option E (Surgical drainage) is incorrect. Surgical drainage is mandated when septic arthritis presents in young children and in prosthetic joints. Otherwise, it is reserved until response to antibiotic therapy can be assessed. Should there be no clinical improvement or reduction in synovial leukocyte count, drainage should be considered.
A 48-year-old man, who is a lawyer with HIV, comes to the office with a 5-day history of fever and shortness of breath. He is febrile at 38.9°C (102°F) with tachycardia and tachypnea. His oxygen saturation on room air is 86%. He has not been on any antiretroviral therapies. Laboratory values from 1 month ago reveal a CD4+ cell count of 83/μL and an HIV viral load of 8000. Radiography of the chest is shown (see figure). These findings are most likely to be caused by which of the following organisms?
(clear chest radiograph)
Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Cryptosporidium
B. Cytomegalovirus
C. Histoplasmosis
D. Pneumocystis carinii
E. Tuberculosis
Option D (Pneumocystis carinii) is correct. Pneumocystis carinii infection presents with hypoxia and respiratory distress in patients with HIV who have CD4+ cell counts less than 200/μL. While pneumococcal pneumonia is still more common than pneumocystis pneumonia, the clear chest radiograph and the absence of pneumococcus as an answer in this series make Pneumocystis carinii the best choice.

Option A (Cryptosporidium) is incorrect. Cryptosporidium infection is typically an infection of the gastrointestinal system in immunocompromised hosts like this patient.

Option B (Cytomegalovirus) is incorrect. Although cytomegalovirus infection is in the differential diagnosis in an immunocompromised host, the patient has hypoxia and a clear chest radiograph.This is inconsistent with cytomegalovirus.

Option C (Histoplasmosis) is incorrect. Although histoplasmosis is in the differential diagnosis in an immunocompromised host, the patient has hypoxia and a clear chest radiograph. This is inconsistent with histoplasmosis.

Option E (Tuberculosis) is incorrect. Although tuberculosis is in the differential diagnosis in an immunocompromised host, the patient has hypoxia and a clear chest radiograph. This is inconsistent with tuberculosis.
A 19-year-old HIV-positive man visits the emergency room (ER) complaining of severe diarrhea. His symptom began 2 days ago and has become progressively worse. Today he reports that he has voluminous watery bowel movements with no sign of blood. He reports no fever, vomiting, or tenesmus. Further discussion reveals the man has been noncompliant with his prescribed highly active antiretroviral therapy regimen. Vital signs are normal and physical exam shows no evidence of skin lesions, ophthalmopathy, or oral thrush. His CD4 count is 150 cells/mm3. Microscopic examination of a stool sample with modified acid-fast staining of stool shows red-stained round oocysts against a blue-green background. No white or red blood cells are seen in the stool. What is the next step in treatment of this patient's likely condition?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Amphotericin B and metronidazole
B. Diphenoxylate, rifampin, isoniazid, chlorambucil, and streptomycin
C. Loperamide, paromomycin, and azithromycin
D. Octreotide, azithromycin, and trimethoprim-sulfamethoxazole
E. Pyrimethamine
Option C (Loperamide, paromomycin, and azithromycin) is correct. The microscopic findings in an AIDS patient with profuse diarrhea and CD4 count less than 200 cell/mm3 strongly indicate intestinal Cryptosporidium infection. The organism is highly resistant to most antibiotic regimens; but this combination along with the antidiarrheal agent of choice, loperamide, has been shown most effective in treatment. Even so, mortality is more than 50%.

Option A (Amphotericin B and metronidazole) is incorrect. Amphotericin B is not indicated for Cryptosporidium infection. Metronidazole is not among the antibiotics of choice. An antidiarrheal agent should be prescribed as well.

Option B (Diphenoxylate, rifampin, isoniazid, chlorambucil, and streptomycin) is incorrect. This is an antituberculosis regimen with an antidiarrheal agent. The patient most likely has an intestinal Cryptosporidium infection.

Option D (Octreotide, azithromycin, and trimethoprim-sulfamethoxazole) is incorrect. Somatostatin inhibitors have been shown effective in symptomatic treatment of Cryptosporidium-associated diarrhea. Sulfa antibiotics and azithromycin have virtually no effect against the organism.

Option E (Pyrimethamine) is incorrect. Pyrimethamine is the drug of choice for Toxoplasma gondii infection and is used to treat AIDS-associated diarrhea. This patient has strong evidence of Cryptosporidium infection. Paromomycin with azithromycin shows better activity against Cryptosporidium than pyrimethamine.
A 44-year-old man presents to the emergency department after being involved in a fist fight yesterday. He has developed cellulitis over the injured fingers. A wound culture is obtained and after 2 days of growth, reveals pitting in agar.

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Aeromonas hydrophila
B. Citrobacter freundii
C. Eikenella corrodens
D. Erysipelothrix rhusiopathiae
E. Haemophilus influenzae
F. Pasteurella multocida
G. Pasteurella multocida
H. Pseudomonas aeruginosa
I. Streptobacillus moniliformis
J. Streptococcus aureus
Option C (Eikenella corrodens) is correct. Most human bites are polymicrobial. A frequent contaminant is Eikenella corrodens, a gram-negative rod. The key finding is the ability of the organism to corrode (i.e., produce pits) in agar, hence the name.
A 44-year-old man presents to the emergency department with a 3-day history of fevers, myalgias, arthralgias, and vomiting. He states the symptoms came on suddenly and the fevers are intermittent. He has also noticed a rash on his arms. He is well known to the staff in the emergency department, as he is homeless and frequently attends the emergency department for minor complaints. Seven days ago, he was bitten by a rat. He is admitted to the hospital for observation. Over the next 3 days, it is noted that his fever is irregularly relapsing.

End of set

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Aeromonas hydrophila
B. Citrobacter freundii
C. Eikenella corrodens
D. Erysipelothrix rhusiopathiae
E. Haemophilus influenzae
F. Pasteurella multocida
G. Proteus vulgaris
H. Pseudomonas aeruginosa
I. Streptobacillus moniliformis
J. Streptococcus aureus
Option I (Streptobacillus moniliformis) is correct. This patient has rat bite fever (also known as Haverhill fever), most often caused by Streptobacillus moniliformis. The presentation is as in the vignette. The condition is associated with a 25% mortality. Intravenous (IV) penicillin is the treatment of choice.

High-yield Hit 1
Streptobacillus moniliformis, the causative agent of rat-bite fever, is a long, thin (0.1 to 0.5 × 1 to 5 μm), gram-negative rod that tends to stain poorly and to be more pleomorphic in older cultures. Granules, bulbous swellings resembling a string of beads, and extremely long filaments may be seen (Figure 39-3).
Streptobacillus is found in the nasopharynx of rats and other small rodents, as well as transiently in animals that feed on rodents (e.g., dogs, cats). Turkeys exposed to rats and mice, as well as contaminated water and milk, have also been implicated in Streptobacillus infections.
Figure 39-3 Gram stain of Streptobacillus moniliformis; note the pleomorphic forms and bulbous swellings.

From Medical Microbiology 5E by Murray et al
High-yield Hit 2
Human infections result from rodent bites (rat-bite fever) or consumption of contaminated food or water (Haverhill fever). After a 2- to 10-day incubation period, the disease onset is abrupt, characterized by irregular fever, headache, chills, myalgia, and arthralgia. A maculopapular rash develops a few days later. Recurrent episodes of headache and arthralgia and complications, such as carditis, meningitis, or pneumonia, can occur in untreated patients. Vomiting and pharyngitis are characteristics of Haverhill fever (named after Haverhill, Mass., where the first epidemic was described).
Blood and joint fluid should be collected for the isolation of S. moniliformis. The organism can grow on enriched media supplemented with 15% blood, 20% horse or calf serum, or 5% ascitic fluid. S. moniliformis is slow growing, taking at least 3 days to be isolated. When grown in broth, it has the appearance of "puffballs"; small, round colonies are seen on agar, as are cell wall defective forms, with their typical fried-egg appearance. It is difficult to identify the organisms because they are relatively inactive, although acid is produced from glucose and other selected carbohydrates. The most reliable method for identifying isolates is sequencing the 16S rRNA gene. The serologic tests that can detect antibodies against Streptobacillus antigens are available in reference laboratories. A titer greater than or equal to 1:80 or a fourfold rise in the titer is considered diagnostic, although this test has not been standardized or carefully evaluated for cross-reactivity. S. moniliformis is susceptible to many antibiotics, including penicillin (not active against cell wall defective forms) and doxycycline.
A 5-year-old girl is brought to the emergency room 2 hours after awakening with a headache, sore throat, and neck stiffness. Since that time, she has complained of nausea and vomited twice. She had been previously well. On arrival, her temperature is 39.2°C (102.5°F), she appears irritable and is adverse to bright light. There is prominent nuchal rigidity. Additionally, there is involuntary flexion of the knees and hips following passive flexion of the neck. A mixed petechial and maculopapular rash is seen on the extensor surfaces of the extremities. What is the most likely cause of these findings?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Haemophilus influenzae
B. Listeria monocytogenes
C. Neisseria meninginitis
D. Streptococcus agalactiae
E. Streptococcus pneumoniae
Option C (Neisseria meningitis) is correct. This patient has meningitis as evidenced by her nuchal rigidity, photophobia, and positive Brudzinski sign. Although from an epidemiologic standpoint, S. pneumoniae is the most common cause of meningitis in this age, a petechial rash is indicative of N. meningitis infection.

Option A (Haemophilus influenzae) is incorrect. With the introduction of a vaccine against H. influenzae type b (HiB), the incidence of meningitis caused by this bacteria has significantly decreased.

Option B (Listeria monocytogenes) is incorrect. Listeria is a common cause of meningitis in neonates, elderly, and alcoholics. Whenever it is suspected, ampicillin should be added to empiric antibiotic therapy for appropriate coverage.

Option D (Streptococcus agalactiae) is incorrect. This is also known as group B streptococcus (GBS). It is the most common cause of meningitis in neonates.

Option E (Streptococcus pneumoniae) is incorrect. S. pneumoniae is the most common cause of meningitis in all ages except the neonatal period.

High-yield Hit 1
Acute bacterial meningitis is an infection of the pia mater and subarachnoid space. The annual incidence in developed countries is approximately 5-10 per 100000. Causative organisms vary with patient age, with three bacteria (NHS) accounting for over three-quarters of all cases:

* Neisseria meningitidis (meningococcus).
* Hemophilus influenzae (if very young and unvaccinated).
* Streptococcus pneumoniae (pneumococcus).

Other organisms to consider:

* Neonates: Escherichia coli, β-hemolytic streptococci, Listeria monocytogenes.
* Elderly and immunocompromised: Listeria, tuberculosis, Gram-negative bacteria.
* Hospital-acquired infections: Klebsiella, Escherichia coli, Pseudomonas, Staphylococcus aureus.

Clinical features are those of:

* Fever, headache, photophobia, painful eye movements. Impaired consciousness is a late and ominous feature.
* Neck stiffness, positive Kernig's sign.
* Occasionally: petechial skin rash (meningococcal meningitis), focal neurological signs, particularly cranial nerve palsies.

From Crash Course: Nervous System by Mihailoff
A 19-year-old man presents to the physician, because he is experiencing difficulty swallowing and speaking. His symptoms have evolved from a 2-week period of a sore throat, fever, and cervical lymphadenopathy. Since yesterday, he has been experiencing difficulty swallowing and speaking because of the pain in his throat. On examination, his tonsils are grossly swollen and he is slightly drooling. There is bilateral, tender cervical lymphadenopathy. The spleen is palpable 1.5 cm below the costal margin. A blood film reveals atypical lymphocytes and there is a positive heterophile antibody test. What is the most appropriate next step in the management of this patient?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Acyclovir
B. Corticosteroids
C. Ganciclovir
D. Plasmapheresis
E. Rest and avoidance of contact sports
Option B (Corticosteroids) is correct. This patient has a positive heterophile antibody test along with classic symptoms for infectious mononucleosis, making the diagnosis Epstein-Barr virus (EBV)-medicated mononucleosis. He also is experiencing severe swollen tonsils resulting in drooling, dysphagia, and odynophagia. Obstructing tonsils, a very enlarged spleen, or severe thrombocytopenia are indications for the use of corticosteroids.

Option A (Acyclovir) is incorrect. Acyclovir is active against EBV, but is not licensed for use in infectious mononucleosis.

Option C (Ganciclovir) is incorrect. Ganciclovir is active against cytomegalovirus. Cytomegalovirus would produce a heterophile-antibody negative infectious mononucleosis.

Option D (Plasmapheresis) is incorrect. Plasmapheresis is useful when patients subsequently develop Guillain-Barré syndrome, but there is no role acutely.

Option E (Rest and avoidance of contact sports) is incorrect. This is the usual management of patients with EBV-related infectious mononucleosis. The prominence of the tonsils warrants therapy, however.

High-yield Hit 1
14. Why is chicken soup so helpful for upper respiratory infections (URIs)?
The benefits of chicken soup have been of lore for hundreds of years, beginning in the 12th century, when physician and philosopher Maimonides extolled its virtue. The precise mechanisms of its anecdotal therapeutic benefits remain elusive. One recent study at the University of Nebraska found that the nonparticulate component of chicken soup in vitro inhibited neutrophil migration in a concentration-dependent manner. This anti-inflammatory effect may be one mechanism by which chicken soup mitigates the symptoms of URIs.
Rennard BO, Ertl RF, Gossman GL, et al: Chicken soup inhibits neutrophil chemotaxis in vitro. Chest 118:1150-1157, 2000.
15. Name the three stages of pertussis infection (whooping cough).

1. Catarrhal (1-2 weeks): Low-grade fever, upper respiratory infection symptoms
2. Paroxysmal (2-4 weeks): Severe cough occurring in paroxysms, onset of inspiratory "whoop"
3. Convalescent (1-2 weeks): Resolution of symptoms

16. What is the most common cause of death in children with whooping cough?
Ninety percent of deaths are attributable to pneumonia, which most often develops as a secondary bacterial infection. These cases can be easily missed during the paroxysmal phase, when respiratory symptoms are so prominent and usually attributed solely to pertussis. A new spiking fever should prompt a careful search for an evolving pneumonia.
17. Is erythromycin of value in pertussis infection?
If used during the first 14 days of illness or before the paroxysmal stage, erythromycin can decrease the severity of symptoms during the paroxysmal stage. If the diagnosis is established later in the course, erythromycin should still be administered to eliminate the nasopharyngeal carriage of Bordetella pertussis and limit the spread of disease. The dose is 50 mg/kg/day (divided into four daily doses) for 14 days, with a maximum total daily dose of 1 gm. Recent evidence suggests that treatment with azithromycin (10-12 mg/kg/day in one dose) or clarithromycin (15-20 mg/kg/day divided into two doses) for 5-7 days is also effective for eradicating carriage and preventing transmission.
18. Do antibiotics prevent the development of pneumonia after a URI?
Over 90% of URIs are caused by viruses, and children <5 years old (especially those in day-care environments) can experience 6-8 URI episodes per year. Multiple studies have shown that antibiotic treatment of URIs does not shorten their course or prevent the development of pneumonia.
Gadomski AM: Potential interventions for preventing pneumonia among young children: Lack of effect of antibiotic treatment for upper respiratory infections. Pediatr Infect Dis J 12:115-120, 1993.
19. Sternal edema is classically the sign of what infection?
20. How does Hatchcock's sign help distinguish swelling as a result of mumps from swelling caused by adenitis?
Upward pressure applied to the angle of the mandible produces tenderness with mumps (Hatchcock's sign); this maneuver produces no tenderness with adenitis.
21. Summarize the distinguishing features of staphylococcal scalded skin syndrome, staphylococcal toxic shock syndrome, and streptococcal toxic shock syndrome.
See Table 11-1.
22. What percentage of cases of staphylococcal toxic shock syndrome are nonmenstrual?
Over the past two decades, the epidemiology of toxic shock syndrome has changed, reflecting changes in tampon composition and a decrease in absorbency. In 1996, >50% of reported cases were nonmenstrual. The syndrome occurs in the setting of focal staphylococcal colonization or focal infections, including empyema, osteomyelitis, soft-tissue abscess, surgical infections, and burns.
23. Which diseases are transmitted by ticks?
Disease Agent
Lyme disease Borrelia burgdorferi
Relapsing fever Borrelia species
Tularemia Francisella tularensis
Rocky Mountain spotted fever Rickettsia rickettsii
Queensland tick typhus Rickettsia australis
Boutonneuse fever Rickettsia conorii
Asian tick typhus Rickettsia sibirica
Colorado tick fever Arbovirus
Tick-borne encephalitis Arbovirus
Ehrlichiosis Ehrlichia chaffeensis, Ehrlichia equi, Ehrlichia phagocytophila, Ehrlichia ewingii
Babesiosis Babesia microti, Babesia divergens, Babesia bovis
Drutz JE: Arthropods. In Feigin RD, Cherry JD (eds): Textbook of Pediatric Infectious Diseases, 5th ed. Philadelphia, W.B. Saunders, 2004, p 2836.
24. What are the two primary types of human ehrlichiosis?
Human monocytic ehrlichiosis and human granulocytic ehrlichiosis. Both are febrile illnesses that are caused by different agents but that have similar clinical pictures of significant systemic symptoms (e.g., intense headache, chills, myalgia) and, sometimes, rash. The presentation of symptoms can mimic Rocky Mountain spotted fever. Laboratory features include anemia, lymphopenia, leukopenia, thrombocytopenia, hyponatremia, elevated liver function tests, and cerebrospinal fluid (CSF) abnormalities (e.g., lymphocytic pleocytosis, elevated total protein).
Jacobs RF, Schultze GE: Ehrlichiosis in children. J Pediatr 131:184-192, 1997.
Clinical features Staphylococcal scalded skin syndrome Staphylococcal toxic shock syndrome Group A streptococcal toxic shock-like syndrome
Organism Staphylococcus aureus
Usually phage group 11, type 71 Staphylococcus aureus
Usually phage group 1, type 29 Group A streptococci
Usually type 1, 3, or 18
Exotoxin A production
Site of infection Usually focal
Mucocutaneous border: nose, mouth, diaper area Mucous membranes
Infected wound or furuncle Blood, abscess, pneumonia, empyema, cellulitis, necrotizing fasciitis
Sometimes inapparent Sometimes inapparent Sometimes inapparent
Skin rash Tender erythroderma: face/neck, generalized Tender erythroderma: trunk, hands, feet Erythroderma: trunk, extremities
Bullae, no petechiae Edema of hands, feet
Desquamation Early, first 1-2 days, generalized Late, 7-10 days, mostly hands and feet Late, 7-10 days, mostly hands and feet
Hyperemia of oral and vaginal mucosa Hyperemia of oral and vaginal mucosa
Mucous membranes Normal Hypertrophy of tongue papillae Hypertrophy of tongue papillae
Conjunctivae Normal Markedly injected Injected
Course Insidious, 4-7 days
Benign, <1% mortality Fulminant, shock with secondary multiple organ failure, 10% mortality Fulminant, shock with early primary multiple organ failure, 30-50% mortality

Adapted from Bass JW: Treatment of skin and skin structure infections. Pediatr Infect Dis J 11:152-155, 1992.
25. What is the preferred treatment for human ehrlichiosis?
Doxycycline is the drug of choice to treat human ehrlichiosis. Early clinical experience suggested that chloramphenicol may also be effective, but in vitro susceptibility testing of E. chaffeensis and the human granulocytic ehrlichiosis agent revealed resistance to chloramphenicol. Although tetracyclines are generally contraindicated in children <8 years old because of associated dental staining, short courses of treatment with these agents-especially doxycycline-are unlikely to cause dental abnormalities.
26. What the heck are the HACEKs?
The HACEK organisms include Haemophilus aphrophilus, Haemophilus paraphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae. These organisms share the property of slow growth in culture and have a predilection for producing endocarditis. They should be considered in cases of apparent culture-negative endocarditis.
27. In the setting of clinical signs and symptoms of encephalitis, what electroencephalogram pattern is suggestive of herpes simplex virus disease?
Periodic lateralized epileptiform discharges. These may be seen in other, rarer forms of encephalitis, such as Epstein-Barr virus encephalitis, Creutzfeldt-Jakob disease, and subacute sclerosing panencephalitis.
28. What is the best approach to diagnosing herpes simplex virus (HSV) encephalitis in children?
In the past, no single noninvasive method could simply and reproducibly diagnose HSV encephalitis; definitive diagnosis relied on brain biopsy. In recent years, a number of studies have demonstrated that analysis of CSF using the polymerase chain reaction (PCR) allows for rapid and accurate diagnosis. According to Lakeman and colleagues, PCR detects >98% of cases and may be more sensitive than brain biopsy. Nowadays, brain biopsy should be considered only when PCR is negative and the diagnosis remains obscure or PCR is positive but the clinical course is atypical for HSV encephalitis and the response to antiviral therapy is slow.
Lakeman FD, Whitley RJ: Diagnosis of herpes simplex encephalitis: Application of polymerase chain reaction to cerebrospinal fluid from brain-biopsied patients and correlation with disease. National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. J Infect Dis 171:857-863, 1995.
Whitley RJ, Lakeman FD. Herpes simplex virus infections of the central nervous system: Therapeutic and diagnostic considerations. Clin Infect Dis 20:414-420, 1995.
29. Can acyclovir be used to prevent or treat oral HSV infections?
In immunocompetent hosts, oral acyclovir offers significant therapeutic benefit in primary HSV gingivostomatitis but has limited efficacy for the treatment of recurrent herpes labialis. Topical acyclovir has not shown consistent benefit in either of these settings. Prophylaxis with oral acyclovir can reduce the number of recurrences in adults with herpes labialis, but it has not been studied in children.
30. How quickly do central lines become colonized?
The timing and rate of central line colonization depend on a number of factors. Manipulation of the catheter (e.g., for blood drawing, medication administration, or flushing) and poor handwashing by health care providers are probably the most important factors that increase the risk of colonization. In general, the likelihood of colonization increases with the length of time that the catheter has been in place. Colonization rates have been reported to be <10% for catheters <3 days old, approximately 15% for catheters 3-7 days old, and about 20% for catheters in place for >7 days.
31. What is the most proper medical term for oral thrush?
Acute pseudomembranous candidiasis. Quite a mouthful. Although thrush is sometimes confused with residual formula in the mouth in infants, formula is more easily removed with a tongue blade. When thrush is scraped, small bleeding points often occur on the underlying mucosa.
32. Which congenital infections cause cerebral calcifications?
Cerebral calcifications are most frequently observed in congenital Toxoplasma and cytomegalovirus (CMV) infections. They are seen occasionally in patients with congenital herpes simplex virus infection and rarely in patients with congenital rubella infection.
33. What are the late sequelae of congenital infections?
The late sequelae of chronic intrauterine infections are relatively common and may occur in infants who are asymptomatic at birth. Most sequelae present symptoms later in childhood rather than infancy.

* CMV: Hearing loss,* minimal to severe brain dysfunction* (motor, learning, language, and behavioral disorders)
* Rubella: Hearing loss,* minimal to severe brain dysfunction* (motor, learning, language, and behavioral disorders), autism,* juvenile diabetes, thyroid dysfunction, precocious puberty, progressive degenerative brain disorder*
* Toxoplasmosis: Chorioretinitis,* minimal to severe brain dysfunction,* hearing loss, precocious puberty
* Neonatal herpes: Recurrent eye and skin infection, minimal to severe brain dysfunction
* Hepatitis B virus: Chronic subclinical hepatitis, rarely fulminant hepatitis

Plotkin SA, Alpert G: A practical guide to the diagnosis of congenital infections in the newborn infant. Pediatr Clin North Am 33:465-479, 1986.
34. What is the most common congenital infection?
Congenital CMV infection, which in some large screening studies occurs in up to 1.3% of newborns. However, 90-95% of infected neonates are asymptomatic. Some infants who are asymptomatic at birth later develop hearing loss.
35. How is CMV transmitted from mother to infant?
CMV can be transmitted by the transplacental route or through contact with cervical secretions or breast milk. On occasion, transmission may occur by contact with saliva or urine.
36. Should congenital CMV be treated?
Treatment is recommended for infants with life- or vision-threatening disease, such as severe retinitis, interstitial pneumonitis, hepatitis, or thrombocytopenia.
37. How do complications vary between newborns with CMV infection who are symptomatic versus those who are asymptomatic at birth?
See Table 11-2.
38. What is the risk to the fetus if the mother is infected with parvovirus B19 during pregnancy?
The risk of fetal loss is 2-10% and is greatest when maternal infection occurs during the first half of pregnancy. Fetal loss occurs as a consequence of hydrops, which develops as a result of parvovirus-induced anemia. An elevated maternal serum alpha-fetoprotein level may be a marker for an adverse outcome. The signs of parvovirus infection in adults are not very distinctive but may include fever, a maculopapular or lace-like rash, and joint pain.
39. What are the consequences of primary varicella infection during the first trimester?
The congenital varicella syndrome consists of a constellation of features:

* Limb atrophy, usually associated with a cicatricial (scarring) lesion
* Neurologic and sensory defects
* Eye abnormalities (chorioretinitis, cataracts, microphthalmia, Horner syndrome)

This syndrome usually follows maternal infection during the first trimester, although it may be seen after infection up to 20 weeks into gestation. The largest prospective study reported to date found four cases of fetal varicella syndrome in 141 pregnancies, yielding an incidence of <3%.
Percentage of occurrence
Complication Symptomatic Asymptomatic
Death 5.8 0.3
Microcephaly 37.5 1.8
Sensorineural hearing loss 58 7.4
Bilateral hearing loss 37 2.7
Moderate-to-profound hearing loss (60-90 dB) 27 1.7
Chorioretinitis 20.4 2.5
Intelligence quotient of <70 55 3.7
Seizures 23.1 0.9
Paresis/paralysis 12.5 0

Adapted from Remington JS, Klein JO: Infections of the Fetus and Newborn Infant, 5th ed. Philadelphia, W.B. Saunders, 2001, p 408.
40. When should varicella zoster immune globulin (VZIG) be given to a newborn?
VZIG should be given as soon as possible to a newborn whose mother developed varicella from 5 days before to 2 days after delivery. During this period of high risk, the fetus is exposed to high circulating titers of the virus without the benefit of maternal antibody synthesis. Premature neonates exposed to varicella during the neonatal period are also candidates for VZIG:

* If the infant is ≥28 weeks' gestation and the mother has no history of chickenpox
* If the infant is <28 weeks' gestation or weighs ≤1,000 gm, regardless of maternal history, because little maternal antibody crosses the placenta before the third trimester of pregnancy.


1. Patients >12 years old
2. Patients with chronic pulmonary or cutaneous disorders
3. Patients receiving long-term salicylate therapy
4. Patients receiving corticosteroids (oral or aerosolized)

41. Do urogenital mycoplasmas have a role in neonatal disease?
Ureaplasma urealyticum has been associated with low birth weight and bronchopulmonary dysplasia. This organism has been recovered from neonates with respiratory distress, pneumonia, and meningitis, but a causative role in these diseases has not been proven. Several reports of apparent Mycoplasma hominis meningitis and eye infection have been published.
42. If a mother is culture positive for Ureaplasma urealyticum or M. hominis, what is the likelihood of transmission to the newborn infant?
Vertical transmission occurs in up to 60% of exposed newborns. Risk of transmission is higher in preterm and low-birthweight infants and correlates with the prolonged rupture of membranes and maternal fever. Infants delivered by cesarean section over intact membranes have a very low rate of colonization as compared with infants delivered vaginally.
43. What are the features of congenital rubella syndrome?
The most characteristic features of congenital rubella syndrome are congenital heart disease, cataracts, microphthalmia, corneal opacities, glaucoma, and radiolucent bone lesions. The features of congenital rubella syndrome can be divided into three broad categories:

* Transient: Low birthweight, hepatosplenomegaly, thrombocytopenia, hepatitis, pneumonitis, and radiolucent bone lesions
* Permanent: Deafness, cataracts, and congenital heart lesions (patent ductus arteriosus > pulmonary artery stenosis > aortic stenosis > ventricular septal defects)
* Developmental: Psychomotor delay, behavioral disorders, and endocrine dysfunction

44. Should all pregnant women be screened for herpes simplex virus (HSV) infection during pregnancy?
Existing data indicate that antepartum cultures of the maternal genital tract fail to predict viral shedding at the time of delivery. As a consequence, routine antepartum cultures are not recommended.
45. What are risk factors for the development of neonatal HSV disease?
Among infants born vaginally to mothers with primary herpes genitalis, 30-50% will develop HSV disease. Only 3-5% of infants born to mothers with active recurrent disease become infected. Distinguishing between primary and recurrent herpes infections by history and clinical examination is often difficult. Low birthweight is an independent risk factor. Fetal scalp monitoring may result in direct inoculation of the virus into the baby's scalp.
Many experts advocate cesarean section for women who are in labor at term and have visual evidence of active genital HSV lesions, especially if membranes have been ruptured for less than 4-6 hours. If membranes have been ruptured for longer periods of time, operative delivery is less effective for reducing the risk of neonatal infection.
46. What are the three forms of neonatal HSV disease?
Occurring with approximately equal frequency, the three patterns of neonatal HSV disease are as follows:

* Mucocutaneous disease (localized to the skin, eye, or mouth)
* Encephalitis
* Disseminated disease (± central nervous system [CNS] involvement) with a picture that resembles bacterial sepsis

It is important to note that only one third of infants with either localized encephalitis or disseminated disease will have visible skin lesions.
47. How should the neonate with suspected HSV disease be treated?
Both acyclovir and vidarabine have activity against HSV. Acyclovir is the preferred drug and is administered in a dose of 20 mg/kg intravenously every 8 hours pending definitive diagnosis. For mucocutaneous disease, treatment is continued for 14 days. For encephalitis and disseminated disease, treatment is continued for 21 days.
48. In which groups of women is prenatal hepatitis B surface antigen (HBsAg) screening recommended?
In the past, women were screened for HBsAg if they fell into a high-risk group based on ethnic origin, immunization status, or history of exposure to blood products, intravenous drugs, or a high-risk partner. However, historic information reveals only a portion of HBsAg carriers were captured using these screening criteria, and thus it is recommended that all pregnant women be screened for HBsAg.
49. What is the relationship between age of acquisition of hepatitis B virus and the likelihood of chronic hepatitis B infection?
Chronic hepatitis B virus infection with persistence of HBsAg occurs in as many as 90% of infants who are infected by perinatal transmission, in an average of 30% of children who are 1-5 years old when infected, and in 2-6% of older children, adolescents, and adults who become infected.
Schiff ER: Update in hepatology. Ann Intern Med 130:52-57, 1999.
50. How should infants born to mothers with hepatitis A infection be managed?
Neonates born to mothers with active hepatitis A infection are unlikely to contract the virus, and efficacy of postnatal prophylaxis with hepatitis A immune globulin has not been proven. With this information in mind, no prophylaxis is recommended.
51. How should infants born to mothers with hepatitis B infection be managed?
For infants born to women who are HBsAg-positive, hepatitis B immune globulin (0.5 mL intramuscularly) and the first dose of hepatitis B vaccine should be administered within 12 hours of delivery to reduce the risk of infection. Although breast milk is capable of transmitting the hepatitis B virus, the risk of transmission in HBsAg-positive mothers whose infants have received timely hepatitis B immune globulin and hepatitis B vaccine is not increased by breast feeding.
52. How should infants born to mothers with hepatitis C infection be managed?
The risk of vertical transmission of hepatitis C virus is approximately 5%, and no preventive therapy exists. Mothers with hepatitis C infection should be advised that transmission of hepatitis C by breast feeding has not been documented. Accordingly, maternal hepatitis C infection is not a contraindication to breast feeding, although mothers with cracked or bleeding nipples should consider abstaining.
53. How do the clinical features of early and late congenital syphilis differ?
The manifestations of congenital syphilis are protean and may be divided into early and late findings. Early manifestations occur during the first 2 years of life; late manifestations occur after 2 years of age (Table 11-3).
54. Describe the appearance of Hutchinson's teeth.
The permanent central incisors are typically peg-shaped or notched.
55. How is the diagnosis of congenital syphilis made?

* Pregnant women and infants should be screened for possible infection with a nontreponemal test for Treponema pallidum. Such tests include the rapid plasma reagin card test and the Venereal Disease Reference Laboratory (VDRL) slide test.
* If blood from the mother or infant yields a positive nontreponemal serologic test, a specific treponemal test should be performed on the infant's blood. Examples include the fluorescent treponemal antibody absorption test and the microhemagglutination test for T. pallidum.
* Evaluation of infants with suspected congenital syphilis should also include a complete blood count, analysis of the cerebrospinal fluid (including a CSF VDRL), and long-bone radiographs (unless the diagnosis has been otherwise established).

Early Congenital Syphilis (310 Patients) Late Congenital Syphilis (271 Patients)
Hepatomegaly 32% Pseudoparalysis of Parrot 87%
Skeletal abnormalities 29% Short maxilla 84%
Splenomegaly 18% High palatal arch 76%
Birthweight <2,500 gm 16% Hutchinson triad 75%
Pneumonia 16% Saddle nose 73%
Severe anemia, hydrops, edema 16% Mulberry molars 65%
Skin lesions 15% Hutchinson teeth 63%
Hyperbilirubinemia 13% Higoumenakia sign 39%
Snuffles, nasal discharge 9% Relative protuberance of mandible 26%
Painful limbs 7% Interstitial keratitis 9%
Cerebrospinal fluid abnormalities 7% Rhagades 7%
Pancreatitis 5% Saber shin 4%
Nephritis 4% VIII nerve deafness 3%
Failure to thrive 3% Scaphoid scapulae 0.7%
Testicular mass 0.3% Clutton joint 0.3%
Chorioretinitis 0.3%
Hypoglobulinemia 0.3%

Adapted from Sanchez PJ, Gutman LT: Syphilis. In Feigin RD, Cherry JE, Demmler GJ, Kaplan SL (eds): Pediatric Infectious Diseases, 5th ed. Philadelphia, W.B. Saunders, 2004, pp 1730-1732.
56. What are the pitfalls of rapid plasma reagin and VDRL testing?

* Cord blood specimens from the infant can produce false-positive results; therefore, serum from the infant is preferred.
* A mother who has been treated adequately for syphilis during pregnancy can still passively transfer antibodies to the neonate, which results in a positive titer in the infant in the absence of infection. In this circumstance, the infant's titer is usually less than the mother's and reverts to negative over several months.

57. If a pregnant woman is found to have Chlamydia trachomatis in her birth canal, what is the most appropriate course of action?
A pregnant woman with a known chlamydial infection should be treated with oral erythromycin, azithromycin, or amoxicillin to reduce the risk of neonatal chlamydial pneumonia and conjunctivitis. Simultaneous treatment of the male partner(s) with doxycycline (100 mg orally twice daily) or azithromycin (1 gm orally as a single dose) should also be undertaken.
58. What is the risk to a fetus after primary maternal Toxoplasma infection?
The risk depends on the time during pregnancy that the mother becomes infected. Assuming that the mother is untreated, first-trimester infection is associated with a fetal infection rate of approximately 25%, second-trimester infection with a rate >50%, and third-trimester infection with a rate of roughly 65%. The severity of clinical disease in congenitally infected infants is inversely related to gestational age at the time of primary maternal infection.
59. If a mother acquires Toxoplasma during pregnancy, can transmission to the fetus be prevented?
The existing literature is conflicting. Some studies suggest that treatment with spiramycin before 17 weeks' gestation or with pyrimethamine plus sulfadiazine after 17 weeks' gestation can reduce the risk of transmission of the parasite to the fetus by 50-60%, although other studies show no effect of treatment on transmission. The rationale for such treatment is based on the observation that there may be a significant lag period between the onset of maternal infection and infection of the fetus.
Gilbert R, Gras L; European Multicentre Study on Congenital Toxoplasmosis: Effect of timing and type of treatment on the risk of mother to child transmission of Toxoplasma gondii. Brit J Obstet Gynecol 110:112-120, 2003.
Wallon M, Liou
The parents of a 13-month-old girl bring their child to the pediatrician for a regular scheduled well-child checkup and appropriate immunizations. There are no current complaints. The child had a high fever and a “slapped cheek"” rash 3 months ago that resolved after 3 days without treatment or sequelae. There is no other history of illness. On examination, the child is well appearing. Vital signs are normal. There are no abnormal physical findings. The parents are concerned about the possible side effects of the recommended mumps-measles-rubella vaccine due at this time. Which of the following is an accurate and appropriate response?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Febrile seizure is the most serious side effect
B. Fewer than 0.1% of children will likely develop mumps after vaccination
C. Side effects are uncommon
D. The chance of moderate side effects is 1 in 100,000
E. The chance of serious side effects is 1 in 100,000
Option E (The chance of serious side effects is 1 in 100,000) is correct. A serious reaction occurs in about 0.001% of cases.

Option A (Febrile seizure is the most serious side effect) is incorrect. Among the most serious side effects are anaphylactic shock, thrombocytopenia, and coma. Febrile seizure is considered a moderate side effect.

Option B (Fewer than 0.1% of children will likely develop mumps after vaccination) is incorrect. About 3 to 4 weeks after the injection, 2% of children develop a mild form of mumps. This only lasts a day or two.

Option C (Side effects are uncommon) is incorrect. Body rash is common 7 to 10 days after the mumps-measles-rubella vaccine.

Option D (The chance of moderate side effects is 1 in 100,000) is incorrect. Febrile seizures, which are considered a moderate side effect, occur in 0.03% of cases.

High-yield Hit 1
Figure 8-11 Vaccination strategies. Examples of different types of vaccines and the nature of the protective immune responses induced by these vaccines are summarized.
Vaccination is the process of stimulating protective adaptive immune responses against microbes by exposure to nonpathogenic forms or components of the microbes. The development of vaccines against infections has been one of the great successes of immunology. The only human disease to be intentionally eradicated from the earth is smallpox, and this was achieved by a worldwide program of vaccination. Polio is likely to be the second such disease, and, as mentioned in Chapter 1, many other diseases have been largely controlled by vaccination (Fig. 1-2, Chapter 1). Several types of vaccines are in use and are being developed (Fig. 8-11). Some of the most effective vaccines are composed of attenuated microbes, which are treated to abolish their infectivity and pathogenicity while retaining their antigenicity. Immunization with these attenuated microbes stimulates the production of neutralizing antibodies against microbial antigens that protect vaccinated individuals from subsequent infections. For some infections, such as polio, the vaccines are given orally, to stimulate mucosal IgA responses that protect individuals from natural infection, which occurs by the oral route. Vaccines composed of microbial proteins and polysaccharides, called subunit vaccines, work in the same way. Some microbial polysaccharide antigens (which cannot stimulate T cell help) are chemically coupled to proteins, so that helper T cells are activated and high-affinity antibodies are produced against the polysaccharides. These are called conjugate vaccines, and they are excellent examples of the practical application of our knowledge of helper T cell-B cell interactions. Immunization with inactivated microbial toxins and with microbial proteins synthesized in the laboratory stimulate antibodies that bind to and neutralize the native toxins and the microbes, respectively.

Taken from Basic Immunology 2E by Abbas & Lichtman