Micro USMLE 8-21 (3) Flashcards
Based on her X-ray findings, leukocytosis, and sputum analysis, this woman has developed bacterial pneumonia (circle in image). The observation of gram-positive cocci in clusters (shown in the vignette image) is diagnostic of Staphylococcus aureus. S. aureus is a common cause of secondary bacterial pneumonia after initial infection with the influenza virus, and its principal virulence factor is protein A. It is also a common cause of hospital-acquired pneumonia. Pneumonia due to this organism frequently leads to complications such as lung abscess or empyema. This patient’s X-ray findings display?
lobar pneumonia. However, postinfluenza pneumonia caused by S. aureus can also lead to bronchopneumonia, which may even be more common. This would instead appear as patchy infiltrates on chest X-ray. If the disease process is rapidly progressive, S. aureus can even lead to extensive infiltrates bilaterally, appearing similar to pulmonary edema on chest X-ray.
Legionella pneumophila is a weakly staining gram-negative bacillus that is the agent behind Legionnaires’ disease. It thrives in aquatic environments and can be acquired from inhalation of aerosol from contaminated water sources, frequently in a hospital setting. It secretes Ank proteins as its primary virulence factor.
Capsular polysaccharide (CPS) and lipopolysaccharide are two important virulence factors in Klebsiella pneumoniae infection. CPS makes up the outer layer of the microbe, protecting it from phagocytic destruction. Klebsiella makes up the ?
normal flora the mouth and intestines, but K. pneumoniae is an important cause of hospital acquired pneumonia, typically seen in immunocompromised patients.
Haemophilus influenzae is a gram-negative bacillus that secretes an IgA protease. It is a common cause of community-acquired pneumonia, particularly in patients with underlying pulmonary pathology such as chronic obstructive pulmonary disease. In unvaccinated children, the encapsulated form of H. influenzae can cause life-threatening acute epiglottitis. In addition, Streptococcus pneumoniae and Neisseria also have IgA protease as an important virulence factor.
Mycoplasma pneumoniae is the most common cause of?
bacterial pneumonia in young adults. It generally causes a mild atypical interstitial pneumonia (“walking pneumonia”) that can be treated on an outpatient basis. M. pneumoniae lacks a cell wall and thus cannot be detected on Gram stain.
Staphylococcus aureus can cause a postviral lobar pneumonia, with the appearance of gram-positive clusters on light microscopy. Notably, S. aureus provides ?
protein A as its primary virulence factor.
A neonate with purulent umbilical discharge for 1 day presents with fever, irritability, and diffuse flushing. One day later she is covered in large, fluid-filled blisters that rupture easily, leaving raw red areas beneath. Blood cultures are taken, which within 24 hours grow an organism that is subsequently Gram stained with the results shown below.
The skin symptoms observed in this case are due to the involvement of which of the following intercellular structures?
Staphylococcal scalded skin syndrome (SSSS) is caused by the release of two exotoxins (epidermolytic toxins A and B) from Staphylococcus aureus. Desmosomes (also called “macula adherens”) are responsible for binding epithelial cells to one another to form a coherent whole. The exotoxins that are released bind to a molecule within the desmosome called desmoglein 1, thereby disrupting cell adhesion. In SSSS, the epidermis separates at the stratum granulosum due to the binding of exotoxins to desmosomes in this layer. Clinically, this results in bullous lesions and a positive Nikolsky’s sign.
Gap junctions are circular intercellular contact areas that permit the passage of small molecules between adjacent cells, allowing communication to facilitate electrotonic and metabolic function.
Hemidesmosomes are present on the basal surface of epithelial cells adjacent to the basement membrane, and serve to connect epithelial cells to the underlying extracellular matrix.
Intermediate junctions lie deep to tight junctions, comprised of actin filaments forming a?
continuous band around the cell, providing structural support just below tight junctions.
Tight junctions are located beneath the luminal surface of simple columnar epithelium (eg, intestinal lining) and seal the intercellular space to prevent diffusion between cells.
In staphylococcal scalded skin syndrome, the epidermis separates at the stratum granulosum as a result of binding of epidermolytic toxins A and B to desmoglein 1 in this layer.
This patient presents with acute chest pain, dry cough, fatigue, malaise, chills, and a systolic murmur secondary to tricuspid regurgitation. This clinical picture, together with his history of intravenous drug use, provide strong diagnostic clues. He most likely has infective endocarditis of the tricuspid valve caused by Staphylococcus aureus bacteremia introduced through intravenous drug use.
More than 50% of cases of infective endocarditis secondary to intravenous drug use will only affect the tricuspid valve. Tricuspid valve vegetations may also seed?
septic emboli from the right side of the heart, resulting in pulmonary emboli, with the presence of cough, pleuritic chest pain, diffuse pulmonary infiltrates, and pyopneumothorax. S. aureus is a catalase-positive, coagulase-positive, β-hemolytic, gram-positive (in clusters) facultative coccus (shown in the image below). S. aureus produces a golden-yellow pigment in culture.
It’s imperative to suspect S. aureus in intravenous drug users who may not manifest with the classic symptoms of infectious endocarditis (Roth spots, Osler nodes, and Janeway lesions) owing to isolated tricuspid valve infection with pulmonary emboli rather than systemic embolization as in left-sided endocarditis.
Catalase-negative β-hemolytic cocci is characteristic of Group A streptococci (Streptococcus pyogenes), which are uncommon causes of endocarditis in injection-drug users. Catalase-positive, coagulase-negative cocci is characteristic of ?
Staphylococcus epidermidis which most commonly grows on and damages cardiac valve replacements, but not native valves. α-hemolytic cocci with optochin resistance is characteristic of viridans streptococci, which damage native cardiac valves, but less commonly than S. aureus in injection-drug users. α-hemolytic cocci with optochin sensitivity is characteristic of Streptococcus pneumoniae, which is a common cause of meningitis, otitis media, and pneumonia, but less common in endocarditis. Non-hemolytic cocci in chains is characteristic of enterococci and Lancefield group D streptococci, which can cause subacute bacterial endocarditis, and are also associated with biliary and urinary tract infections
Staphylococcus aureus (S. aureus) can cause an acute infective endocarditis of native heart valves resulting in high fevers, chills, and an acute heart murmur. It’s imperative to suspect S. aureus in intravenous drug users who may not manifest with ?
the classic symptoms of infectious endocarditis (Roth spots, Osler nodes, and Janeway lesions) owing to isolated tricuspid valve infection with pulmonary, rather than systemic emboli.
A 70-year-old woman presents to the emergency department with fever, chills, swelling, erythema, and decreased range of motion in the left knee. She had a left total knee replacement two weeks ago and had a prosthetic joint implanted. Her surgeon decides to tap the joint and sends the fluid for Gram stain and culture.
Which of the following is most likely to be observed upon laboratory examination of the joint fluid?
Gram-positive, catalase-positive cocci could refer to either Staphylococcus aureus or Staphylococcus epidermidis. Overall, S. aureus is the most common cause of septic arthritis in adults and children. However, S. epidermidis is also known for causing nosocomial infections of implanted foreign bodies such as catheters, joint prosthetics, and prosthetic heart valves. S. aureus and S. epidermidis can be differentiated by coagulase testing: S. aureus is coagulase-positive while S. epidermidis is coagulase-negative.
Gram-negative, glucose-fermenting cocci identifies an organism such as Neisseria gonorrhoeae. N. gonorrhoeae is a common cause of septic arthritis in young, sexually active adults. It is sexually transmitted and causes a purulent infiltration of the synovium. N. gonorrhoeae ferments only glucose, whereas N. meningitidis ferments both glucose and maltose.
Gram-negative, lactose-fermenting bacilli identifies an organism such as Escherichia coli. E. coli is the most common cause of urinary tract infections. It is not implicated as a cause of postsurgical septic arthritis.
Gram-negative, non-lactose fermenting bacilli identifies an organism such as?
Salmonella. Salmonella species are usually implicated in bloody diarrhea. When infecting bone, Salmonella causes osteomyelitis rather than septic arthritis, particularly in asplenic individuals such as adults with sickle cell anemia.
Gram-positive, catalase-negative cocci identifies an organism such as Streptococcus. S. pyogenes is implicated in bacterial pharyngitis and scarlet fever, among other diseases. It could cause polyarthralgias in a patient with rheumatic fever, but it is not a likely cause of postsurgical septic arthritis.
Staphylococcus aureus and Staphylococcus epidermidis are gram-positive, catalase-positive cocci that are likely to cause?
septic arthritis after joint replacement surgery.
The patient’s strong muscle contractions and trismus (contraction of the jaw muscles) are symptoms of tetanus. Tetanus is caused by?
Clostridium tetani spores that are found in the soil. These organisms classically enter the body as spores through a puncture wound. In the low-oxygen environment of a deep wound, the anaerobic bacteria sporulate and grow, producing tetanus toxin.
Clostridium tetani is a spore-forming, gram-positive bacillus that is transmitted through contaminated soil and animal feces, whose entrance into the body is often facilitated by puncture wounds from spore-contaminated sharp objects like nails. It produces an?
exotoxin that blocks glycine and GABA from inhibiting muscular contractions, resulting in tonic contraction (tetanus).
The disease pathology is associated with the production of an exotoxin known as tetanospasmin or tetanus toxin. This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. The net result of this is to?
prevent the inhibitory signal from reaching motor neurons downstream, thus predisposing motor neurons to tonic contraction, or tetanus.
Prevention of tetanus is accomplished by vaccination using an inactivated form of tetanus toxin called tetanus toxoid. Protection against tetanus is excellent after immunization but wanes over time. It is unlikely that our patient has followed an adequate vaccination schedule, as she has not seen a doctor in over 10 years.
