A 67-year-old man presents to the physician with profuse watery diarrhea along with fever and crampy abdominal pain. He has been taking an antibiotic course of cefixime for about a week to treat a respiratory tract infection. At the doctor’s office, his pulse is 112/min, the blood pressure is 100/66 mm Hg, the respirations are 22/min, and the temperature is 38.9°C (102.0°F). His oral mucosa appears dry and his abdomen is soft with vague diffuse tenderness. A digital rectal examination is normal. Laboratory studies show:
Hemoglobin 11.1 g/dL
Hematocrit 33%
Total leucocyte count 16,000/mm3
Serum lactate 0.9 mmol/L
Serum creatinine 1.1 mg/dL
What is most likely to confirm the diagnosis?
Q242
A 2-year-old boy is brought to the emergency department by his parents after they found him to be lethargic and febrile. His current symptoms started 1 week ago and initially consisted of a sore throat and a runny nose. He subsequently developed a fever and productive cough that has become worse over time. Notably, this patient has previously presented with pneumonia and gastroenteritis 8 times since he was born. On presentation, the patient's temperature is 103°F (39.4°C), blood pressure is 90/50 mmHg, pulse is 152/min, and respirations are 38/min. Based on clinical suspicion, an antibody panel is obtained and the results show low levels of IgG and IgA relative to the level of IgM. The expression of which of the following genes is most likely abnormal in this patient?
Q243
A 4-year-old boy is brought to the emergency department by his parents. He is lethargic and confused and has a severe headache, vomiting, and a high-grade fever since earlier that day. His mother reports that the child was doing well until 2 days ago when he developed a fever and green nasal discharge. The patient has a history of neonatal sepsis, meningococcemia at 18 months of age, and pneumococcal pneumonia at 2 and 3 years of age. His scheduled vaccinations are up to date. His blood pressure is 70/50 mm Hg, heart rate is 120/min, respiratory rate is 22/min, and temperature is 39.3°C (102.4°F). On examination, the child is lethargic and his skin is pale, with several petechiae over his buttocks. There is a purulent nasal discharge from both nostrils. The lungs are clear to auscultation bilaterally. Heart sounds are normal. There is marked neck rigidity. Cerebrospinal fluid analysis shows the following results:
Opening pressure 100 mm H2O
Appearance cloudy
Protein 500 mg/dL (5 g/L)
White blood cells 2500/μL (polymorphonuclear predominance)
Glucose 31 mg/dL (1.7 mmol/L)
Culture positive for N. meningitidis
Which of the following immunological processes is most likely to be impaired in this child?
Q244
A 6-year-old male who recently immigrated to the United States from Asia is admitted to the hospital with dyspnea. Physical exam reveals a gray pseudomembrane in the patient's oropharynx along with lymphadenopathy. The patient develops myocarditis and expires on hospital day 5. Which of the following would have prevented this patient's presentation and decline?
Bacteria US Medical PG Practice Questions and MCQs
Question 241: A 67-year-old man presents to the physician with profuse watery diarrhea along with fever and crampy abdominal pain. He has been taking an antibiotic course of cefixime for about a week to treat a respiratory tract infection. At the doctor’s office, his pulse is 112/min, the blood pressure is 100/66 mm Hg, the respirations are 22/min, and the temperature is 38.9°C (102.0°F). His oral mucosa appears dry and his abdomen is soft with vague diffuse tenderness. A digital rectal examination is normal. Laboratory studies show:
Hemoglobin 11.1 g/dL
Hematocrit 33%
Total leucocyte count 16,000/mm3
Serum lactate 0.9 mmol/L
Serum creatinine 1.1 mg/dL
What is most likely to confirm the diagnosis?
A. Identification of C. difficile toxin in stool (Correct Answer)
B. Colonoscopy
C. CT scan of the abdomen
D. Abdominal X-ray
E. Stool culture
Explanation: ***Identification of C. difficile toxin in stool***
- The patient's presentation with **profuse watery diarrhea**, fever, and abdominal pain following a course of **antibiotics (cefixime)** is highly suggestive of *Clostridioides difficile* infection (CDI).
- **Detecting *C. difficile* toxins A or B in stool** is the most reliable and definitive method to confirm the diagnosis of CDI.
*Colonoscopy*
- While colonoscopy can reveal **pseudomembranes** characteristic of severe *C. difficile* colitis, it is an **invasive procedure** and not the primary diagnostic tool.
- Endoscopy is typically reserved for cases where the diagnosis is uncertain despite positive toxin tests, or to assess severity when there is concern for complications like **toxic megacolon**.
*CT scan of the abdomen*
- A CT scan may show signs of colitis, such as **bowel wall thickening**, but it cannot definitively diagnose *C. difficile* infection.
- It is more useful for identifying **complications** like toxic megacolon, bowel perforation, or ascites, rather than initial diagnosis.
*Abdominal X-ray*
- An abdominal X-ray is primarily used to look for signs of **toxic megacolon** or **bowel perforation** (e.g., free air under the diaphragm).
- It is **not diagnostic for *C. difficile* infection itself** and would not confirm the presence of the pathogen or its toxins.
*Stool culture*
- A stool culture for common bacterial pathogens would likely be **negative** in a case of *C. difficile* infection, as *C. difficile* is a distinct entity.
- While *C. difficile* can be cultured, **toxin detection** is preferred for diagnosis because not all *C. difficile* strains produce toxins, and asymptomatic carriage can occur.
Question 242: A 2-year-old boy is brought to the emergency department by his parents after they found him to be lethargic and febrile. His current symptoms started 1 week ago and initially consisted of a sore throat and a runny nose. He subsequently developed a fever and productive cough that has become worse over time. Notably, this patient has previously presented with pneumonia and gastroenteritis 8 times since he was born. On presentation, the patient's temperature is 103°F (39.4°C), blood pressure is 90/50 mmHg, pulse is 152/min, and respirations are 38/min. Based on clinical suspicion, an antibody panel is obtained and the results show low levels of IgG and IgA relative to the level of IgM. The expression of which of the following genes is most likely abnormal in this patient?
A. STAT3
B. LYST
C. NADPH oxidase
D. CD40L (Correct Answer)
E. CD18
Explanation: ***CD40L***
- This patient's history of **recurrent infections** (pneumonia and gastroenteritis), fever, and persistent productive cough, coupled with **low IgG and IgA levels** but **normal or elevated IgM**, is characteristic of **hyper-IgM syndrome**.
- **Hyper-IgM syndrome** is most commonly caused by a genetic defect in **CD40L (CD154)** on T cells, which is essential for B cell class switching from IgM to other immunoglobulin isotopes (e.g., IgG, IgA, IgE).
*STAT3*
- Abnormalities in **STAT3** are associated with **hyper-IgE syndrome (Job's syndrome)**, characterized by recurrent skin abscesses, eczema, facial dysmorphism, and very high IgE levels, none of which are consistent with this patient's presentation.
- While it involves immune dysregulation and infections, the **immunoglobulin profile** (low IgG/IgA, normal/high IgM) does not fit hyper-IgE syndrome.
*LYST*
- Defects in the **LYST gene** cause **Chediak-Higashi syndrome**, characterized by partial oculocutaneous albinism, recurrent pyogenic infections, peripheral neuropathy, and giant lysosomes in phagocytes.
- The presented symptoms and **immunoglobulin abnormalities** do not align with the features of Chediak-Higashi syndrome.
*NADPH oxidase*
- Deficiencies in **NADPH oxidase** lead to **chronic granulomatous disease (CGD)**, where phagocytes cannot produce reactive oxygen species to kill certain microbes, resulting in recurrent severe bacterial and fungal infections and granuloma formation.
- While recurrent infections are present, the **humoral immunity profile** (low IgG/IgA, high IgM) is not typical for CGD.
*CD18*
- Defects in **CD18**, a component of the **beta-2 integrin LFA-1**, cause **leukocyte adhesion deficiency (LAD)**.
- LAD presents with recurrent bacterial infections, impaired wound healing, and a characteristic **leukocytosis** with **neutrophilia** due to the inability of leukocytes to extravasate to sites of infection. The immunoglobulin profile described is not associated with LAD.
Question 243: A 4-year-old boy is brought to the emergency department by his parents. He is lethargic and confused and has a severe headache, vomiting, and a high-grade fever since earlier that day. His mother reports that the child was doing well until 2 days ago when he developed a fever and green nasal discharge. The patient has a history of neonatal sepsis, meningococcemia at 18 months of age, and pneumococcal pneumonia at 2 and 3 years of age. His scheduled vaccinations are up to date. His blood pressure is 70/50 mm Hg, heart rate is 120/min, respiratory rate is 22/min, and temperature is 39.3°C (102.4°F). On examination, the child is lethargic and his skin is pale, with several petechiae over his buttocks. There is a purulent nasal discharge from both nostrils. The lungs are clear to auscultation bilaterally. Heart sounds are normal. There is marked neck rigidity. Cerebrospinal fluid analysis shows the following results:
Opening pressure 100 mm H2O
Appearance cloudy
Protein 500 mg/dL (5 g/L)
White blood cells 2500/μL (polymorphonuclear predominance)
Glucose 31 mg/dL (1.7 mmol/L)
Culture positive for N. meningitidis
Which of the following immunological processes is most likely to be impaired in this child?
A. Formation of C5-9 complex (Correct Answer)
B. Production of IL-2 by Th1 cells
C. Oxidative burst in macrophages
D. Activation of TCRs by MHC-II
E. Cleavage of C2 component of complement into C2a and C2b
Explanation: ***Formation of C5-9 complex***
- The recurrent infections with **encapsulated bacteria** like *N. meningitidis* and *S. pneumoniae*, along with recurrent **meningococcemia**, strongly suggest a deficiency in the **terminal complement pathway (C5-C9)**, which is crucial for forming the **membrane attack complex (MAC)**.
- The MAC is essential for **lysing gram-negative bacteria** such as *N. meningitidis*, and a defect here increases susceptibility to recurrent infections by this pathogen.
*Production of IL-2 by Th1 cells*
- **Interleukin-2 (IL-2)** is vital for **T-cell proliferation** and differentiation, particularly of **cytotoxic T lymphocytes (CTLs)**, important for viral and intracellular bacterial infections.
- While important for overall immune function, a deficiency in IL-2 production does not specifically or primarily explain recurrent encapsulated bacterial infections and meningococcemia.
*Oxidative burst in macrophages*
- The **oxidative burst** is critical for phagocytic cells (neutrophils and macrophages) to kill ingested pathogens, especially **catalase-positive bacteria** and fungi.
- A defect here (e.g., in **chronic granulomatous disease**) leads to recurrent severe bacterial and fungal infections, typically forming granulomas, which is not the specific pattern observed with recurrent meningococcal disease.
*Activation of TCRs by MHC-II*
- **T-cell receptor (TCR)** activation by **MHC-II** is central to **CD4+ helper T cell** function, essential for coordinating immune responses and antibody production.
- While critical for adaptive immunity, a defect here would lead to broader immune deficiencies, including impaired antibody responses and susceptibility to various pathogens, but does not preferentially predispose to recurrent *N. meningitidis* infections like terminal complement deficiency.
*Cleavage of C2 component of complement into C2a and C2b*
- The cleavage of **C2** is part of the **classical and lectin complement pathways**, which are important for opsonization and inflammation.
- **C2 deficiency** is often associated with recurrent pyogenic infections and autoimmune diseases (e.g., SLE), but not specifically with recurrent infections by *N. meningitidis*, which is more characteristic of **terminal complement component deficiencies**.
Question 244: A 6-year-old male who recently immigrated to the United States from Asia is admitted to the hospital with dyspnea. Physical exam reveals a gray pseudomembrane in the patient's oropharynx along with lymphadenopathy. The patient develops myocarditis and expires on hospital day 5. Which of the following would have prevented this patient's presentation and decline?
A. Increased CD4+ T cell count
B. Circulating IgG against AB exotoxin (Correct Answer)
C. Increased IgM preventing bacterial invasion
D. Improved IgE release from mast cells
E. Secretory IgA against viral proteins
Explanation: ***Circulating IgG against AB exotoxin***
- This clinical presentation (gray pseudomembrane, dyspnea, lymphadenopathy, and myocarditis) is classic for **diphtheria**, caused by **Corynebacterium diphtheriae**.
- The severe manifestations, including myocarditis, are due to the **diphtheria exotoxin**, an AB toxin. **Circulating IgG antibodies** against this toxin would neutralize it, preventing its toxic effects and the ensuing severe disease.
*Increased CD4+ T cell count*
- While T cells are crucial for overall immune function, diphtheria's pathogenicity is primarily mediated by its **exotoxin**, not directly by bacterial invasion or intracellular survival requiring a strong cellular immune response.
- An increased CD4+ T cell count alone would not directly neutralize the circulating diphtheria toxin, which is the key to preventing the severe systemic complications like myocarditis.
*Increased IgM preventing bacterial invasion*
- IgM antibodies are important in the **primary immune response** and can agglutinate bacteria, but they are generally less effective at neutralizing toxins compared to IgG.
- The critical determinant of severe diphtheria is the **systemic spread of the exotoxin**, not simply bacterial invasion, and IgM would be less effective in preventing toxin-mediated damage.
*Improved IgE release from mast cells*
- IgE antibodies are primarily involved in **allergic reactions** and defense against parasites.
- They play no significant role in immunity against bacterial infections like diphtheria or in neutralizing bacterial exotoxins.
*Secretory IgA against viral proteins*
- Secretory IgA primarily functions in **mucosal immunity** to prevent the adherence and invasion of pathogens at mucosal surfaces.
- It is effective against **viral and bacterial pathogens** at mucosal sites but would not prevent the systemic effects of a bacterial exotoxin that has already been absorbed, nor would it specifically target viral proteins in a bacterial infection.
