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30 Cards in this Set

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A 16-year-old female comes to the emergency room after an altercation with her cat. She has several bite marks over the dorsum of her hand. She has no reported allergies and her vital signs are normal. X-ray is negative for retained teeth. Prophylactic antibiotic amoxicillin (Augmentin) is prescribed to protect against infection from which organism?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Bartonella
B. Clostridium
C. Eikenella
D. Kingella
E. Pasteurella
Option E (Pasteurella) is correct. Pasteurella is a common bacterium that can cause skin infections after a cat bite. Because of the shape of the cat's teeth, the bacteria is injected deep into the soft tissue. Wounds should be cored out and left open. Treatment with intravenous ampicillin sodium (Unasyn) or oral amoxicillin (Augmentin) is warranted as prophylaxis for infection.

Option A (Bartonella) is incorrect. Bartonella is a bacteria that causes cat scratch disease. Regional lymphadenopathy is the hallmark of this infection. It is a less common cause of infection from cat-caused injuries.

Option B (Clostridium) is incorrect. Clostridium infection can cause gas gangrene or tetanus. This patient needs a tetanus shot if she has not had one in the last 5 years, but clostridium is not typically found in the mouths of cats.

Option C (Eikenella) is incorrect. Eikenella is an uncommon cause of bacterial endocarditis. They are not pathogens that cause infection in cat bites.

Option D (Kingella) is incorrect. Kingella is an uncommon cause of bacterial endocarditis. They are not pathogens that cause infection in cat bites.

High-yield Hit 1
Figure 35-4 Pasteurella multocida in respiratory specimen from patient with pneumonia.
Pasteurella are small, facultatively anaerobic, fermentative coccobacilli (Figure 35-4) commonly found as commensals in the oropharynx of healthy animals. Most human infections result from animal contact (e.g., animal bites, scratches, shared food). Pasteurella multocida (the most common isolate) and Pasteurella canis are human pathogens; the other Pasteurella species are rarely associated with human infections (Table 35-4). The following three general forms of disease are reported: (1) localized cellulitis and lymphadenitis that occur after an animal bite or scratch (P. multocida from contact with cats or dogs; P. canis from dogs); (2) an exacerbation of chronic respiratory tract disease in patients with underlying pulmonary dysfunction (presumably related to colonization of the patient's oropharynx followed by the aspiration of oral secretions); and (3) a systemic infection in immunocompromised patients, particularly those with underlying hepatic disease.

From Medical Microbiology 5E by Murray et al
A 71-year-old man is brought to the emergency department with an altered mental status, cough, fevers, nausea, diarrhea, and abdominal pain. His wife states that he has complained of a dry cough for the last 3 days, which has been gradually worsening, as well as abdominal pain and diarrhea. The mental status changes have been present since this morning. He has a history of hypercholesterolemia and regularly takes simvastatin. On arrival his blood pressure is 125/82 mm Hg; pulse, 66 beats/min; temperature, 40.4°C (104.7°F); and respirations, 23 breaths/min. There are prominent rales on auscultation of the lung fields. Abdominal examination is within normal limits. Mental status examination reveals disorientation to place and time, as well as impaired cognitive functions. Initial laboratory investigation reveals leukocytosis and hyponatremia. What is the most appropriate next step in the diagnosis of this patient?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Bronchoalveolar lavage
B. Diagnostic peritoneal lavage
C. Head computed tomography (CT)
D. Stool culture
E. Urinary antigen testing
Option E (Urinary antigen testing) is correct. This patient has a dry cough, gastrointestinal symptoms, mental status changes, fever, and rales on chest auscultation. Laboratory investigation reveals hyponatremia. This is strongly suggestive of Legionella pneumophila pneumonia. Urinary antigen testing is a rapid, effective method of diagnosing Legionnaires disease and will most likely lead to the correct diagnosis in this patient. Treatment is with either levofloxacin or azithromycin.

Option A (Bronchoalveolar lavage) is incorrect. Bronchoalveolar lavage is used in the diagnosis of Pneumocystis carinii infection. This patient does not have a history of human immunodeficiency virus infection or immunosuppression.

Option B (Diagnostic peritoneal lavage) is incorrect. Diagnostic peritoneal lavage is a technique used in trauma situations to determine if there is abdominal bleeding. This technique has been replaced in many centers with focused abdominal sonography.

Option C (Head computed tomography [CT]) is incorrect. Head CT is not diagnostic in this patient.

Option D (Stool culture) is incorrect. Stool culture may yield a cause for the diarrhea, but the most likely explanation for these findings is infection with Legionella pneumophila.

High-yield Hit 1
Urinary Antigen Tests
Enyzme-linked immunoassays (EIAs) are used to detected soluble Legionella-specific lipopolysaccharide antigens excreted in the urine of infected patients. The sensitivity of these assays for L. pneumophila serogroup 1 is relatively high (range, 60% to >90%), particularly with concentrated urines, but the sensitivity for other serogroups and Legionella species is low. A genus-specific lipoprotein associated with the cell surface has been identified in the urine of infected patients and may prove to be a more useful diagnostic target. Antigens persist in the urine of treated patients, with almost 50% of patients remaining positive at 1 month and 25% at 2 months. Persistence is particularly common with immunosuppressed patients, in which antigens can persist for up to 1 year.

From Medical Microbiology 5E by Murray et al
A 48-year-old woman presents to her physician complaining of diarrhea for the last 2 days. The diarrhea came on suddenly, and she has not had any solid bowel movements since. She describes the diarrhea as watery and specifically denies seeing any blood or mucous. One month earlier, she had been hospitalized for administration of intravenous antibiotics after developing a productive cough, fever, and rigors. She does not take any regular medications and has no known allergies. She denies any recent ill contacts, visits to daycare, consumption of restaurant food, or travel. Her vital signs are as follows: blood pressure, 120/80 mm Hg; pulse, 84 beats/minute; temperature, 38.2°C (100.7°F); and respirations, 11 breaths/minute. Her abdomen is soft and diffusely tender to palpation. Bowel sounds are present, and the abdomen is tympanic to percussion throughout. A rectal examination is within normal limits. Laboratory investigations reveal the following:
Serum
Leukocyte count 14,000/mm3
Segmented neutrophils 65%
Bands 8%
Eosinophils 2%
Basophils 0%
Lymphocytes 25%
Monocytes 2%

Stool analysis
Clostridium difficile toxin [stool toxin assay] negative


What is the most appropriate next step in the management of this patient?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. C. difficile toxin assay
B. Colonoscopy
C. Stool electrolytes
D. Stool ova and parasite analysis
E. Trimethoprim-sulfamethoxazole (TMP-SMX)
Option A (C. difficile toxin assay) is correct. In a patient with watery diarrhea and recent (within 6 weeks) hospitalization or antibiotic use, pseudomembranous colitis caused by C. difficile overgrowth must be strongly suspected. In 80% of patients with pseudomembranous colitis, the toxin is identified after three stool samples. Thus, in this case, repeat stool sample analysis is warranted.

Option B (Colonoscopy) is incorrect. Pseudomembranous colitis, as the name suggests, has visible pseudomembranes, exudates, and plaques on colonoscopy. Although colonoscopy is a relatively safe procedure, it remains an invasive procedure with risk of bowel perforation. It is rarely used in the diagnosis of pseudomembranous colitis and should not be undertaken unless the condition is still strongly suspected after three negative stool toxin analyses.

Option C (Stool electrolytes) is incorrect. Stool electrolytes are used in the diagnosis of secretory versus osmotic diarrhea. In the present case, the recent antibiotic use strongly suggest pseudomembranous colitis.

Option D (Stool ova and parasite analysis) is incorrect. Stool ova and parasite analysis is not cost effective, and thus not warranted, in most cases of diarrhea unless specific predisposing events in the history suggest a cause. This includes patients with recent contacts to infants, travel to endemic regions, acquired immune deficiency syndrome (AIDS), and homosexual males.

Option E (Trimethoprim-sulfamethoxazole [TMP-SMX]) is incorrect. TMP-SMX is a commonly used antibiotic for severe infectious/invasive diarrhea. This patient is suspected of having C. difficile overgrowth, which is treated with metronidazole or vancomycin.

High-yield Hit 1
Pseudomembranous colitis
Pseudomembranous colitis is caused by colonization of the colon with Clostridium difficile, which produces toxins. It usually follows antibiotic therapy and should be suspected in patients in hospital who develop diarrhea after a period of antibiotics. It is usually of acute onset but may run a chronic course. The most frequently implicated antibiotic is clindamycin but few antibiotics are free of this side effect. Clinical features include diarrhea, fever and abdominal cramps.
Diagnosis
Diagnosis is by identification of the toxin in stool specimens. Sigmoidoscopy reveals an erythematous, ulcerated mucosa, which is covered by a membrane. Sigmoidoscopy, however, is not essential for the diagnosis.
Management
Suspected antibiotics should be stopped and patients should be isolated. Oral vancomycin or metronidazole is used as specific treatment.

From Crash Course: Internal Medicine by Baliga
A 23-year-old man has developed hypopigmented, sharply marginated, oval macules that coalesce over his chest and shoulders. A fine white scale is observed when the macules are scraped with a scalpel blade. He denies any pruritus or pain. Examination under ultraviolet light reveals blue-green florescence. Direct microscopic examination of scales prepared with potassium hydroxide shows a “spaghetti-and-meatballs” appearance. What is the most appropriate next step in the management of this patient?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Oral griseofulvin
B. Oral prednisone
C. Topical corticosteroids
D. Topical fluconazole
E. UV-B phototherapy
Option D (Topical fluconazole) is correct. This patient has pityriasis (tinea) versicolor. A topical antifungal is the initial therapy of choice because the condition is caused by Malassezia furfur, a fungal species. Normal pigmentation will return, but it can typically take months to years after the fungus has been eradicated. Oral antifungal therapy may be required if there is widespread involvement or for patients who do not respond to topical therapy.

Option A (Oral griseofulvin) is incorrect. Griseofulvin is not active against Malassezia furfur, the causative agent of pityriasis versicolor. Also, its side effects limit its use in adults. However, it is one of the treatments of choice for tinea capitis.

Option B (Oral prednisone) is incorrect. This is a treatment option for vitiligo and many other dermatologic conditions. This patient has pityriasis versicolor and requires antifungal therapy.

Option C (Topical corticosteroids) is incorrect. Topical steroids are not indicated in the therapy of pityriasis versicolor.

Option E (UV-B phototherapy) is incorrect. This is a treatment option for vitiligo, which does not fluoresce under ultraviolet examination and does not demonstrate hyphae and spores under potassium hydroxide (KOH) preparation.

High-yield Hit 1
Tinea Versicolor (PTG)
BASIC INFORMATION
DEFINITION
Tinea versicolor is a fungal infection of the skin caused by the yeast Pityrosporum orbiculare (Malassezia furfur).

From Ferri's Clinical Advisor 2006 by Ferri
High-yield Hit 2
EPIDEMIOLOGY & DEMOGRAPHICS

* Increased incidence in adolescence and young adulthood
* More common during the summer (hypopigmented lesions are more evident when the skin is tanned)

PHYSICAL FINDINGS & CLINICAL PRESENTATION

* Most lesions begin as multiple small, circular macules of various colors.
* The macules may be darker or lighter than the surrounding normal skin and will scale with scraping.
* Most frequent site of distribution is trunk.
* Facial lesions are more common in children (forehead is most common facial site).
* Eruption is generally of insidious onset and asymptomatic.
* Lesions may be hyperpigmented in blacks.
* Lesions may be inconspicuous in fair-complexioned individuals, especially during the winter.
* Most patients become aware of the eruption when the involved areas do not tan (Fig. 1-240).

ETIOLOGY
The infection is caused by the lipophilic yeast P. orbiculare (round form) and P. ovale (oval form); these organisms are normal inhabitants of the skin flora; factors that favor their proliferation are pregnancy, malnutrition, immunosuppression, oral contraceptives, and excess heat and humidity.

From Ferri's Clinical Advisor 2006 by Ferri
High-yield Hit 3
WORKUP
Diagnosis is based on clinical appearance; identification of hyphae and budding spores (spaghetti and meatballs appearance) with microscopy confirms diagnosis.
LABORATORY TESTS
Microscopic examination using potassium hydroxide confirms diagnosis when in doubt.
TREATMENT
NONPHARMACOLOGIC THERAPY
Sunlight accelerates repigmentation of hypopigmented areas.
ACUTE GENERAL Rx

* Topical treatment: selenium sulfide 2.5% suspension (Selsun or Exsel) applied daily for 10 min for 7 consecutive days results in a cure rate of 80% to 90%.
* Antifungal topical agents (e.g., miconazole, ciclopirox, clotrimazole) are also effective but generally expensive.
* Oral treatment is generally reserved for resistant cases. Effective agents are ketoconazole (Nizoral) 200 mg qd for 5 days, or single 400-mg dose (cure rate >80%), fluconazole (Diflucan) 400 mg given as a single dose (cure rate >70% at 3 wk after treatment), or itraconazole 200 mg/day for 5 days.

DISPOSITION
The prognosis is good, with death of the fungus usually occurring within 3-4 wk of treatment; however, recurrence is common.
PEARLS & CONSIDERATIONS
COMMENTS
Patients should be informed that the hypopigmented areas will not disappear immediately after treatment and that several months may be necessary for the hypopigmented areas to regain their pigmentation.

From Ferri's Clinical Advisor 2006 by Ferri
A 44-year-old woman presents to the emergency room with severe right upper quadrant abdominal pain. The pain began 4 hours ago. Laboratory values include: mean corpuscular value (MCV) 130 fL; red cell distribution width (RDW) 17%; aspartate transaminase (AST) 230 U/L; alanine transanimase (ALT) 95 U/L, alkaline phosphatase 525 U/L, total bilirubin 5 mg/dL, direct bilirubin 4 mg/dL, albumin 3.2 g/dL. Urine urobilinogen is positive. An ultrasound of the right upper quadrant reveals no visible abnormalities. Based on this evidence, which of the choices below most likely explains these findings?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Acalculus cholecystitis
B. Alcoholic hepatitis
C. Hepatitis B
D. Hepatitis C
E. Sclerosing cholangitis
Option B (Alcoholic hepatitis) is correct. Patterns of liver function test abnormalities can help one determine the category of hepatobiliary disease. Alcoholic hepatitis tends to have an AST/ALT ratio of greater than 2 (thought to be because of pyridoxal phosphate deficiency in alcoholic patients, which affects ALT synthesis). Macrocytic anemia from folate or vitamin B12 deficiency may also be a clue to a history of alcohol use, but further questioning is warranted.

Option A (Acalculus cholecystitis) is incorrect. Ultrasound has a sensitivity and specificity greater than 90% in patients in the outpatient setting who present with acalculus cholecystitis. Thus, a negative test provides a high degree of reassurance. In addition, hepatobiliary obstruction tends to cause a more elevated serum alkaline phosphatase, total and direct bilirubin, and a negative urobilinogen on urinalysis.

Option C (Hepatitis B) is incorrect. Most hepatocellular diseases, such as viral hepatitis or acetaminophen hepatotoxicity, are characterized by an AST/ALT ratio of less than 1. Furthermore, the elevated transaminases are usually in the hundreds range.

Option D (Hepatitis C) is incorrect. Most hepatocellular diseases, such as viral hepatitis or acetaminophen hepatotoxicity, are characterized by an AST/ALT ratio of less than 1. Furthermore, the elevated transaminases are usually in the hundreds range.

Option E (Sclerosing cholangitis) is incorrect. Sclerosing cholangitis is a condition in which the bile ducts become progressively sclerotic and eventually close off, causing signs and symptoms of biliary obstruction. This is classically seen in association with inflammatory bowel disease.

High-yield Hit 1
ALCOHOLIC HEPATITIS. This is characterized by the following:

* Hepatocyte swelling and necrosis. Single or scattered foci of cells undergo swelling (ballooning) and necrosis. The swelling results from the accumulation of fat and water, as well as proteins that normally are exported.
* Mallory bodies. Scattered hepatocytes accumulate tangled skeins of cytokeratin intermediate filaments and other proteins, visible as eosinophilic cytoplasmic inclusions in degenerating hepatocytes (Fig. 16-15). These inclusions are a characteristic but not specific feature of alcoholic liver disease, because they are also seen in primary biliary cirrhosis, Wilson disease, chronic cholestatic syndromes, and hepatocellular tumors.
* Neutrophilic reaction. Neutrophils permeate the lobule and accumulate around degenerating hepatocytes, particularly those containing Mallory bodies. Lymphocytes and macrophages also enter portal tracts and spill into the parenchyma.
* Fibrosis. Alcoholic hepatitis is almost always accompanied by a brisk sinusoidal and perivenular fibrosis; occasionally periportal fibrosis may predominate, particularly with repeated bouts of heavy alcohol intake. In some cases there is cholestasis and mild deposition of hemosiderin (iron) in hepatocytes and Kupffer cells. Macroscopically, the liver is mottled red with bile-stained areas. Although the liver may be normal or increased in size, it often contains visible nodules and fibrosis, indicative of evolution to cirrhosis.


Taken from Robbins Basic Pathology 7E by Kumar et al
High-yield Hit 2
Figure 16-15 Alcoholic hepatitis. A, The cluster of inflammatory cells marks the site of a necrotic hepatocyte. A Mallory body is present in a second hepatocyte (arrow). B, Eosinophilic Mallory bodies are seen in hepatocytes, which are surrounded by fibrous tissue. (H & E.)

Taken from Robbins Basic Pathology 7E by Kumar et al
High-yield Hit 3
Pathogenesis. Short-term ingestion of up to 80 g of ethanol per day (eight beers or 7 ounces of 80-proof liquor) generally produces mild, reversible hepatic changes, such as fatty liver. Daily ingestion of 160 g or more of ethanol for 10 to 20 years is associated more consistently with severe injury; chronic intake of 80 to 160 g/day is considered a borderline risk for severe injury. For reasons that may relate to decreased gastric metabolism of ethanol and differences in body composition, women appear to be more susceptible to hepatic injury than men. However, only 10% to 15% of alcoholics develop cirrhosis. Individual, possibly genetic, susceptibility must exist, but no reliable genetic markers of susceptibility have been identified. In addition, there is an inconstant relationship between hepatic steatosis and alcoholic hepatitis as precursors to cirrhosis. Moreover, cirrhosis may develop without antecedent evidence of steatosis or alcoholic hepatitis. In the absence of a clear understanding of the pathogenetic factors influencing liver damage, no "safe" upper limit for alcohol consumption can be proposed (despite the current popularity of red wines for amelioration of coronary vascular disease).
The pharmacokinetics and metabolism of alcohol were examined in Chapter 8. Pertinent to this discussion are the detrimental effects of alcohol and its byproducts on hepatocellular function:

* Hepatocellular steatosis results from (1) the shunting of normal substrates away from catabolism and toward lipid biosynthesis, owing to generation of excess reduced nicotinamide-adenine dinucleotide by the two major enzymes of alcohol metabolism, alcohol dehydrogenase and acetaldehyde dehydrogenase (generating acetate); (2) impaired assembly and secretion of lipoproteins; and (3) increased peripheral catabolism of fat.
* Induction of cytochrome P-450 leads to augmented transformation of other drugs to toxic metabolites. In particular, this can accelerate the metabolism of acetaminophen into highly toxic metabolites and increase the risk of liver injury even with therapeutic doses of this commonly used analgesic.
* Free radicals are generated during oxidation of ethanol by the microsomal ethanol oxidizing system; the free radicals react with membranes and proteins.
* Alcohol directly affects microtubular and mitochondrial function and membrane fluidity.
* Acetaldehyde (the major intermediate metabolite of alcohol en route to acetate production) induces lipid peroxidation and acetaldehyde-protein adduct formation, further disrupting cytoskeletal and membrane function.
* Neutrophil infiltration of the liver is common in alcoholic hepatitis, and it is thought that activated neutrophils release toxic oxygen metabolites. Elevated levels of interleukin 8, a chemoattractant of neutrophils, is seen in plasma of patients with alcoholic hepatitis.
* Alcohol induces an immunologic attack on hepatocytes that are antigenically altered by alcohol or by acetaldehyde-induced alterations in hepatic proteins.
* Because generation of acetaldehyde and free radicals is maximal in the centrilobular region of the parenchyma, this region is most susceptible to toxic injury.
* Concurrent viral hepatitis, particularly hepatitis C, is a major factor that accelerates liver disease in alcoholics. The prevalence of hepatitis C in patients with alcoholic disease is about 30%.


Taken from Robbins Basic Pathology 7E by Kumar et al
A 35-year-old man is seen aboard a luxury cruise ship by the staff physician after developing diarrhea. The diarrhea first began this morning and was initially watery in nature. He has had 10 bowel movements today, and the stools are now bloody. There is associated abdominal cramps, nausea, vomiting, and headache. On examination, his vital signs are as follows: blood pressure, 120/80 mm Hg; pulse, 85 beats/minute; temperature, 38.3°C (100.9°F); and respirations, 12 breaths/minute. His mucous membranes are moist and skin turgor normal. Capillary refill is 1 second. His abdomen is diffusely tender to palpation. There are five other individuals aboard the ship who have all presented within the last hour with the same symptoms. Direct questioning has revealed all ate shellfish from the same source approximately 20 hours ago. Stool examination results from all six patients reveal comma-shaped organisms.

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Bacillus cereus
B. Clostridium perfringens
C. Clostridium botulinum
D. Escherichia coli OH157
E. Giardia lamblia
F. Salmonella species
G. Staphylococcus aureus
H. Vibrio cholera
I. Vibrio parahaemolyticus
Option I (Vibrio parahaemolyticus) is correct. Comma-shaped organisms on stool analysis indicates that the likely agent is of the Vibrio species. Although infection with most Vibrio produces a watery diarrhea (especially Vibrio cholera), approximately one fourth of the cases of V. parahaemolyticus results in bloody diarrhea. Transmission is usually via shellfish.

High-yield Hit 1
Vibrio Parahaemolyticus (Box 32-4)
The severity of gastroenteritis caused by V. parahaemolyticus can range from a self-limited diarrhea to a mild, cholera-like illness. In general, the disease develops after a 5- to 72-hour incubation period (mean, 24 hours), with explosive, watery diarrhea. No grossly evident blood or mucus is found in stool specimens except in severe cases. Headache, abdominal cramps, nausea, vomiting, and low-grade fever may persist for 72 hours or more. The patient usually experiences an uneventful recovery. Wound infections with this organism can occur in people exposed to contaminated seawater.

From Medical Microbiology 5E by Murray et al
High-yield Hit 2
BOX 32-4. Summary of Vibrio parahaemolyticus Infections

* Physiology and StructureCurved gram-negative rods, facultative anaerobe; fermenter
* Simple nutritional requirements but requires salt for growth

* VirulenceRefer to Table 32-3

* EpidemiologyOrganism found in estuarine and marine environments worldwide
* Associated with consumption of contaminated shellfish
* Not commonly isolated in the United States but is a major pathogen in countries where raw fish is eaten

* DiseasesRefer to Box 32-3

* DiagnosisCulture should be performed as with V. cholerae

* Treatment, Prevention, and ControlSelf-limited disease, although antibiotics can shorten length of symptoms and fluid loss
* Disease prevented by proper cooking of shellfish
* No vaccines are available


From Medical Microbiology 5E by Murray et al
High-yield Hit 3
The severity of gastroenteritis caused by V. parahaemolyticus can range from a self-limited diarrhea to a mild, cholera-like illness. In general, the disease develops after a 5- to 72-hour incubation period (mean, 24 hours), with explosive, watery diarrhea. No grossly evident blood or mucus is found in stool specimens except in severe cases. Headache, abdominal cramps, nausea, vomiting, and low-grade fever may persist for 72 hours or more. The patient usually experiences an uneventful recovery. Wound infections with this organism can occur in people exposed to contaminated seawater.

From Medical Microbiology 5E by Murray et al
A 55-year-old female presents to the emergency room with a sudden onset of intense vomiting and diarrhea 3 hours ago. The diarrhea is described as watery, and she specifically denies any blood or mucous. There are seven other individuals currently in the emergency room with the same symptoms, all of whom attended a church picnic earlier in the day. Direct questioning reveals they all ate from the same batch of potato salad.

End of set

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Bacillus cereus
B. Clostridium perfringens
C. Clostridium botulinum
D. Escherichia coli OH157
E. Giardia lamblia
F. Salmonella species
G. Staphylococcus aureus
H. Vibrio cholera
I. Vibrio parahaemolyticus
Option G (Staphylococcus aureus) is correct. Picnics, potato salad, and pastries with cream are all clues to S. aureus toxin contamination. Because the clinical effects are the result of a preformed toxin, onset of symptoms is rapid and often with 1 to 6 hours of ingestion. Antibiotics are not indicated because there is no infection.

High-yield Hit 1
Staphylococcal food poisoning, one of the most common foodborne illnesses, is an intoxication rather than an infection. Disease is caused by bacterial toxin present in food, rather than from a direct effect of the organisms on the patient. The most commonly contaminated foods are processed meats such as ham and salted pork, custard-filled pastries, potato salad, and ice cream. Growth of S. aureus in salted meats is consistent with the ability of this organism to grow in the presence of high salt concentrations. Unlike many other forms of food poisoning in which an animal reservoir is important, staphylococcal food poisoning results from contamination of the food by a human carrier. Although contamination can be prevented by not allowing individuals with an obvious staphylococcal skin infection to prepare food, approximately half of the infections originate from carriers with asymptomatic nasopharyngeal colonization. After the staphylococci have been introduced into the food (through a sneeze or contaminated hand), the food must remain at room temperature or warmer for the organisms to grow and release the toxin. The contaminated food will not appear or taste tainted. Subsequent heating of the food will kill the bacteria but not inactivate the heat-stable toxin.

From Medical Microbiology 5E by Murray et al
High-yield Hit 2
After ingestion of contaminated food, the onset of disease is abrupt and rapid, with a mean incubation period of 4 hours, which is, again, consistent with a disease mediated by preformed toxin. Further toxin is not produced by ingested staphylococci, so the disease has a rapid course, with symptoms generally lasting less than 24 hours. Severe vomiting, diarrhea, and abdominal pain or nausea are characteristic of staphyloccoal food poisoning. Sweating and headache may occur, but fever is not seen. The diarrhea is watery and nonbloody, and dehydration may result from the considerable fluid loss.
The toxin-producing organisms can be cultured from the contaminated food if the organisms are not killed during food preparation. The enterotoxins are heat-stable, so contaminated food can be tested for toxins at a public health facility; however, these tests are rarely performed.

From Medical Microbiology 5E by Murray et al
High-yield Hit 3
Treatment is for the relief of abdominal cramping and diarrhea and for the replacement of fluids. Antibiotic therapy is not indicated because, as already noted, the disease is mediated by preformed toxin and not by replicating organisms. Neutralizing antibodies to the toxin can be protective, and limited cross-protection occurs among the different enterotoxins. Short-lived immunity means that second episodes of staphylococcal food poisoning can occur, particularly with serologically distinct enterotoxins.

From Medical Microbiology 5E by Murray et al
A 29-year-old African American woman presents to her local physician, because she has experienced diffuse lower abdominal pain in the previous week. She also noticed that sexual intercourse has become noticeably painful during this time. She states that she was surprised by the pain because she usually experiences a small amount of pelvic region discomfort during her menses and that her present symptoms had begun shortly after she completed her monthly menstrual cycle. Otherwise, she has been well and denies nausea, vomiting, or recent fevers. She currently has one sexual partner of 2 months’ duration, and her only medication is the oral contraceptive pill (OCP). She has had 14 lifetime sexual partners since the age of 13. On examination, her blood pressure is 115/75 mm Hg; temperature, 37.7°C (99.8°F); heart rate, 72 beats/minute; and respirations, 12 breaths/minute. Palpation of the abdomen demonstrates lower quadrant pain bilaterally, with the left side being greater in intensity than the right. There is also mild rebound tenderness and voluntary guarding. Bimanual pelvic examination reveals distinct cervical tenderness. The remainder of the physical examination is unremarkable. Laboratory results are as follows:

Urine
Specific gravity 1.023
Blood 0–1/high-power field (hpf)
Glucose negative
Ketones negative
Leukocyte esterase negative
Nitrites negative
Protein negative
Squamous epithelial cells scant
Chlamydial ligase chain reaction negative
White blood cells (WBCs) 4/hpf
Serum
Human chorionic gonadotropin 0 mIU/mL

What is the most likely diagnosis?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Appendicitis
B. Ectopic pregnancy
C. Ovarian torsion
D. Pelvic inflammatory disease (PID)
E. Urinary tract infection (UTI)
Option D (Pelvic inflammatory disease [PID]) is correct. This patient is most likely suffering from pelvic inflammatory disease (PID), because the risk factors are consistent, the examination is most suggestive, and the pregnancy test is negative.

Option A (Appendicitis) is incorrect. Appendicitis is certainly in the differential, but the protracted time course makes this option less likely than pelvic inflammatory disease (PID).

Option B (Ectopic pregnancy) is incorrect. This patient has a negative serum pregnancy test, effectively ruling out an ectopic pregnancy.

Option C (Ovarian torsion) is incorrect. Ovarian torsion is also in the differential, but is more commonly associated with a sudden onset of abdominal pain and accompanying nausea and vomiting.

Option E (Urinary tract infection [UTI]) is incorrect. She is unlikely to be experiencing a urinary tract infection (UTI) in light of the classic pelvic inflammatory disease (PID) physical examination and the absence of findings on urinalysis.

High-yield Hit 1
1. How is pelvic inflammatory disease (PID) defined?
The term PID describes a spectrum of infection and inflammation involving, in varying degrees depending on the severity of the disease, the upper genital tract (endometrium, tubes, and ovaries) as well as the surrounding peritoneum. In more severe cases, the infection can spread along the upper peritoneum to the liver capsule, causing perihepatic adhesions. When this happens, it is referred to as Fitz-Hugh-Curtis syndrome.
2. What is the cause of PID?
PID comprises, for the most part, sequelae of cervical infection with sexually transmitted organisms, chiefly Neisseria gonorrhoeae and Chlamydia trachomatis. Cervical infection with these organisms breaks down cervical barriers to ascending infection, allowing endogenous super infection of the upper genital tract by aerobic as well as anaerobic organisms normally inhabiting the lower genital tract. In addition, though less commonly the cause, instrumentation of the cervix and uterus during surgical procedures (such as surgical abortion, dilation and curettage, hysteroscopy, endometrial and cervical biopsy, insertion of intrauterine device [IUD], and intrauterine insemination) can cause auto-inoculation of the endometrium with endogenous bacteria and lead to PID.

From Ob/Gyn Secrets 3E by Bader
High-yield Hit 2
4. What is the relationship of PID to bacterial vaginosis?
It is believed that similar organisms cause bacterial vaginosis (a vaginal infection) and PID. While studies have shown that the diagnosis of bacterial vaginosis is more common in women with PID, a cause-and-effect relationship has not been proven.

From Ob/Gyn Secrets 3E by Bader
High-yield Hit 3
5. How does PID present in the clinical setting?
History: Classic PID presents with a history of acute onset of pelvic pain and fever, frequently beginning during or after a menstrual period in a sexually active woman. However, especially when Chlamydia is the initiating organism, the onset of pelvic pain can be more gradual and less severe. Nausea and vomiting, as well as loss of appetite, especially in more severe cases, may accompany these symptoms.
Physical exam: Fever and mild to severe tachycardia are frequently found on investigation of vital signs. Abdominal exam shows varying degrees of bilateral lower abdominal tenderness and possible rebound and/or guarding in more severe cases. Right upper quadrant tenderness will be found with accompanying Fitz-Hugh-Curtis syndrome. On pelvic exam, the classic sign of PID is the "chandelier sign"-cervical motion tenderness-which describes severe tenderness and accompanying reaction by the patient on movement of the cervix. Palpation of the uterus and adnexa also elicits tenderness, and frequently an adequate exam is limited by guarding. When a tubo-ovarian abscess (TOA) is present, this can be palpated, either as a unilateral adnexal mass or as a mass in the cul-de-sac. Tubo-ovarian abscesses occasionally will point into the cul-de-sac as well.
On speculum exam, mucopurulent discharge is seen originating from the cervix. In advanced cases, this sign may have resolved since as endogenous super infection advances, inciting organisms (e.g., Neisseria and Chlamydia) are frequently eliminated.
Laboratory: Cervical cultures or DNA-based testing is frequently positive, especially early in the disease process. White blood cell (WBC) count is elevated, and erythrocyte sedimentation rate and C-reactive protein (though not usually obtained in the clinical setting) are usually elevated as well. There are no specific ultrasound findings in PID, but complex adnexal masses will be seen on ultrasound when TOAs or inflammatory complexes are present. In the presence of Fitz-Hugh-Curtis syndrome, liver function tests may be elevated.

From Ob/Gyn Secrets 3E by Bader
A 44-year-old woman, with a 2-year history of human immunodeficiency virus (HIV) infection, presents to the emergency department, because of progressively worsening shortness of breath for the last 10 days. She has also experienced fevers and a nonproductive cough during this time that has also been worsening. Her allergies include an anaphylactic reaction to sulfa at the age of 10. Laboratory evaluation reveals a CD4+ count of 165/μL and a lactate dehydrogenase level of 410 U/L. Chest X-ray (CXR) is unremarkable. Microscopic examination of bronchoalveolar lavage fluid reveals cysts and trophozoites. What is the most appropriate next step in the management of this patient?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Azithromycin
B. Clarithromycin and ethambutol
C. Isoniazid, rifampin, ethambutol, and pyrazinamide
D. Pyrimethamine
E. Trimethoprim and dapsone
Option E (Trimethoprim and dapsone) is correct. This patient has Pneumocystis carinii pneumonia (PCP). The standard of care for treating PCP is trimethoprim-sulfamethoxazole (TMP-SMX), but several new agents have been studied and found efficacious against PCP. However, in this particular case, the patient has a severe allergy to sulfa and thus cannot take TMP-SMX. Combining trimethoprim with dapsone has been found to be an efficacious alternative in such situations. Additionally, many patients develop rashes and gastrointestinal disturbances on TMP-SMX and thus, alternatives are important to note, because they are used.

Option A (Azithromycin) is incorrect. Azithromycin can be used to prevent Mycobacterium avium complex (MAC), and should be started when the CD4+ count is below 50.

Option B (Clarithromycin and ethambutol) is incorrect. This is appropriate therapy for Mycobacterium avium complex (MAC), which affects individuals who have CD4+ count is below 50.

Option C (Isoniazid, rifampin, ethambutol, and pyrazinamide) is incorrect. This is appropriate therapy for tuberculosis, which would present with acid-fast bacilli.

Option D (Pyrimethamine) is incorrect. Pyrimethamine is used with sulfadiazine for the treatment of toxoplasmosis.

High-yield Hit 1
Table 8-9. Prophylaxis to Prevent First Episode of Opportunistic Disease among Adults and Adolescents Infected with HIV Preventive Regimen
Preventive Regimen
Pathogen Indication First Choice Alternative
I. Strongly Recommended as Standard of Care
Pneumocystis carinii CD4+counts of <200/μL or oropharyngeal candidiasis Trimethoprim-sulfamethoxazole (TMP-SMX), 1 double-strength tablet (DS) by mouth daily or TMP-SMX, 1 single-strength tablet (SS) by mouth daily Dapsone 50 mg by mouth twice daily or 100 mg by mouth daily; dapsone 50 mg by mouth daily plus pyrimethamine 50 mg by mouth weekly plus leucovorin 25 mg by mouth weekly; dapsone 200 mg by mouth plus pyrimethamine 75 mg by mouth plus leucovorin 25 mg by mouth weekly; aerosolized pentamidine 300 mg monthly via Respirgard II nebulizer (Marquest Englewood, CO); atovaquone 1500 mg by mouth daily; TMP-SMX 1 DS by mouth three times weekly

From Practical Guide to the Care of the Medical Patient 7E by Ferri
A 21-year-old man presents to the community health center complaining of a sore throat, lymphadenopathy, and fevers to 38.7°C (101.6°F). He states the symptoms have been presents for 5 days and are associated with fatigue and malaise. His girlfriend had similar symptoms 3 weeks ago and she gave him leftover amoxicillin when he first noticed his sore throat. A day after taking the antibiotic, he developed a erythematous maculopapular rash over his entire body. He does not take any regular medications and does not have any known allergies. He drinks 20 to 40 g of ethanol weekly, smokes 1 pack of tobacco per day, and occasionally uses marijuana. He has one current sexual partner that he has been monogamous with for the last 2 years and uses barrier contraception regularly. On examination, there is bilateral cervical lymphadenopathy and pharyngeal erythema. What is the most likely cause of these findings?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Cytomegalovirus infection (CMV)
B. Epstein-Barr Virus infection (EBV)
C. Hepatitis B virus (HBV) infection
D. Human immunodeficiency virus (HIV) infection
E. Varicella zoster virus infection (VZV)
Option B (Epstein-Barr Virus infection [EBV]) is correct. Fever, malaise, lymphadenopathy, and pharyngitis suggest a diagnosis of infectious mononucleosis. However, a very characteristic finding is the development of a rash following the administration of amoxicillin. The most common cause of infectious mononucleosis is EBV.

Option A (Cytomegalovirus infection [CMV]) is incorrect. Cytomegalovirus can produce symptoms very similar to EBV and is often impossible to distinguish clinically. However, CMV often affects older individuals and is typically milder. A heterophile-antibody test is negative.

Option C (Hepatitis B virus [HBV] infection) is incorrect. Although HBV can produce similar symptoms, it is not as common. Symptoms could also include right upper quadrant pain and jaundice.

Option D (Human immunodeficiency virus [HIV] infection) is incorrect. Although HIV can present with a mononucleosis-type picture, finding a rash developing following amoxicillin suggests EBV as a cause.

Option E (Varicella zoster virus infection) is incorrect. Varicella zoster virus presents as an intensely pruritic vesicular rash, along with lethargy and fever.

High-yield Hit 1
Roughly 80% of clinically manifest cases of infectious mononucleosis are caused by EBV. This acute illness usually develops late in adolescence after intimate contact with asymptomatic oropharyngeal shedders of EBV. Patients develop sore throat, fever, and generalized lymphadenopathy and sometimes experience headache and myalgias. Five to 10% of patients have a transient rash that may be macular, petechial, or urticarial. Palatal petechiae are often present, as is pharyngitis, which may be exudative. Cervical lymphadenopathy, particularly involving the posterior lymphatic chains, is prominent, although some involvement elsewhere is common. The spleen is enlarged in about 50% of patients. Autoimmune hemolytic anemia, thrombocytopenia, encephalitis or aseptic meningitis, Guillain-Barré syndrome, hepatitis, or splenic rupture, although rare, may dominate the clinical presentation. The enlarged spleen may be very fragile. This dictates gentleness in palpation of the left upper quadrant. Three fourths of patients present with an absolute lymphocytosis. At least one third of their lymphocytes are atypical in appearance: large, with vacuolated basophilic cytoplasm; rolled edges often deformed by contact with other cells; and lobulated, eccentric nuclei. Immunologic studies indicate that some circulating B cells are infected with EBV and that the cells involved in the lymphocytosis are mainly cytotoxic T cells capable of damaging EBV-containing lymphocytes. Atypical lymphocytes may also be seen in other viral illnesses (Table 94-4).

From Cecil Essentials of Medicine 6E by Andreoli et al
High-yield Hit 2
B-cell infection with EBV is a stimulus to production of polyclonal antibodies. The Monospot rapid diagnostic test is sensitive and specific; false-positive results occur in rare cases in patients with lymphoma or hepatitis. The presence of IgM antibody to viral capsid antigen is diagnostic of acute infectious mononucleosis. The appearance of antibody to EBV nuclear antigen is also indicative of EBV infection.
Infectious mononucleosis usually pursues a benign course even in patients with neurologic involvement. The fever resolves after 1 to 2 weeks, although residual fatigue may be protracted. Occasional patients have a persistent or recurrent syndrome with fever, headaches, pharyngitis, lymphadenopathy, arthralgias, and serologic evidence of chronic active EBV infection. Patients should be managed symptomatically. Acetaminophen may be useful for sore throat. Antibiotics, particularly ampicillin, should be avoided. The use of ampicillin causes a rash in almost all patients with EBV infection, and this phenomenon can also be a diagnostic clue to the occurrence of EBV infection. Corticosteroids are indicated in the rare individual with serious hematologic involvement (i.e., thrombocytopenia, hemolytic anemia) or impending airway obstruction as a result of massive tonsillar swelling.

From Cecil Essentials of Medicine 6E by Andreoli et al
High-yield Hit 3
Table 94-3. Fever and Rash in Viral Infection
Acute HIV infection Maculopapular truncal rash may occur as early manifestation of infection. Associated fever, sore throat, and lymph node enlargement may persist for 2 or more weeks.
Coxsackievirus/echovirus Maculopapular "rubelliform": 1-3mm, faint pink, begins on face, spreading to chest and extremities. "Herpetiform": vesicular stomatitis with peripheral exanthem (papules and clear vesicles on an erythematous base), including palms and soles (hand, foot, and mouth disease). Summertime, no itching or lymphadenopathy; multiple cases in household or community-wide epidemic; mostly diseases of children.
Measles Erythematous, maculopapular rash begins on upper face and spreads down to involve extremities, including palms and soles; Koplik's spots are bluish-gray specks on a red base found on buccal mucosa near second molars; atypical measles occurs in individuals who receive killed vaccine, then are exposed to measles; the rash begins peripherally and is urticarial, vesicular, or hemorrhagic. Incubation period 10-14 days; first severe upper respiratory symptoms, coryza, cough, conjunctivitis; then Koplik's spots; then rash.
Rubella Maculopapular rash beginning on face and moving downward; petechiae on soft palate. Incubation 12-35 days; adenopathy: posterior auricular, posterior cervical, and suboccipital.
Varicella Generalized vesicular eruption; lesions in different stages from erythematous macules to vesicles to crusted; spreads from trunk centrifugally. Zoster-see text. Incubation 14-15 days; late winter, early spring.
Herpes simplex virus Oral primary: small vesicles on pharynx, oral mucosa, which ulcerate; painful and tender.
Recurrent: vermillion border, one or few lesions. Genital: see Chapter 106. Incubation 2-12 days.
Hepatitis B Prodrome in one fifth: erythematous maculopapular rash, urticaria. Arthralgias, arthritis, abnormal liver function tests; hepatitis B antigenemia.
EBV Erythematous, maculopapular rash on trunk and proximal extremities; occasionally urticarial or hemorrhagic. Transiently occurs in 5-10% of patients during first week of illness.

From Cecil Essentials of Medicine 6E by Andreoli et al
A 33-year-old woman visits her primary care physician with complaints of a 2-day history of fever and chills. Today she also notes the appearance of a painful rash on her lower left leg. Further questioning reveals there is a mosquito bite on the affected leg that appeared several days before the rash. Medical history is significant for type 1 diabetes. She reports developing a rash and breathing difficulty in the one instance that she was treated with penicillin. Vital signs are temperature: 39°C (102.2°F), blood pressure (BP): 115/75, heart rate (HR): 78 beats/min, and respiratory rate (RR): 14 breaths/min. Physical exam is notable for a 4 cm × 9 cm fiery red edematous rash with sharply raised, abruptly demarcated, irregular borders on the posteromedial aspect of the left lower leg. Which antibiotic is most appropriate for the treatment of this patient's condition?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Ceftazidime
B. Ciprofloxacin
C. Erythromycin
D. Gentamicin
E. Vancomycin
Option C (Erythromycin) is correct. The clinical picture is most suggestive for erysipelas. The most common cause is group A beta-hemolytic streptococci infection. The treatment of choice is penicillin. Erythromycin is the treatment of choice in patients with significant penicillin allergy.

Option A (Ceftazidime) is incorrect. Ceftazidime has poor gram-positive activity. The patient's likely diagnosis is erysipelas. The most common cause is group A beta-hemolytic streptococci infection.

Option B (Ciprofloxacin) is incorrect. Ciprofloxacin is a poor gram-positive antibiotic. The patient's likely diagnosis is erysipelas. The most common cause is group A beta-hemolytic streptococci infection.

Option D (Gentamicin) is incorrect. Aminoglycoside antibiotics have poor gram-positive activity. The patient's likely diagnosis is erysipelas. The most common cause is group A beta-hemolytic streptococci infection.

Option E (Vancomycin) is incorrect. Vancomycin is certainly not the initial alternative to penicillin in a mild case of erysipelas. Diabetics can develop life-threatening erysipelas infections where this would be the appropriate treatment.

High-yield Hit 1
Erysipelas
Erysipelas (erythros, "red"; pella, "skin") is an acute infection of the skin. Patients experience localized pain, inflammation (erythema, warmth), lymph node enlargement, and systemic signs (chills, fever, leukocytosis). The involved skin area is typically raised and distinctly differentiated from the uninvolved skin (Figure 23-3). Erysipelas occurs most commonly in young children or older adults, historically on the face but now more commonly on the legs, and usually is preceded by infections of the respiratory tract or skin with S. pyogenes (less commonly with group C or G streptococci).

From Medical Microbiology 5E by Murray et al
High-yield Hit 2
Figure 23-3 Acute stage of erysipelas of the leg. Note the erythema in the involved area and bullae formation. (From Emond RTD, Rowland HAK: A color atlas of infectious diseases, ed 2, London, 1989, Wolfe.)

From Medical Microbiology 5E by Murray et al
presents with well-defined, erythematous plaques that have silvery white scales at places of repeated trauma.
Psoriasis vulgaris
is a benign epithelial tumor that presents as a well-defined, waxy papule that has a warty surface and appears stuck on to the skin.
Seborrheic keratosis
presents with a pruritic, scaly, round plaque that has an erythematous margin and central clearing.
Tinea corporis
is a close differential diagnosis in patients with pityriasis versicolor. Distinguishing features are distribution (periorbital and perioral, perineum, axillae, and areas of repeated trauma or pressure such as elbows, knees, sacrum, and malleoli), absence of scale, and a predilection of the areas to burn when suntanning. The lesions do not fluoresce under ultraviolet light, and there are no fungal elements observed with KOH preparation.
Vitiligo
hey are different colors in different seasons. In winter months, these lesions are typically slightly hyperpigmented (and thus, less noticeable) than in the summer, when they become hypopigmented. The infected areas do not tan and thus, when patients sunbathe causing their skin to tan, the contrast can be stark, resulting in presentation to the physician. The lesions typically have a fine scale that is observed best when scraped with a scalpel or glass slide. A KOH preparation shows filamentous hyphae and globose yeast forms, which has been termed a spaghetti and meatballs appearance.
Pityriasis versicolor
A 55-year-old man presents to the emergency department with a 2-week history of fevers, chills, weakness, and shortness of breath. He was previously well and does not take any regular medications. On arrival, his blood pressure, is 130/70 mm Hg; pulse, 110 beats/min; temperature 39.3°C (102.7°F); and respirations, 32 breaths/min. Linear, red streaks are seen under the fingernails and are most prominent in the proximal nail bed. There is a pansystolic murmur heard over the apex that was not noticed 6 months ago during his annual health maintenance examination. An echocardiogram is performed and reveals mitral valve vegetations. Blood cultures are drawn. While awaiting results from the blood cultures, what is the most appropriate antibiotic regimen?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Ceftriaxone
B. Nafcillin, penicillin, gentamicin
C. Nafcillin, vancomycin
D. Penicillin
E. Vancomycin, gentamicin, rifampin
Option B (Nafcillin, penicillin, gentamicin) is correct. This patient has infective endocarditis (IE) and is otherwise healthy. He is not predisposed to any unusual organisms and thus, the most appropriate empiric coverage is with nafcillin, penicillin, and gentamicin. This provides adequate coverage for the most likely causes of IE, including Staphylococcus, Streptococcus, and Enterococcus.

Option A (Ceftriaxone) is incorrect. Ceftriaxone is useful as outpatient therapy in patients who have Streptococcus viridans-associated IE.

Option C (Nafcillin, vancomycin) is incorrect. This is not appropriate empiric coverage for any situation as there is insufficient coverage of gram-negative organisms.

Option D (Penicillin) is incorrect. Monotherapy with penicillin can be started after the causative agent, usually Streptococcus viridans or Streptococcus bovis, has been identified as susceptible.

Option E (Vancomycin, gentamicin, rifampin) is incorrect. This is appropriate empiric coverage for patients who have prosthetic heart valves and are more likely to have gram-negative infections, as well as the more common Staphylococcus aureus and Staphylococcus epidermidis.

High-yield Hit 1
MANAGEMENT

1. Medical:
1. Box 8-2 describes antibiotic treatment of adults, based on positive blood culture results.
1. Antibiotic therapy (after identification of the organism) should be guided by susceptibility testing (minimum inhibitory concentration, minimum bactericidal concentration).
2. Peak serum bactericidal titers of 1:64 or greater and trough bactericidal titers of 1:32 or greater are recommended.
2. Initial intravenous antibiotic therapy (before culture results) is aimed at the most likely organism.
1. In patients with prosthetic valves or patients with native valves but allergic to penicillin: vancomycin plus rifampin and gentamicin
2. In intravenous drug addicts: penicillinase-resistant penicillin (oxacillin or nafcillin) plus gentamicin
3. In native-valve endocarditis: combination of penicillin and gentamicin; a penicillinase-resistant penicillin or vancomycin should be added if acute bacterial endocarditis is present or if S. aureus is suspected as one of the possible causative organisms; the combination of vancomycin and gentamicin provides broad empiric coverage while awaiting culture results.
2. Surgical: indications for cardiac surgery in patients with active native valve infective endocarditis are listed in Box 8-3. Box 8-4 describes indications for surgery in patients with prosthetic valve endocarditis.


From Practical Guide to the Care of the Medical Patient 7E by Ferri
High-yield Hit 2
BOX 8-2 Antibiotic Treatment of Infective Endocarditis
Streptococci
Viridans streptococci and Streptococcus bovis
Penicillin G susceptible (MIC ≤0.1 μg/mL)
Regimen A: Penicillin G at 12-18 million U/d IV in divided doses q4h for 4 weeks
Regimen B: Penicillin as in regimen A plus gentamicin 1 mg/kg IV q8h both for 2 weeks
Regimen C: Penicillin plus gentamicin for 2 weeks as in regimen B with penicillin continued 2 weeks longer
*Regimen D: Ceftriaxone at 2 g IV or IM daily for 4 weeks
*Regimen E: Vancomycin at 15 mg/kg IV q12h for 4 weeks
Relatively penicillin G resistant (MIC >0.1 μg/mL but <0.5 μg/mL)
Regimen C
*Regimen D or E
Enterococci and viridans streptococci (MIC ≥0.5 μg/mL)
Regimen F: Penicillin G 18-30 million U/d or ampicillin at 12 g/d IV in divided doses q4h, plus gentamicin at 1 mg/kg IV q8h or streptomycin at 7.5 mg/kg IM q12h, both for 4 to 6 weeks
*Regimen G: Vancomycin at 15 mg/kg IV q12h plus gentamicin or streptomycin as in regimen F, both for 4 to 6 weeks
Prosthetic valve (see text)
Staphylococci
Native valve
Methicillin susceptible (Staphylococcus epidermidis, Staphylococcus aureus)
Regimen H: Nafcillin at 2 g IV q4h for 4 to 6 weeks with or without gentamicin 1 mg/kg IV q8h for the first 3 to 5 days
*Regimen I: Cefazolin at 2 g IV q8h for 4 to 6 weeks with or without gentamicin as in regimen H
Regimen J: Vancomycin at 15 mg/kg IV q12h for 4 to 6 weeks
Methicillin resistant
Regimen J
Prosthetic valve
Methicillin susceptible
Regimen H, I, or J: for 6 to 8 weeks with gentamicin for the first 2 weeks and rifampin at 300 mg orally q8h for 6 to 8 weeks
Methicillin resistant
Regimen J: for 6 to 8 weeks with gentamicin for the first 2 weeks and rifampin at 300 mg orally q8h for 6 to 8 weeks

*Regimens for patients allergic to penicillin.
MIC, minimal inhibitory concentration.
From Gorbach SL: Infectious Diseases, 2nd ed. Philadelphia, WB Saunders, 1998.

From Practical Guide to the Care of the Medical Patient 7E by Ferri
A 37-year-old woman is brought to the emergency department because she awoke with fever, severe headache, neck stiffness, and photophobia. Physical examination reveals spontaneous flexion of the hips during attempted passive flexion of the neck and an inability to touch the chin to the chest. A lumbar puncture is performed along with a Gram stain of the cerebrospinal fluid (CSF) and shows Gram positive bacteria. 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 meningitidis
D. Streptococcus agalactiae
E. Streptococcus pneumoniae
Option E (Streptococcus pneumoniae) is correct. The Gram stain shows gram-positive diplococci, making the most likely diagnosis Streptococcus pneumoniae . Overall, in adults, S. pneumoniae is the most common cause of meningitis.

Option A ( Haemophilus influenzae) is incorrect. Haemophilus influenzae was the most common cause of meningitis in children until immunization to type b H. influenzae . It is now a relatively infrequent cause. It is a gram-negative rod.

Option B ( Listeria monocytogenes) is incorrect. Listeria meningitis is the third most common cause of meningitis is neonates. It is much more common in immunosuppressed adults, the elderly and pregnant women. It is not usually visualized on cerebrospinal fluid (CSF) Gram stain. When it does appear, it can be resemble diplococci.

Option C ( Neisseria meningitidis) is incorrect. This is the second most common cause of meningitis in adults and often presents with a classic petechial/purpuric rash. It is the most common cause of meningitis in children. It appears as gram-negative diplococci.

Option D ( Streptococcus agalactiae) is incorrect. This is the most common cause of bacterial meningitis is neonates. It appears as gram-positive cocci in chains.

High-yield Hit 1
Laboratory Diagnosis
The CSF in acute bacterial meningitis usually contains 500 to 10,000 cells/μL, mostly neutrophils (see Table 96-1). Glucose concentration falls below 40 mg/dL, and the protein level rises above 150 mg/dL in most patients. The Gram-stained preparation of CSF is positive in 80 to 88% of cases. However, certain cautionary notes are appropriate. Cell counts can be lower (occasionally zero) early in the course of meningococcal and pneumococcal meningitis. Also, predominantly mononuclear cell pleocytosis may occur in patients who have received antibiotics before the lumbar puncture (Table 96-3). A similar mononuclear pleocytosis may be seen in Listeria monocytogenes meningitis, tuberculous meningitis, and acute syphilitic meningitis. Gram-stained preparations of CSF may be negative or misinterpreted when meningitis is caused by H. influenzae, N. meningitidis, or L. monocytogenes because the presence of gram-negative diplococci and coccobacilli may be difficult to appreciate, particularly when the background consists of amorphous pink material. In addition, bacteria tend to be pleomorphic in CSF and may assume atypical forms. Compared with patients with acute meningitis caused by other bacterial pathogens, patients with Listeria infection have a significantly lower incidence of meningeal signs, and the CSF profile is significantly less likely to have a high white blood cell count or a high protein concentration. Gram stain is negative in two thirds of cases of listerial meningitis and meningoencephalitis and may be misleading in many of the remaining cases. Gram stain of CSF is negative in two thirds of cases of CNS listeriosis. If interpretation of the Gram-stained CSF is not clear-cut, broad-spectrum antibiotics should be instituted while results of cultures are pending. If the initial Gram-stained preparation does not contain organisms, examining the stained sediment prepared by concentrating up to 5 mL of CSF with a cytocentrifuge may reveal the causative organism.

From Cecil Essentials of Medicine 6E by Andreoli et al
A 29-year-old man presents to the physician for his regular health maintenance examination. He was diagnosed with human immunodeficiency virus (HIV) 2 years ago and has been taking highly active antiretroviral therapy (HAART). His CD4+ count today is 180/μL. His physician starts him on prophylactic therapy against Pneumocystis jiroveci (Pneumocystis carinii) infection. This therapy is also prophylactic against infection with what other organism?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Cryptococcus neoformans
B. Cryptosporidium parvum
C. Histoplasma capsulatum
D. Mycobacterium avium complex (MAC)
E. Toxoplasma gondii
Option E (Toxoplasma gondii) is correct. Trimethoprim-sulfamethoxazole (TMP-SMX) is the first-line against for prophylaxis against toxoplasmosis and Pneumocystis carinii pneumonia (PCP). Toxoplasmosis usually presents as central nervous system (CNS) mass and appears as a ring-enhancing lesion on computed tomography (CT).

Option A (Cryptococcus neoformans) is incorrect. Classically associated with visualization on India ink preparation, this condition can be prevented with fluconazole. However, routine prophylaxis is not recommended, because the condition is infrequent.

Option B (Cryptosporidium parvum) is incorrect. This causes a diarrheal illness. Prophylaxis has been demonstrated with rifabutin or clarithromycin, but has not been yet approved.

Option C (Histoplasma capsulatum) is incorrect. Histoplasmosis presents as an acute pulmonary condition, but may also have abdominal pains and significant lymphadenopathy. It can be prevented with itraconazole.

Option D (Mycobacterium avium complex [MAC]) is incorrect. MAC prophylaxis usually begins when the CD4+ count is below 50. Prophylaxis is achieved with azithromycin, clarithromycin, and rifabutin.

High-yield Hit 1
Table 8-9. Prophylaxis to Prevent First Episode of Opportunistic Disease among Adults and Adolescents Infected with HIV Preventive Regimen
Preventive Regimen
Pathogen Indication First Choice Alternative
I. Strongly Recommended as Standard of Care
Pneumocystis carinii CD4+counts of <200/μL or oropharyngeal candidiasis Trimethoprim-sulfamethoxazole (TMP-SMX), 1 double-strength tablet (DS) by mouth daily or TMP-SMX, 1 single-strength tablet (SS) by mouth daily Dapsone 50 mg by mouth twice daily or 100 mg by mouth daily; dapsone 50 mg by mouth daily plus pyrimethamine 50 mg by mouth weekly plus leucovorin 25 mg by mouth weekly; dapsone 200 mg by mouth plus pyrimethamine 75 mg by mouth plus leucovorin 25 mg by mouth weekly; aerosolized pentamidine 300 mg monthly via Respirgard II nebulizer (Marquest Englewood, CO); atovaquone 1500 mg by mouth daily; TMP-SMX 1 DS by mouth three times weekly
Mycobacterium tuberculosis
Isoniazid-sensitive Tuberculin skin test (TST) reaction ≥5 mm or prior positive TST result without treatment or contact with person with active tuberculosis, regardless of TST result Isoniazid 300 mg by mouth plus pyridoxine 50 mg by mouth daily for 9 months, or isoniazid 900 mg by mouth plus pyridoxine 100 mg by mouth twice weekly for 9 months Rifampin 600 mg by mouth daily for 4 months or rifabutin 300 mg by mouth daily for 4 months; pyrazinamide 15-20 mg/kg body weight by mouth daily for 2 months plus either rifampin 600 mg by mouth daily for 2 months or rifabutin 300 mg by mouth daily for 2 months
Isoniazid-resistant Same as previous pathogen; increased probability of exposure to isoniazid-resistant tuberculosis Rifampin 600 mg by mouth daily or rifabutin 300 mg by mouth daily for 4 months Pyrazinamide 15-20 mg/kg body weight by mouth daily for 2 months plus either rifampin, 600 mg by mouth daily for 2 months or rifabutin, 300 mg by mouth daily for 2 months
Multidrug-resistant (isoniazid and rifampin) Same as previous pathogen; increased probability of exposure to multidrug-resistant tuberculosis Choice of drugs requires consultation with public health authorities; depends on susceptibility of isolate from source patient -
Toxoplasma gondii Immunoglobulin G (IgG) antibody to Toxoplasma and CD4+count of <100/μL TMP-SMX 1 DS by mouth daily TMP-SMX 1 SS by mouth daily; dapsone 50 mg by mouth daily plus pyrimethamine 50 mg by mouth weekly plus leucovorin 25 mg by mouth weekly; dapsone 200 mg by mouth plus pyrimethamine 75 mg by mouth plus leucovorin 25 mg by mouth weekly; atovaquone 1500 mg by mouth daily with or without pyrimethamine 25 mg by mouth daily plus leucovorin 10 mg by mouth daily
Mycobacterium avium complex CD4+count of <50/μL Azithromycin 1200 mg by mouth weekly or clarithromycin 500 mg by mouth twice daily Rifabutin 300 mg by mouth daily; azithromycin 1200 mg by mouth daily plus rifabutin 300 mg by mouth daily
Varicella-zoster virus (VZV) Substantial exposure to chickenpox or shingles for patients who have no history of either condition or, if available, negative antibody to VZV Varicella-zoster immune globulin (VZIG) 5 vials (1.25 mL each) intramuscularly administered ≤ 96 hours after exposure, ideally in ≤ 48 hours -

From Centers for Disease Control and Prevention: Guidelines for using antiretroviral agents among HIV-infected adults and adolescents. MMWR 51(RR-7), 2002.

From Practical Guide to the Care of the Medical Patient 7E by Ferri
A 24-year-old woman sees her family physician for a cough. The cough is nonproductive and first appeared 3 days ago. The patient has also felt feverish with a headache and sore throat. Both of her roommates are having similar symptoms. On exam, she has erythematous tympanic membranes and pharyngeal erythema with no exudate. There are fine rhonchi and inspiratory and expiratory wheezes heard on chest exam. A chest radiograph is ordered and shows diffuse patchy infiltrates in both lungs. What is this patient’s most likely diagnosis?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Adult-onset asthma
B. Haemophilus influenzae pneumonia
C. Hypersensitivity pneumonitis
D. Mycoplasma pneumonia
E. Viral pneumonia
Option D (Mycoplasma pneumonia) is correct. This patient has classic Mycoplasma pneumonia, which is the most common cause of community-acquired pneumonia in young adults. Macrolide antibiotics are the treatment of choice.

Option A (Adult-onset asthma) is incorrect. History signs and symptoms of a communicable disease in this case make this an unlikely diagnosis.

Option B (Haemophilus influenzae pneumonia) is incorrect. This would be uncommon in someone in this age group without obvious risk factors.

Option C (Hypersensitivity pneumonitis) is incorrect. This diagnosis shares many of the signs and symptoms of the patient, but has a somewhat different radiologic appearance, usually does not have involvement of the middle ear, and is not infectious. The patient’s history suggests this condition is infectious.

Option E (Viral pneumonia) is incorrect. A common and similar disease to Mycoplasma pneumonia, but this patient’s chest radiograph makes Mycoplasma a more likely diagnosis.

High-yield Hit 1
Regardless of cause, the morphologic patterns in atypical pneumonias are similar. The process may be patchy, or it may involve whole lobes bilaterally or unilaterally. Macroscopically, the affected areas are red-blue, congested, and subcrepitant. Histologically, the inflammatory reaction is largely confined within the walls of the alveoli (Fig. 13-27). The septa are widened and edematous; they usually contain a mononuclear inflammatory infiltrate of lymphocytes, histiocytes, and, occasionally, plasma cells. In contrast to bacterial pneumonias, alveolar spaces in atypical pneumonias are remarkably free of cellular exudate. In severe cases, however, full-blown diffuse alveolar damage with hyaline membranes may develop. In less severe, uncomplicated cases, subsidence of the disease is followed by reconstitution of the native architecture. Superimposed bacterial infection, as expected, results in a mixed histologic picture.
Clinical Course. The clinical course of primary atypical pneumonia is extremely varied, even among cases caused by a single pathogen. It may masquerade as a severe upper respiratory tract infection or "chest cold" that goes undiagnosed, or it may present as a fulminant, life-threatening infection in immunocompromised patients. More typically, the onset is that of an acute, nonspecific febrile illness characterized by fever, headache, and malaise, and, later, cough with minimal sputum. Chest radiographs usually reveal transient, ill-defined patches, mainly in the lower lobes. Physical findings are characteristically minimal and indistinguishable from bronchopneumonia, although, particularly with Mycoplasma, lobar consolidations may occur. Because the edema and exudation are both in a strategic position to cause an alveolocapillary block, there may be respiratory distress seemingly out of proportion to the physical and radiographic findings.

Taken from Robbins Basic Pathology 7E by Kumar et al
A 35-year-old man presents to the physician with a 3-day history of malaise, fatigue, lethargy, headache, and fever. He has also noticed a rash on his lower leg that has changed in appearance since the onset 4 days ago. The rash is neither painful nor pruritic. He was previously well, does not take any regular medications and has no known allergies. Physical examination reveals a temperature of 38.4°C (101.1°F) and a 5-cm erythematous patch with central clearing on the lateral portion of the left lower leg. The remainder of the examination is within normal limits. What is the most likely diagnosis?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Babesiosis
B. Ehrlichiosis
C. Erythema infectiosum
D. Lyme disease
E. Rocky mountain spotted fever (RMSF)
Option D (Lyme disease) is correct. The described rash is that of erythema migrans and it is virtually pathognomonic of Lyme disease, the most common vector-borne disease in North America. It is caused by the spirochete Borrelia burgdorferi and is spread by Ixodes scapularis ticks. Only 30% of individuals with Lyme recall a tick bite, because the tick is so small. Lyme disease has several clinical stages and this patient presents with the earliest. There is often a flu-like illness combined with erythema migrans. Secondary Lyme includes a migratory polyarthropathy, as well as Bell palsy. Tertiary Lyme can present with arthritis and subacute encephalitis.

Option A (Babesiosis) is incorrect. Also transmitted as Ixodes ticks, there is a flu-like illness with petechiae, hepatosplenomegaly, and jaundice.

Option B (Ehrlichiosis) is incorrect. Ehrlichiosis is thought to be transmitted by the same tick as Lyme disease. The initial flu-like symptoms are similar, but erythema migrans does not appear.

Option C (Erythema infectiosum) is incorrect. Erythema infectiosum, also known as fifth disease, presents in children as a maculopapular rash on the arms that spreads to the face as a “slapped cheek” appearance.

Option E (Rocky mountain spotted fever [RMSF]) is incorrect. This is another tick-borne condition, caused by Rickettsia rickettsii and transmitted by the Dermacentor tick. The rash begins on the wrists, palms, ankles, and soles as blanching erythematous macules and spreads to the trunk to form nonblanching petechiae or purpura.

High-yield Hit 1
Lyme Disease (PTG)
DIFFERENTIAL DIAGNOSIS

* Chronic fatigue/fibromyalgia
* Acute viral illnesses
* Babesiosis
* Ehrlichiosis

WORKUP

* ELISA testing-Western blot
* Immunofluorescent assay
* Early disease often difficult to diagnose serologically secondary to slow immune response
* Culturing of skin lesions (ECM) and polymerase chain reaction (PCR) of skin biopsy and blood to give definitive diagnosis (available only in reference laboratories)

Figure 1-140 Erythema migrans. Note expanding erythematous lesion with central clearing on trunk. (Courtesy John Cook, M.D. From Goldstein B [ed]: Practical dermatology, ed 2, St Louis, 1997, Mosby.)

From Ferri's Clinical Advisor 2006 by Ferri
High-yield Hit 2
TREATMENT

* Early Lyme disease
Doxycycline 100 mg bid or amoxicillin 500 mg qid for 10-14 days (doxycycline should be avoided in children/pregnant females)
Alternative treatments: cefuroxime axetil 500 mg bid for 10-14 days, azithromycin 500 mg PO qd for 1 day followed by 250 mg qd for 6 days
* Early Disseminated and late persistent infection: 30 days of treatment necessary; doxycycline and ceftriaxone appear equally effective for acute disseminated Lyme disease
* Arthritis: 30 days of doxycycline or amoxicillin plus probenecid (repeated courses of therapy are often needed)
* Neurologic involvement requires
Parenteral antibiotics
Ceftriaxone 2 g/day for 21 to 28 days
Alternative: cefotaxime 2 g q8h Alternative: penicillin G 5 million U qid
* Cardiac involvement: IV ceftriaxone or penicillin plus cardiac monitoring
* Evidence from recent study suggests that prolonged treatment with IV or PO antibiotic therapy for up to 90 days did not improve symptoms more than placebo


From Ferri's Clinical Advisor 2006 by Ferri
High-yield Hit 3
PEARLS & CONSIDERATIONS

* The U.S. Advisory Committee on immunization practices (ACIP) has recommended that "vaccination should be considered for patients 15 to 70 years of age who live, work, and recreate in high- or moderate-risk areas, and are exposed to ticks either frequently or for long periods of time."
* In some patients with Lyme disease, nonspecific complaints such as headache, fatigue, and arthralgia may persist for months after appropriate (and ultimately successful) antibiotic treatment. These patients undergo slow spontaneous resolution; further therapy for Lyme disease should not be given unless there are objective findings of active disease (including physical findings; abnormalities on cerebrospinal or synovial fluid analysis; changes on formal neuropsychologic testing).
* A single dose of 200 mg doxycycline given within 72 hr of Ixodes tick bite can prevent development of Lyme disease.


From Ferri's Clinical Advisor 2006 by Ferri
transmitted as Ixodes ticks, there is a flu-like illness with petechiae, hepatosplenomegaly, and jaundice.
Babesiosis
is thought to be transmitted by the same tick as Lyme disease. The initial flu-like symptoms are similar, but erythema migrans does not appear.
Ehrlichiosis
presents in children as a maculopapular rash on the arms that spreads to the face as a “slapped cheek” appearance.
Erythema infectiosum, also known as fifth disease
The rash begins on the wrists, palms, ankles, and soles as blanching erythematous macules and spreads to the trunk to form nonblanching petechiae or purpura.
Rocky mountain spotted fever [RMSF], caused by Rickettsia rickettsii and transmitted by the Dermacentor tick.
A 29-year-old man presents to the physician because his roommate was recently diagnosed with active pulmonary tuberculosis (TB). At present he has no symptoms and has been otherwise well. His medical record indicates that he was vaccinated with Bacille-Calmette-Guérin (BCG) at the age of 4 years. Physical examination is within normal limits. A Mantoux purified protein derivative (PPD) test is performed and reveals 16 mm of induration at the site 48 hours after administration. What is the most appropriate next step in the management of this patient?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Isoniazid
B. No further management required
C. Rifampin
D. Rifampin and pyrazinamide
E. Sputum induction due to previous BCG vaccine
Option A (Isoniazid) is correct. In patients who have had a previous BCG vaccine, all PPD skin tests should be compared to baseline skin tests performed shortly after vaccination. However, in most cases, this baseline value is not available. Consequently, skin test reactivity is interpreted in the same fashion as in nonvaccinated individuals. This is an individual with close contacts to active TB with a reactive skin test. The most appropriate therapy is isoniazid.

Option B (No further management required) is incorrect. This patient requires therapy as he has a reactive skin test.

Option C (Rifampin) is incorrect. Rifampin is used when treating latent TB that is isoniazid resistant.

Option D (Rifampin and pyrazinamide) is incorrect. This therapy was previously considered second line therapy for latent TB, but because of elevated rates of liver toxicity, it has since been stopped.

Option E (Sputum induction due to previous BCG vaccine) is incorrect. The BCG vaccine is not a contraindication to skin testing; and if there is no baseline skin test reactivity value available, skin tests are interpreted as though the individual had never been vaccinated.

High-yield Hit 1
TREATMENT OF LATENT TUBERCULOSIS INFECTION

1. A chest radiograph is indicated for all individuals being considered for treatment of LTBI to exclude active pulmonary tuberculosis. If chest radiographs are normal and no symptoms consistent with active tuberculosis are present, tuberculin-positive people may be candidates for treatment of LTBI. If radiographic or clinical findings are consistent with pulmonary or extrapulmonary tuberculosis, further studies (e.g., medical evaluation, bacteriologic examinations, and a comparison of the current and old chest radiographs) should be done to determine whether treatment for active tuberculosis is indicated.
2. Once patients have been identified with and then tested for LTBI, they should receive an initial clinical evaluation. They should also receive follow-up evaluations at least monthly (if receiving isoniazid alone or rifampin alone) and at 2, 4, and 8 weeks (if receiving rifampin and pyrazinamide). This evaluation should include questioning about side effects and a brief physical assessment checking for signs of hepatitis. Patients should be educated about the side effects associated with treatment of LTBI and advised to stop treatment and promptly seek medical evaluation when they occur.
3. Baseline laboratory testing is not routinely indicated for all patients at the start of treatment for LTBI. Patients whose initial evaluation suggests a liver disorder should have baseline hepatic measurements of serum aspartate aminotransferase (AST) or alanine aminotransferase (ALT) and bilirubin. Baseline testing is also indicated for patients with HIV infection, pregnant women, and women in the immediate postpartum period (i.e., within 3 months of delivery), persons with a history of chronic liver disease (e.g., hepatitis B or C, alcoholic hepatitis, or cirrhosis), persons who use alcohol regularly, and persons at risk for chronic liver disease. Baseline testing is not routinely indicated in older persons.


From Practical Guide to the Care of the Medical Patient 7E by Ferri
A 5-year-old boy is brought to the physician, because of a 10-day history of cough, bilateral nasal discharge, and nasal congestion. He has also been febrile, with a temperature ranging between 38.5°C (101.3°F) and 39.0°C (102.2°F). There has not been any vomiting, diarrhea, or earache. He has been otherwise well and has received all recommended vaccinations. Vital signs are as follows: blood pressure (BP), 96/65 mm Hg; pulse, 110 beats/minute; temperature, 39.0°C (102.2°F); and respirations, 24 breaths/minute. There is a thick, purulent nasal discharge bilaterally, along with a mild erythema of the nasal mucosa. Otoscopic examination demonstrates a translucent, pearly grey tympanic membrane and presence of the light reflex. What organism is a sinus aspirate culture is most likely to grow ?

Answer Choices Correct AnswerCorrect answer Your AnswerYour answer
A. Aspergillus species
B. Haemophilus influenzae
C. Moraxella catarrhalis
D. Staphylococcus aureus
E. Streptococcus pneumoniae
Option E (Streptococcus pneumoniae) is correct. This child has acute bacterial sinusitis. Sinusitis is primarily a clinical diagnosis and a sinus aspirate culture is not routinely performed. Nevertheless, the most common cause of acute bacterial sinusitis is S. pneumoniae and would thus be the most likely organism cultured.

Option A (Aspergillus species) is incorrect. Aspergillus has been implicated as one of the most common fungal causes of invasive sinusitis. Fungal sinusitis usually occurs in immunocompromised patients but can occur in immunocompetent patients as well. When occurring in immunocompetent patients, the signs and symptoms are to the result of an immunoglobulin E (IgE)-mediated type I hypersensitivity reaction, not the fungus itself. Suspect acute fungal sinusitis in an atopic patient who has had recurrent sinusitis that has been resistant to antibacterial treatment.

Option B (Haemophilus influenzae) is incorrect. This is the second most common cause of acute bacteria sinusitis. It is usually nontypeable H. influenzae, and, as such, will not decrease because of H. influenzae type b (Hib) immunization.

Option C (Moraxella catarrhalis) is incorrect. Moraxella is the third most common cause of acute bacterial sinusitis.

Option D (Staphylococcus aureus) is incorrect. Suspect S. aureus in a patient who presents with chronic sinusitis.

High-yield Hit 1
1. Define sinusitis.
Strictly speaking, sinusitis is inflammation of the mucosal lining of the paranasal sinuses secondary to many potential triggers. The term rhinosinusitis has been emphasized recently to highlight the importance of nasal cavity mucosal pathology in the overall disease process.
2. Describe the pathophysiology of sinusitis.
Mucosal edema of the paranasal sinuses is the basic event leading to both acute and chronic disease. Edema may lead to obstruction of the drainage routes of the sinuses, causing stasis of secretions and an overall physiologic change in the sinus cavity. These local changes lead to impaired mucociliary clearance, alteration in local immune defenses, and ultimately bacterial overgrowth.
Perhaps the two most important potenital triggers underlying sinusitis are upper respiratory viral infection and upper airway allergy. Additional factors include environmental hypersensitivites, mucociliary dysfunction (primary and acquired), anatomic relationships (septal deviation, nasal polyposis), immunodeficiencies, and fungal hypersensitivities.

From ENT Secrets 3E by Jafek & Murrow
High-yield Hit 2
4. Which sinus is most often involved in rhinosinusitis?
In the majority of cases, the maxillary sinus and anterior ethmoid sinuses are involved. This can be predicted by the anatomy of the middle meatus or infundibulum, the location for drainage of the "anterior sinuses" (maxillary, anterior ethmoid, frontal sinuses) (Fig. 18-1).
5. How is rhinosinusitis classified?
Figure 18-1 Acute bacterial rhinosinusitis. Nasal endoscopy of the left nasal cavity reveals purulent material in the middle meatus.
Clinical categories of rhinosinusitis are largely based on the duration of symptoms and include the following: acute (up to 4 weeks), subacute (4-12 weeks), chronic (> 12 weeks), recurrent-acute (> 4 episodes/year with absence of intervening signs), and acute exacerbations of chronic (sudden worsening of chronic sinusitis). This classification scheme is symptom based and should serve only as a general guideline.

From ENT Secrets 3E by Jafek & Murrow
High-yield Hit 3
6. Describe the signs and symptoms of acute bacterial rhinosinusitis (ABRS).
In can be very difficult to distinguish between ABRS and other causes of acute nasal congestion (viral rhinitis, allergic/nonallergic rhinitis). The 1996 Task Force on Rhinosinusitis developed a list of symptoms and signs to serve as a guideline in making the diagnosis of ABRS (Table 18-1). A diagnosis of ABRS may be made in adults or children with a viral upper respiratory infection does not dissipate within 10 days (or worsens after 5-7 days) and is accompanied by some or all of these symptoms.
Table 18-1. SIGNS AND SYMPTOMS OF ABRS
Nasal drainage
Nasal congestion
Facial pain/pressure (especially when unilateral and focused in the region of a particular sinus group)
Postnasal drip
Hyposmia/anosmia
Fever
Cough
Fatigue
Maxillary dental pain
Ear fullness/pressure
7. What are the most common organisms associated with ABRS?
Streptococcus pneumoniae (20-40%), Haemophilus influenzae (20-35%), and Moraxella catarrhalis (2-10%) are the most common pathogens associated with ABRS. Less common pathogens include Staphylococcus aureus (0-9%), anaerobes (0-9%), and streptococcal species (3-9%).
A relatively new issue in the management of ABRS is evolving antibiotic resistance. Essentially all of the most common pathogens in ABRS now demonstrate decreased antibiotic sensitivities to many of the commonly used drugs and related drug classes. This has directly affected antibiotic selection in the treatment of ABRS. Table 18-2 presents the current antibiotic resistence rates for isloates of S. pneumoniae. The incidence of beta-lactamase production in isolates of H. influenzae is 30-40%, and for isolates of M. catarrhalis it is 92%.

From ENT Secrets 3E by Jafek & Murrow
the most common cause of acute bacterial sinusitis
Streptococcus pneumoniae
the second most common cause of acute bacteria sinusitis
nontypeable H. influenzae, and, as such, will not decrease because of H. influenzae type b (Hib) immunization.
the third most common cause of acute bacterial sinusitis
Moraxella catarrhalis