Micro USMLE 8-29(15) (qmax 8/22- 1-5) Flashcards
This patient presents with abdominal pain, vomiting, diarrhea containing mucus and blood, and high temperature. She most likely has an infection caused by Shigella, an invasive pathogen producing febrile gastroenteritis. It is a Gram-negative, oxidase-negative rod which does not ferment lactose (white colonies on MacConkey agar) or produce hydrogen sulfide (no blackening on TSI). Shigella is extremely virulent, requiring only 10 organisms for infection, and it invades via?
the M cells found in the Peyer patches of the small intestine, spreading between cells by actin rockets. Outbreaks are most common in daycare centers and nursing homes.
Shigella is an invasive, Gram-negative non-lactose fermenter that does not produce hydrogen sulfide, and can cause dysentery with fever. Shigella dysenteriae also produces a toxin that may cause?
hemolytic uremic syndrome, which manifests with the typical triad of anemia, thrombocytopenia, and acute renal failure.
Shigella dysenteriae also produces Shiga toxin, which can cause hemolytic uremic syndrome (HUS). The pathogenesis of HUS is incompletely understood, but is thought to involve Shiga toxin binding to endothelial cell surface receptors, causing endothelial cell apoptosis and release of thrombogenic factors and cytokines. Shiga toxin also inactivates ADAMTS-13, producing formation of von Willebrand factor multimers, as well as complement factor H, leading to increased activation of the complement cascade. These pathways result in local activation of the coagulation cascade, leading to the formation of microthrombi. Consumption and destruction of platelets cause ?
thrombocytopenia. Shearing of blood cells by microthrombi results in microangiopathic hemolytic anemia.
Microvascular damage and ischemia cause renal cortical necrosis, leading to uremia. Treatment for HUS consists of supportive care. Note that S. dysenteriae is not common in the United States. The most common species in the United States, Shigella sonnei, does not produce Shiga toxin, and rarely causes HUS.
Ascending flaccid paralysis is characteristic of Guillain-Barre syndrome, associated with Campylobacter jejuni dysentery. Liver abscess and toxic megacolon result from Entamoeba histolytica infection. Meningitis is a complication of invasive listeriosis, caused by?
Listeria monocytogenes. Subcutaneous nodules, polyarthritis, chorea, and a heart murmur are features of rheumatic fever following Streptococcus pyogenes infections.
This patient presents with palpitations, chest pain, and mitral regurgitation, along with a recent history of an upper respiratory illness (fever, congestion). Her elevated cardiac enzyme levels and inflammatory infiltrate with necrosis on a biopsy specimen (shown in the image) signal acute myocardial damage. In an otherwise healthy adult, her symptoms and lab results suggest ventricular dysfunction typical of ?
acute viral myocarditis. Although myocarditis can be asymptomatic, it often starts with fever and mild symptoms, which are then followed by chest pain, palpitations, shortness of breath, and congestive heart failure.
Some of the most common viral causes of myocarditis include human herpesvirus-6, parvovirus B19, and the enteroviruses, most notably, coxsackievirus B. Other infectious causes of myocarditis include Trypanosoma cruzi, Borrelia burgdorferi, and Corynebacterium diphtheriae.
Hepatitis B and rubella are not typical causes of myocarditis.
Staphylococcus aureus and Staphylococcus epidermidis can lead to ?
endocarditis, but not myocarditis.
Myocarditis damages the cardiac myocytes, leading to signs of ventricular dysfunction, elevated cardiac enzyme levels, inflammatory infiltration, and myocardial necrosis. Although there are many causes of inflammation of the myocardium, one of the most common viral infections associated with myocarditis is ?
coxsackievirus B.
This patient’s cough with green sputum, together with his other non-specific symptoms, suggests a pneumonia of unknown etiology. However, the presence of numerous yeast cells within a macrophage (as indicated by the arrow in the histology image below) points to a likely diagnosis of histoplasmosis, caused by ?
the fungus Histoplasma capsulatum. Histoplasmosis is endemic in central, mid-Atlantic, and southeastern states, particularly in the Ohio and Mississippi River valleys. The fungus is common in soil contaminated with bat or bird droppings; people who work with soil or around these animals are at increased risk for histoplasmosis. The primary infection is in the lungs and may be latent, or brief and self-limited. (Immunocompromised people are at particular risk for disseminated infection.) Symptoms include fever, cough, and sweats. X-ray of the lungs will shows calcified coin lesions and hilar lymphadenopathy.
Blastomycosis appears as broad-based buds, while coccidiomycosis is described as spherules filled with endospores. The multiple budding yeasts seen with Paracoccidiomycosis have a characteristic ?
“captain’s wheel” formation. Cryptococcus demonstrates heavily encapsulated yeast that appears best on India ink or mucicarmine stain.
Histoplasmosis is endemic in central, mid-Atlantic, and southeastern United States. It primarily infects the lungs, and causes fever, cough, and sweats. Because the fungus is common in soil contaminated with?
bat or bird droppings, working with or near these animals increases the risk of contracting the disease.
This 6-month-old patient presents with wheezing and ronchi, along with signs of a worsening upper respiratory infection (rhinorrhea and cough) of 3-day duration. She has no previous medical history, and is experiencing tachypnea, nasal flaring, suprasternal retraction, and hypoxemia, indicated by a SpO2 of 90%, meeting the criteria for the diagnosis of bronchiolitis caused by ?
respiratory syncytial virus (RSV).
This virus is the most common cause of lower respiratory tract infection (LRTI) in children younger than 1 year of age. RSV is a single-stranded, non-segmented, negative-sense enveloped RNA virus and a member of the Paramyxoviridae family.
The virus begins replicating in the nasopharynx, then infects the small bronchiolar epithelium, sparing the basal cells, and then extends to the type 1 and 2 alveolar pneumocytes in the lung. The immune response leads to airway obstruction, air trapping, and increased airway resistance, as seen in this patient.
In a child <2 years of age, bronchiolitis is diagnosed clinically with one of the following:?
I
ncreased respiratory effort Tachypnea Nasal flaring Accessory muscle use Intercostal, subcostal, or suprasternal retractions Grunting Hypoxemia (SpO2 <95%) Apnea Acute respiratory failure Initial management for a pediatric patient with bronchiolitis is nasal suctioning and supplemental oxygen.
An enveloped RNA virus with a single-stranded, positive-sense, and non-segmented genome describes coronavirus, which is responsible for the common cold. An enveloped RNA virus with a single-stranded, negative-sense, and segmented genome describes influenza virus, which presents with the classic symptoms of dyspnea, fever, headache, cold chills, nausea, vomiting, and diarrhea and can cause severe secondary respiratory infections. However, it would not be the most common etiology at this patient’s age. A non-enveloped RNA virus with a double-stranded, and segmented genome describes the Reoviridae family which is not associated with respiratory involvement. A non-enveloped RNA virus with a single stranded, positive-sense, and non-segmented genome describes ?
rhinovirus, which is responsible for symptoms of the common cold and does not manifest with symptoms of respiratory decompensation in a child of this age.
Respiratory syncytial virus is a single-stranded, non-segmented, negative-sense, enveloped RNA virus and is the most common cause of ?
bronchiolitis in children <1 year of age.
This patient presents with nonproductive cough, fever, headache, and malaise, plus late inspiratory crackles. The chest x-ray shows bilateral diffuse patchy interstitial infiltrate. The patient’s symptoms and the findings on the chest x-ray are most suggestive of atypical pneumonia. The infectious agent most likely responsible is Mycoplasma pneumoniae.
M. pneumoniae organisms do not have cell walls, and their cell membranes contain cholesterol. Therefore culture of M. pneumoniae requires a ?
cholesterol-rich medium for maintaining and building outer membranes, and M. pneumoniae will not appear on Gram staining.
