0% 0% Micro USMLE 8-30(22) (qmax 8/30 incorrect qs) Flashcards
This patient presents with lower abdominal cramping, fever and watery non-bloody diarrhea several days after being treated in the hospital for cellulitis with clindamycin. He most likely has pseudomembranous colitis, which is found primarily in hospitalized patients and caused by ?
Clostridium difficile. This organism causes diarrhea (usually watery, but small amounts of blood may be present), abdominal cramping (generalized or lower abdomen), and fever through the production of two exotoxins: toxin A and toxin B. This infection usually manifests after treatment with broad-spectrum antibiotics for several days such as clindamycin, ampicillin and fluoroquinolones.
Oral vancomycin can be used for 10 to 14 days to treat the type of infection seen in this patient. Vancomycin inhibits cell wall peptidoglycan formation by?
binding D-ala D-ala. Metronidazole works by forming cytotoxic intermediates that damage bacterial DNA. Ampicillin works by inhibiting transpeptidase cross-linking and is associated with causing, not treating CDI. Tigecycline and fidaxomicin work by inhibiting protein synthesis by inhibiting the 30S subunit and RNA polymerase, respectively. Although oral vancomycin, tigecycline and fidaxomicin are options in the treatment of CDI, they are not first-line therapy.
Clostridium difficile pseudomembranous colitis can manifest following treatment with broad-spectrum antibiotics, particularly with ampicillin and clindamycin. The first-line initial therapy recommended by treatment guidelines for this infection is vancomycin, which inhibits?
cell wall peptidoglycan formation by binding D-ala D-ala.
An epidemic of a diarrhea has broken out in a city hospital. Colonoscopy of one of the affected patients reveals colonic inflammation with exudates and necrosis of the mucosal surface. Assays for toxin A and toxin B are positive.
Which of the following is the microbiology laboratory likely to isolate from the affected patients?
A gram-positive anaerobe
The description of colonic inflammation with exudates and necrosis of the mucosal surface describes the pseudomembranous colitis of Clostridium difficile, of which there have been several outbreaks. C. difficile is a gram-positive anaerobe spore-former that produces toxin A (which causes diarrhea) and toxin B (which is cytotoxic). AB toxin causes cell apoptosis. Later stages of C. difficile infection can result in necrosis as described in the vignette. Strains that produce an increased amount of these toxins have led to increased morbidity and even death associated with C. difficile colitis.
Clostridium difficile is a?
gram-positive anaerobic organism that produces toxin A and toxin B, causing diarrhea and necrosis of the colonic mucosa, respectively. It is a source of increasing morbidity, and appropriate preventive measures, most notably hand washing and judicious use of antibiotics, must be employed.
This HIV-positive patient with weakness of right upper and lower limbs (hemiparesis), disorganized meaningless speech (aphasia), ataxia (loss of muscle control), seizures, and increased signal intensity in the temporal lobe on MRI most likely has temporal lobe encephalitis.
Herpes simplex virus type 1 (HSV-1) is a ?
double-stranded DNA virus that can cause temporal lobe encephalitis in immunocompromised patients. Following the primary infection, the HSV-1 virus may enter a latent period, lying dormant in the trigeminal ganglion. During the latent phase, viral genetic material is preserved as an episome: circular, double-stranded DNA that is not yet integrated into the host chromosome and therefore can be detected in infected neurons.
Initial infection with HSV-1 occurs in the skin and mucous membranes in the oropharynx. During this initial stage, the virus actively replicates and produces vesicular skin lesions that contain numerous viral particles. Subsequently, the virus may be reactivated by various stimuli including stress, menstruation, and exposure to ultraviolet light. On reactivation, viral proteins are synthesized and a reactivated infection can occur.
DNA is copied by viral DNA polymerase during lytic, not latent, replication.
Parvovirus B19 is a ?
single-stranded DNA virus that manifests in adults with prodromal symptoms (fever, malaise, headache) followed by pure RBC aplasia and/or symmetric arthritis of the hands, wrists, and knees. This patient’s symptoms are not consistent with parvovirus B19 infection.
Viral nucleocapsids are not produced during the latent period of virus replication.
Reverse transcriptase is not associated with this patient’s condition and therefore would not be detected in infected neurons.
During the latent phase, HSV-1 viral genetic material is preserved as ?
an episome: circular, double-stranded DNA that is not yet integrated into the host chromosome and therefore can be detected in infected neurons.
This patient with pearly white/skin-colored papules with central umbilication has the classic dermatological finding associated with molluscum contagiosum. Caused by?
a poxvirus, an enveloped virus with double-stranded, linear DNA, molluscum contagiosum virus is most frequently seen in children. In this population, the virus is often transmitted through skin-to-skin contact or indirect contact with fomites (e.g. gymnasium equipment). Lesions commonly occur on the chest, arms, trunk, legs, face, and intertriginous areas.
Molluscum contagiosum also occurs in adults and may be transmitted sexually. In such cases, if the patient is immunocompetent, lesions tend to be located around the genitalia and surrounding areas, as seen in this patient. Widespread, persistent, and atypical presentations may be seen in immunocompromised patients. The infection often resolves spontaneously, but may require topical therapy or surgery in immunocompromised patients.
The organisms named in the alternate answer choices do not produce the pearly white or skin-colored papules with central umbilication seen in this patient’s skin. Among the non-enveloped RNA viruses, coxsackie virus, which causes hand, foot, and mouth disease, is most closely associated with a rash; however, this is described as red, blister-like lesions. Microsporum, a mold, (and several similar organisms) cause cutaneous infections with a pruritic, flat rash on several parts of the body. Malassezia species, al-shaped, budding yeasts, are responsible for tinea versicolor, an infection in which patches of skin become discolored due to melanocyte damage by the infecting fungus. Rickettsia are?
gram-negative, obligate intracellular bacteria capable of causing a rash, which is erythematous; other similar organisms also cause rashes different from those in the illustration. Infections caused by this pathogen often present with systemic symptoms, as well. Dermatological findings of Treponema pallidum, a spiral-shaped bacterium, include maculopapular rashes, characterized by flat, coarse red areas of skin; other spirochetes also cause rashes.
This patient presents with bloody diarrhea after eating undercooked ground beef. Given her fever, tachycardia, petechiae (a sign of thrombocytopenia), elevated creatinine (which is concerning for renal failure), elevated WBC count, and decreased hemoglobin (which is concerning for anemia), without coagulopathy, this child is likely suffering from hemolytic-uremic syndrome (HUS).
HUS is most commonly associated with infection with Shigella dysentariae and Escherichia coli O157:H7– both express shiga-toxin.
Composed of two components, A and B, these toxins can cause renal failure, microangiopathic hemolytic anemia, and disseminated intravascular coagulation, as well as thrombocytopenia and fever. The B component binds to the cell membrane and allows entry of the A toxin. This component?
inactivates ribosomes, thereby stopping protein synthesis, which leads to cell death
Since these pathogens are commonly acquired via the digestive tract, the cells exposed die and slough off, leading to the bloody diarrhea experienced by the patient. Both Shigella and Escherichia coli O157:H7 attach to?
intestinal epithelium, and the toxin (not the bacteria) invades the cell. The two pathogens can be differentiated on stool cultures.
Clinical features of HUS include:
thrombocytopenia
microangiopathic hemolytic anemia
acute renal failure
The toxin produced by Bordetella pertussis (B. pertussis) over-activates adenylate cyclase by disabling the G-inhibitory protein. Infection with B. pertussis is not characterized by the bloody diarrhea, fever, tachycardia, and petechiae seen in this patient. The toxin produced by Corynebacterium diphtheriae (C. diphtheriae) inactivates elongation factor (EF)-2 by adenosine diphosphate ribosylation, but EF-2 is not a G protein. Infection with C. diphtheriae is not characterized by the signs and symptoms seen in this patient.
The venom produced by Latrodectus (the black widow spider), drastically increases the amount of ?
acetylcholine released, which causes muscle contraction until all of the acetylcholine has been used; paralysis can then occur as a result. There is no history of spider bite – which in the case of the black widow is usually immediately painful – in this patient. Staphylococcus aureus produces an exotoxin that binds major histocompatibility complex II and T-lymphocyte receptor, causing the massive release of cytokines, resulting in toxic shock syndrome.
E. coli O157:H7 (EHEC) and Shigella are two foodborne pathogens that can lead to hemolytic-uremic syndrome (HUS). These bacteria secrete protein toxins that enter intestinal cells and inhibit protein synthesis by?
binding ribosomes. Some of the more common manifestations are bloody diarrhea, acute renal failure, and thrombocytopenia.
A “barking” cough, hoarse voice, inspiratory stridor, and a positive “steeple sign” on a chest x-ray are found in patients with croup. Croup is caused by the parainfluenza virus, which is ?.
a single-stranded, negative-sense, linear, nonsegmented RNA virus