Micro USMLE 8-27(10) Flashcards
This patient has classic symptoms of subacute bacterial endocarditis, including Osler nodes (tender raised lesion on finger, first image), Janeway lesions (nontender erythematous lesions on the palms or soles, second image), fever, and a new heart murmur on auscultation. Other symptoms not mentioned in this patient’s presentation include: Roth spots (hemorrhages within the retina) and glomerulonephritis. The Duke criteria are used to make a clinical diagnosis of infective endocarditis (see the table).
This patient’s endocarditis was likely precipitated by his recent dental examination. Viridans streptococci are a common cause of ?
subacute bacterial endocarditis, which generally occurs in the setting of dental procedures on patients with diseased heart valves. Viridans streptococci are normal flora in the mouth, so dental procedures can increase the chance of this bacteria going into the bloodstream and damaging a heart previously damaged from rheumatic fever. Viridans streptococci are gram-positive, catalase-negative, a-hemolytic cocci that are optochin-resistant. Having rheumatic fever as a child put the patient at increased risk of developing diseased heart valves later in life and therefore an increased risk of endocarditis. The patient should have been given antibiotics before the dental procedure to prevent the development of bacterial endocarditis.
Gram-positive cocci, catalase-negative, ß-hemolytic, and bacitracin-resistant describes Streptococcus agalactiae. ?????
Gram-positive cocci, catalase-negative, ß-hemolytic, and bacitracin-sensitive describes?
Streptococcus pyogenes.
Gram-positive, catalase-positive cocci describes Staphylococcus aureus.
Gram-positive, weakly acid-fast rod describes Nocardia asteroides.
Viridans streptococci are a group of gram-positive cocci, catalase-negative, α-hemolytic, and optochin resistant. They can cause?
subacute endocarditis, generally in the setting of previously diseased heart valves and recent dental procedures.
This patient’s symptoms of fever, desquamating rash, and hypotension in the setting of retained nasal packing are consistent with toxic shock syndrome caused by Staphylococcus aureus. S aureus produces a toxin called toxic shock syndrome toxin (TSST-1) that acts as a superantigen. TSST-1 cross-links?
major histocompatibility complex II (MHC II) molecules on antigen-presenting cells to T-cell receptors on T cells independent of antigen. This results in T-cell proliferation, which can induce a cytokine storm. The presence of these cytokines (ie, interleukin-1, interleukin-2, interferon-γ, and tumor necrosis factor-α) gives rise to fever, hypotension, and a diffuse macular rash (like that shown in the image), which desquamates after a few days. Retained foreign bodies that can serve as a conduit for infection, such as nasal packing or tampons, make S aureus the most likely culprit, as this organism naturally colonizes the nose and skin.
Toxic shock syndrome is mediated by inappropriate T-cell activation by TSST-1. This mechanism differs from molecular mimicry (binding of antibodies that recognize a similar epitope on normal tissue), which is classically associated with?
rheumatic fever and occurs 2 to 3 weeks after infection (typically with Streptococcus pyogenes).
Although this patient’s inflammatory response is mediated by cytokines, it is not due to excess cytokine release by B-cell activation. B cells do not secrete the constellation of cytokines that cause the pathology described.
A type 1 hypersensitivity reaction, cross-linking of IgE on presensitized mast cells and basophils, triggering release of their contents, is seen with anaphylaxis (eg, after a bee sting) or an atopic condition (eg, eczema) and causes a rash that occurs within minutes and is accompanied by urticaria, edema, and pruritus.
Although Streptococcus pyogenes can mediate a toxic shock–like syndrome due to nonspecific T-cell activation by exotoxin A, the patient&’s history of retained nasal packing makes ?
S aureus and TSST-1 exotoxin more likely. Streptococcal pyrogenic exotoxin A has identical superantigen activity and could be a plausible cause if the patient had a history of prior streptococcal skin infection (eg, cellulitis).
Staphylococcus aureus produces a superantigen, toxic shock syndrome toxin (TSST-1), which activates a large population of T lymphocytes by ?
cross-linking MHC II and T-cell receptors. This results in a clinical triad of fever, shock, and a desquamating rash in the setting of a retained foreign body, such as nasal packing or a tampon, which provides a rich nutrient source (blood) for the bacteria.
This 10-day-old infant presents with poor feeding, irritability, fever, and lethargy, which is concerning for neonatal sepsis or meningitis. The results from the cerebrospinal fluid (CSF) analysis suggest a bacterial meningitis (gram-positive rods on microscopy, low glucose, elevated protein, elevated leukocyte count with left shift). The most common pathogens causing meningitis in neonates include (in descending order):
Group B streptococci (GBS)
Escherichia coli
Listeria monocytogenes
Of these organisms, Listeria is the only gram-positive bacilli (E. coli = gram-negative bacillus; GBS = gram-positive cocci). Additionally, Listeria is a common cause of meningitis in the elderly and the immunocompromised. Transmission of Listeria generally occurs through placental transmission, vaginal transmission, or ingestion of bacteria in food. Ingestion of ?
poorly pasteurized milk and/or soft cheese is most commonly implicated in the pathogenesis of listeriosis in the elderly, the immunocompromised, or pregnant patients.
Neonatal listeriosis is acquired transplacentally or transvaginally. Neonates with early-onset disease often present with low birth weight, have associated complications, and show evidence of sepsis soon after birth, with circulatory and/or respiratory insufficiency. Neonates with the delayed-onset form, like this patient, are usually full-term, previously healthy neonates presenting with meningitis or sepsis.
Listeria is an intracellular bacteria that must survive inside host cell macrophages. Listeriolysin O, an exotoxin produced by Listeria, facilitating this survival, forms a pore in phagosomes, which prevents fusion of ?
the phagosome and lysosome. Therefore, patients must have intact cell-mediated immunity to eliminate this pathogen. If cell-mediated immunity is impaired (as in neonates, the immunocompromised, the elderly, and pregnant patients), there is a greater risk of serious infection from this organism, which explains why serious Listeria infections have a predilection to these types of patients.
Transmission through an ascending urinary tract infection is characteristic of E. coli, a gram-negative bacillus. It is the number one cause of neonatal meningitis, but it is not classically associated with meningitis in the elderly and the immunocompromised, nor is it consistent with the CSF analysis.
Direct inoculation into an open wound is not a common method by which Listeria is transmitted, and is more consistent with ?
transmission of a superficial bacterial infection of staphylococcal or streptococcal species.
Listeriosis is not an airborne infection, so transmission via inhalation of aerosolized bacteria is an unlikely mode of transmission.
Listeria monocytogenes is a gram-positive rod that causes meningitis in neonates and the immunocompromised. It is commonly found in ?
unpasteurized milk, soft cheeses, coleslaw, and packaged cold cuts.
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.
