Microbiome and immune system interactions US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Microbiome and immune system interactions. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Microbiome and immune system interactions US Medical PG Question 1: A 72-year-old woman presents to the clinic complaining of diarrhea for the past week. She mentions intense fatigue and intermittent, cramping abdominal pain. She has not noticed any blood in her stool. She recalls an episode of pneumonia last month for which she was hospitalized and treated with antibiotics. She has traveled recently to Florida to visit her family and friends. Her past medical history is significant for hypertension, peptic ulcer disease, and hypercholesterolemia for which she takes losartan, esomeprazole, and atorvastatin. She also has osteoporosis, for which she takes calcium and vitamin D and occasional constipation for which she takes an over the counter laxative as needed. Physical examination shows lower abdominal tenderness but is otherwise insignificant. Blood pressure is 110/70 mm Hg, pulse is 80/min, and respiratory rate is 18/min. Stool testing is performed and reveals the presence of anaerobic, gram-positive bacilli. Which of the following increased this patient’s risk of developing this clinical presentation?
- A. Hypercholesterolemia treated with atorvastatin
- B. Constipation treated with laxatives
- C. Osteoporosis treated with calcium and vitamin D
- D. Peptic ulcer disease treated with esomeprazole
- E. Recent antibiotic use for pneumonia treatment (Correct Answer)
Microbiome and immune system interactions Explanation: ***Recent antibiotic use for pneumonia treatment***
- **Antibiotic exposure** is the single most important risk factor for *Clostridioides difficile* infection (CDI), present in approximately 70% of cases.
- Antibiotics disrupt the normal protective gut microbiota, eliminating competitive bacteria and allowing *C. difficile* spores to germinate, colonize, and produce toxins.
- The patient's recent hospitalization and antibiotic treatment for pneumonia directly precipitated this infection by creating an ecological niche for *C. difficile* overgrowth.
- Common culprit antibiotics include fluoroquinolones, clindamycin, cephalosporins, and penicillins.
*Peptic ulcer disease treated with esomeprazole*
- **Proton pump inhibitors (PPIs)** like esomeprazole are an independent risk factor for CDI, increasing risk approximately 2-3 fold.
- PPIs reduce gastric acid production, which normally serves as a defense mechanism against ingested *C. difficile* spores.
- However, PPIs alone do not typically cause CDI without concurrent disruption of gut flora (usually by antibiotics).
- While this is a contributory risk factor in this patient, it is not the primary cause.
*Hypercholesterolemia treated with atorvastatin*
- **Statins** like atorvastatin have no established association with increased risk of *Clostridioides difficile* infection.
- They work by inhibiting HMG-CoA reductase to lower cholesterol and do not affect gastric pH or gut microbiota composition.
*Constipation treated with laxatives*
- Occasional **over-the-counter laxative use** is not a risk factor for *Clostridioides difficile* infection.
- While laxatives affect gut motility, they do not disrupt the protective gut microbiota or increase susceptibility to CDI.
*Osteoporosis treated with calcium and vitamin D*
- **Calcium and vitamin D supplementation** has no association with increased risk of *Clostridioides difficile* infection.
- These supplements support bone health and calcium metabolism without affecting gut flora or gastric acid production.
Microbiome and immune system interactions US Medical PG Question 2: A medical student is reading about a specific type of T cells that plays an important role in immunologic tolerance. Most of these cells develop in the thymus, but some of them also develop in peripheral lymphoid organs. Usually, they are CD4+ cells and also express CD25 molecules. The functions of these cells are dependent on forkhead box P3 (Foxp3). Their function is to block the activation of lymphocytes that could react with self-antigens in a potentially harmful manner. Which of the following interleukins is secreted by these cells?
- A. Interleukin-6
- B. Interleukin-10 (Correct Answer)
- C. Interleukin-2
- D. Interleukin-12
- E. Interleukin-17
Microbiome and immune system interactions Explanation: ***Interleukin-10***
- The description points to **regulatory T cells (Tregs)**, which are CD4+, CD25+, and Foxp3+. A key function of Tregs in maintaining **immunologic tolerance** is the secretion of **IL-10** and TGF-β.
- **IL-10** is a potent **anti-inflammatory cytokine** that suppresses the activation and proliferation of various immune cells, including T cells, macrophages, and dendritic cells, thereby preventing immune responses against self-antigens.
*Interleukin-6*
- **IL-6** is a **pro-inflammatory cytokine** primarily involved in the acute phase response, hematopoiesis, and differentiation of Th17 cells, which is contrary to the immunosuppressive role of Tregs.
- It promotes inflammation and is secreted by various cells, including macrophages, T cells, and B cells, but not typically by Tregs as part of their suppressive function.
*Interleukin-2*
- **IL-2** is an important **T cell growth factor**, crucial for the proliferation and differentiation of T cells, including Tregs themselves, but it is primarily secreted by activated helper T cells (Th1).
- While Tregs express the **CD25 (IL-2 receptor alpha chain)** and require IL-2 for their survival and function, they do not typically secrete IL-2 as their primary immunomodulatory cytokine.
*Interleukin-12*
- **IL-12** is a cytokine mainly produced by antigen-presenting cells (APCs) like dendritic cells and macrophages, and plays a critical role in promoting **Th1 differentiation** and cell-mediated immunity.
- It is a **pro-inflammatory cytokine** that drives immune responses, which is opposite to the suppressive function described for these cells.
*Interleukin-17*
- **IL-17** is the signature cytokine of **Th17 cells**, which are primarily involved in host defense against extracellular bacteria and fungi, but also play a significant role in mediating autoimmune diseases.
- It is a **pro-inflammatory cytokine** and its production is antagonistic to the immunosuppressive function of regulatory T cells.
Microbiome and immune system interactions US Medical PG Question 3: A 21-year-old G3P2 woman presents to her obstetrician at 6 weeks gestation for routine prenatal care. Her past medical history includes obesity and gestational diabetes. She has had two spontaneous vaginal deliveries at term. One infant was macrosomic with hypoglycemia, but otherwise, she has had no complications. Her physician informs her that she must start taking a multivitamin with folic acid daily. The defect that folic acid supplementation protects against arises in tissue that is derived from which germ cell layer?
- A. Mesoderm
- B. Notochord
- C. Endoderm
- D. Mesenchyme
- E. Ectoderm (Correct Answer)
Microbiome and immune system interactions Explanation: ***Ectoderm***
- Folic acid supplementation primarily prevents **neural tube defects**, such as **spina bifida** and **anencephaly**.
- The **neural tube**, which forms the brain and spinal cord, is derived from the **ectoderm**.
*Mesoderm*
- The **mesoderm** gives rise to structures like muscle, bone, connective tissue, and the cardiovascular system.
- Defects in mesodermal development are not primarily prevented by folic acid supplementation.
*Notochord*
- The **notochord** is a transient embryonic structure that induces the formation of the neural plate from the ectoderm.
- While critical for nervous system development, it is not a germ cell layer itself, and defects in its development are not directly prevented by folic acid.
*Endoderm*
- The **endoderm** forms the lining of the gastrointestinal and respiratory tracts, as well as glands like the thyroid and pancreas.
- Anomalies of these internal organs are not the primary target of folic acid supplementation.
*Mesenchyme*
- **Mesenchyme** is embryonic connective tissue, largely derived from the mesoderm, but can also come from neural crest (ectoderm).
- It differentiates into connective tissues, blood, and lymphatic vessels; neural tube defects are not considered mesenchymal in origin.
Microbiome and immune system interactions US Medical PG Question 4: A 25-year-old man presents to the physician with 2 days of profuse, watery diarrhea. He denies seeing blood or mucus in the stools. On further questioning, he reveals that he eats a well-balanced diet and generally prepares his meals at home. He remembers having some shellfish from a street vendor 3 days ago. He takes no medications. His past medical history is unremarkable. Which of the following mechanisms most likely accounts for this patient’s illness?
- A. Tyrosine kinase phosphorylation
- B. ADP-ribosylation of Gs protein (Correct Answer)
- C. Tyrosine kinase dephosphorylation
- D. Osmotic effect of intestinal contents
- E. Inflammation of the gastrointestinal wall
Microbiome and immune system interactions Explanation: ***ADP-ribosylation of Gs protein***
- The patient's history of consuming **shellfish from a street vendor** and presenting with **profuse, watery diarrhea** strongly suggests **cholera**.
- **Cholera toxin** works by irreversibly ADP-ribosylating the **Gs alpha subunit**, leading to constitutive activation of **adenylate cyclase** and increased intracellular **cAMP**, which causes excessive fluid and electrolyte secretion into the intestinal lumen.
*Tyrosine kinase phosphorylation*
- This mechanism is characteristic of signaling pathways involved in growth and differentiation, often seen with **growth factor receptors**, and is not the primary cause of acute, watery diarrhea from food poisoning.
- While some bacterial toxins can affect intracellular signaling, **tyrosine kinase phosphorylation** is not the direct mechanism for the massive fluid loss seen in cholera.
*Tyrosine kinase dephosphorylation*
- This process typically downregulates cell signaling pathways, which would likely **decrease** cellular activity, rather than trigger the profuse secretion seen in this patient's presentation.
- It is not a known mechanism for the pathogenesis of infectious diarrheal diseases such as cholera.
*Osmotic effect of intestinal contents*
- While **osmotic diarrhea** is characterized by the presence of non-absorbable solutes in the gut lumen, drawing water in, the history here points more to an actively secreted fluid loss.
- The sheer volume and rapid onset of the diarrhea suggest an active secretory mechanism rather than simply an osmotic effect from malabsorption.
*Inflammation of the gastrointestinal wall*
- **Inflammatory diarrhea** typically involves blood or mucus in the stool, fever, and abdominal pain, none of which are reported by the patient.
- The patient's "profuse, watery" diarrhea without blood or mucus signifies a non-inflammatory, secretory etiology often caused by toxins.
Microbiome and immune system interactions US Medical PG Question 5: A 24-year-old man comes to the physician with a 2-day history of fever, crampy abdominal pain, and blood-tinged diarrhea. He recently returned from a trip to Mexico. His temperature is 38.2°C (100.8°F). Abdominal examination shows diffuse tenderness to palpation; bowel sounds are hyperactive. Stool cultures grow nonlactose fermenting, oxidase-negative, gram-negative rods that do not produce hydrogen sulfide on triple sugar iron agar. Which of the following processes is most likely involved in the pathogenesis of this patient's condition?
- A. Dissemination via bloodstream
- B. Overactivation of adenylate cyclase
- C. Flagella-mediated gut colonization
- D. Invasion of colonic microfold cells
- E. Inhibition of host cytoskeleton organization (Correct Answer)
Microbiome and immune system interactions Explanation: ***Inhibition of host cytoskeleton organization***
- The patient's symptoms (fever, crampy abdominal pain, blood-tinged diarrhea) and the microbiological findings (**nonlactose fermenting, oxidase-negative, gram-negative rods** that do not produce hydrogen sulfide) are characteristic of **Shigella infection**.
- **Shigella** invades colonic epithelial cells and manipulates the host cell's **actin cytoskeleton** through effector proteins (IpaA, IpaB, IpaC) delivered via a **Type III secretion system**.
- This cytoskeletal disruption enables **intracellular movement** via actin-based motility and **cell-to-cell spread**, allowing Shigella to evade immune defenses while causing characteristic inflammatory dysentery.
*Dissemination via bloodstream*
- While some bacterial infections cause bacteremia, **Shigella** infections are typically localized to the **gastrointestinal tract** and do not commonly disseminate systemically via the bloodstream.
- **Bacteremia** due to *Shigella* is rare and usually occurs only in immunocompromised individuals or young children with severe disease.
*Overactivation of adenylate cyclase*
- **Overactivation of adenylate cyclase** producing **cyclic AMP** and leading to **secretory diarrhea** is characteristic of toxins like **cholera toxin** or **heat-labile enterotoxin of E. coli**.
- **Shigella** primarily causes **inflammatory dysentery** through mucosal invasion and damage, not through this mechanism of fluid secretion.
*Flagella-mediated gut colonization*
- Many bacteria use **flagella** for motility and colonization, but **Shigella** species are notably **non-motile** and **lack flagella**.
- Their pathogenesis relies on invasion and intracellular spread rather than flagella-driven colonization.
*Invasion of colonic microfold cells*
- While **Shigella does initially invade through M cells (microfold cells)** in the colonic epithelium to gain entry into the lamina propria, this is just the **initial entry step**, not the primary pathogenic mechanism that causes disease.
- The key pathogenic process that leads to the characteristic symptoms is the **disruption of the host cytoskeleton** that enables intracellular replication and lateral spread through epithelial cells, causing the inflammatory dysentery seen in this patient.
Microbiome and immune system interactions US Medical PG Question 6: A 21-year-old woman comes to the physician because of a 4-day history of abdominal cramps and bloody diarrhea 5 times per day. Her symptoms began after she ate an egg sandwich from a restaurant. Her vital signs are within normal limits. Physical examination shows diffuse abdominal tenderness. Stool culture shows gram-negative rods that produce hydrogen sulfide and do not ferment lactose. Which of the following effects is most likely to occur if she receives antibiotic therapy?
- A. Orange discoloration of bodily fluids
- B. Pruritic maculopapular rash on the extensor surface
- C. Self-limiting systemic inflammatory response
- D. Prolonged fecal excretion of the pathogen (Correct Answer)
- E. Thrombocytopenia and hemolytic anemia
Microbiome and immune system interactions Explanation: ***Prolonged fecal excretion of the pathogen***
- The patient's symptoms (abdominal cramps, bloody diarrhea after eating an egg sandwich) and stool culture results (gram-negative rods, hydrogen sulfide producers, non-lactose fermenting) are highly suggestive of **Salmonella enterica** infection.
- Antibiotic treatment for non-typhoidal Salmonella gastroenteritis typically **prolongs fecal excretion** and does not shorten the illness, reserving antibiotics for severe cases or immunocompromised individuals.
*Orange discoloration of bodily fluids*
- **Orange discoloration of bodily fluids** (urine, sweat, tears) is a known side effect of **rifampin**, an antibiotic primarily used for tuberculosis and some bacterial meningitides.
- Rifampin is not indicated nor commonly used for Salmonella gastroenteritis.
*Pruritic maculopapular rash on the extensor surface*
- A **pruritic maculopapular rash on the extensor surfaces** is a common presentation of drug reactions, often associated with **penicillins** or **cephalosporins**, especially in viral infections (e.g., amoxicillin rash in mononucleosis).
- This is a general antibiotic side effect and not specifically linked to the outcome of treating Salmonella.
*Self-limiting systemic inflammatory response*
- A self-limiting systemic inflammatory response could be a general reaction to an active infection or a drug, but it's not the most likely or specific outcome of **antibiotic therapy in Salmonella gastroenteritis**.
- Worsening of symptoms can occur in some cases due to toxemia from bacterial lysis (e.g., Jarisch-Herxheimer reaction), but "self-limiting systemic inflammatory response" is too generic for this specific scenario.
*Thrombocytopenia and hemolytic anemia*
- **Thrombocytopenia and hemolytic anemia** in the setting of diarrheal illness strongly suggest **hemolytic uremic syndrome (HUS)**, which is typically associated with **Shiga toxin-producing E. coli** (STEC), particularly E. coli O157:H7.
- While Salmonella can cause severe disease, HUS is not a typical complication of its treatment, and antibiotics are often avoided in STEC infections due to increased risk of HUS.
Microbiome and immune system interactions US Medical PG Question 7: A 28-year-old male presents to his primary care physician with complaints of intermittent abdominal pain and alternating bouts of constipation and diarrhea. His medical chart is not significant for any past medical problems or prior surgeries. He is not prescribed any current medications. Which of the following questions would be the most useful next question in eliciting further history from this patient?
- A. "Does the diarrhea typically precede the constipation, or vice-versa?"
- B. "Is the diarrhea foul-smelling?"
- C. "Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life"
- D. "Are the symptoms worse in the morning or at night?"
- E. "Can you tell me more about the symptoms you have been experiencing?" (Correct Answer)
Microbiome and immune system interactions Explanation: ***Can you tell me more about the symptoms you have been experiencing?***
- This **open-ended question** encourages the patient to provide a **comprehensive narrative** of their symptoms, including details about onset, frequency, duration, alleviating/aggravating factors, and associated symptoms, which is crucial for diagnosis.
- In a patient presenting with vague, intermittent symptoms like alternating constipation and diarrhea, allowing them to elaborate freely can reveal important clues that might not be captured by more targeted questions.
*Does the diarrhea typically precede the constipation, or vice-versa?*
- While knowing the sequence of symptoms can be helpful in understanding the **pattern of bowel dysfunction**, it is a very specific question that might overlook other important aspects of the patient's experience.
- It prematurely narrows the focus without first obtaining a broad understanding of the patient's overall symptomatic picture.
*Is the diarrhea foul-smelling?*
- Foul-smelling diarrhea can indicate **malabsorption** or **bacterial overgrowth**, which are important to consider in some gastrointestinal conditions.
- However, this is a **specific symptom inquiry** that should follow a more general exploration of the patient's symptoms, as it may not be relevant if other crucial details are missed.
*Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life*
- Quantifying pain intensity is useful for assessing the **severity of discomfort** and monitoring changes over time.
- However, for a patient with intermittent rather than acute, severe pain, understanding the **character, location, and triggers** of the pain is often more diagnostically valuable than just a numerical rating initially.
*Are the symptoms worse in the morning or at night?*
- Diurnal variation can be relevant in certain conditions, such as inflammatory bowel diseases where nocturnal symptoms might be more concerning, or functional disorders whose symptoms might be stress-related.
- This is another **specific question** that should come after gathering a more complete initial picture of the patient's symptoms to ensure no key information is overlooked.
Microbiome and immune system interactions US Medical PG Question 8: An immunology expert is explaining the functions of macrophages to biology students. He describes a hypothetical case scenario as follows: a potentially harmful gram-negative bacillus encounters a macrophage in the tissues. The Toll-like receptor (TLR) on the macrophage recognizes the bacterial lipopolysaccharide (LPS). The macrophage is activated by the binding of TLR with bacterial LPS and by interferon-γ (IFN-γ). Which of the following cytokines is most likely to be secreted by the activated macrophage?
- A. Interleukin-4 (IL-4)
- B. Interleukin-1 receptor antagonist (IL-1RA)
- C. Interleukin-10 (IL-10)
- D. Interleukin-2 (IL-2)
- E. Interleukin-12 (IL-12) (Correct Answer)
Microbiome and immune system interactions Explanation: ***Interleukin-12 (IL-12)***
- Macrophage activation by **LPS (a PAMP recognized by TLR4)** and **IFN-γ (a macrophage-activating cytokine)** leads to the secretion of pro-inflammatory cytokines, with **IL-12** being a key mediator.
- **IL-12** is crucial for promoting **Th1 differentiation** and enhancing **NK cell activity**, thus linking innate and adaptive immunity against intracellular pathogens and tumor cells.
*Interleukin-4 (IL-4)*
- **IL-4** is primarily secreted by **Th2 cells, mast cells, and basophils**, and is involved in **allergic responses** and humoral immunity.
- It promotes **Th2 differentiation** and IgE production, which is not the primary response to a Gram-negative bacterial encounter as described.
*Interleukin-1 receptor antagonist (IL-1RA)*
- **IL-1RA** is an **anti-inflammatory cytokine** that blocks the effects of IL-1α and IL-1β, thereby downregulating inflammatory responses.
- While it can be produced by macrophages, initial activation by LPS and IFN-γ would trigger pro-inflammatory mediators before the release of antagonists to temper the response.
*Interleukin-10 (IL-10)*
- **IL-10** is a potent **anti-inflammatory cytokine** that suppresses the immune response, particularly by inhibiting cytokine production by macrophages and Th1 cells.
- Macrophage activation in response to a pathogen initially leads to pro-inflammatory cytokine secretion, with IL-10 typically arising later to resolve the inflammation.
*Interleukin-2 (IL-2)*
- **IL-2** is predominantly produced by **T lymphocytes**, especially **Th1 cells**, upon activation.
- Its main roles include **T cell proliferation**, differentiation, and maintenance of regulatory T cells, rather than being a primary cytokine secreted by activated macrophages in this context.
Microbiome and immune system interactions US Medical PG Question 9: A 29-year-old woman presents with shortness of breath and chest pain for the past week. She says her chest pain is aggravated by deep breathing and she becomes short of breath while walking upstairs in her home. She also has been feeling feverish and fatigued for the past week, as well as pain in her wrists, hands, and left knee. Review of systems is significant for a 4.5 kg (10.0 lb) weight loss over the previous month. Past medical history consists of 2 spontaneous abortions, both of which occurred in the 1st trimester. On physical examination, there is a pink rash present over her face, which is aggravated by exposure to sunlight. There are decreased breath sounds on the right. A chest radiograph is performed which reveals evidence of a right pleural effusion. Serum ANA and anti-dsDNA autoantibodies are positive. Urinalysis is unremarkable. Errors with which of the following is most likely to lead to her disease?
- A. Intrinsic pathway
- B. Cytotoxic CD8+ T cells
- C. Bcl-2 overexpression
- D. Necrosis
- E. Fas-FasL interaction (Correct Answer)
Microbiome and immune system interactions Explanation: ***Fas-FasL interaction***
- This patient presents with multiple symptoms suggestive of **systemic lupus erythematosus (SLE)**, including photosensitive rash, arthritis, serositis (pleural effusion), weight loss, recurrent spontaneous abortions, and positive ANA/anti-dsDNA.
- Genetic defects in the **Fas** or **Fas ligand (FasL) apoptotic pathway** are strongly associated with increased risk of autoimmunity, particularly SLE, as they impair the deletion of autoreactive lymphocytes.
*Intrinsic pathway*
- The intrinsic apoptotic pathway is primarily activated by intracellular stress and mitochondria-dependent signals.
- While essential for cell death, defects in the intrinsic pathway are not as specifically implicated in the pathogenesis of SLE as the Fas-FasL (extrinsic) pathway.
*Cytotoxic CD8+ T cells*
- **CD8+ T cells** are primarily involved in killing virally infected or cancerous cells and are crucial for cellular immunity.
- While involved in some autoimmune processes, their dysfunction is not the primary or most common error leading to the development of SLE, which is largely mediated by autoantibodies.
*Bcl-2 overexpression*
- **Bcl-2** is an anti-apoptotic protein, and its overexpression inhibits apoptosis.
- While Bcl-2 overexpression could theoretically prevent the deletion of autoreactive cells, specific defects in the direct Fas-FasL signaling pathway are more directly and commonly linked to the immune dysregulation seen in SLE.
*Necrosis*
- **Necrosis** is an uncontrolled form of cell death often associated with inflammation and tissue damage.
- While certainly present in tissues affected by SLE due to inflammation, necrosis itself is a consequence of the disease process, not an upstream error in cell death regulation that leads to the autoimmunity of SLE.
Microbiome and immune system interactions US Medical PG Question 10: A 21-year-old woman comes to the physician because of a 1-week history of white discoloration of the tongue. She has had similar, recurrent episodes over the past 5 years. Examination shows white plaques on the tongue that easily scrape off and thick, cracked fingernails with white discoloration. KOH preparation of a tongue scraping shows budding yeasts with pseudohyphae. This patient's condition is most likely caused by decreased activity of which of the following?
- A. Neutrophils
- B. Complement C1–4
- C. B cells
- D. T cells (Correct Answer)
- E. Complement C5–9
Microbiome and immune system interactions Explanation: ***T cells***
- The recurrent oral **candidiasis** with **pseudohyphae** (thrush) and **onychomycosis** (thick, cracked fingernails) suggests a defect in **cell-mediated immunity**, which is primarily mediated by **T cells**.
- **T cells** are crucial for controlling fungal infections, particularly *Candida* species, and their decreased activity makes individuals susceptible to **recurrent mucocutaneous candidiasis** (affecting skin, nails, and mucous membranes).
*Neutrophils*
- Defective **neutrophil** function would lead to **invasive or disseminated candidiasis** (bloodstream, deep tissues) rather than the chronic mucocutaneous pattern seen here.
- Neutrophil defects also cause recurrent **bacterial infections**, especially from *Staphylococcus* and *Pseudomonas* species.
*Complement C1–4*
- Deficiencies in early **complement components** (C1-C4) are associated with an increased risk of encapsulated **bacterial infections** and **immune complex disorders** like lupus.
- These deficiencies are not typically linked to recurrent fungal infections such as candidiasis.
*B cells*
- **B cells** are responsible for **humoral immunity** (antibody production), and their deficiency would lead to recurrent **bacterial and viral infections**, particularly those affecting the respiratory tract.
- While antibodies can play a supportive role, they are not the primary defense against localized candidal infections.
*Complement C5–9*
- Deficiencies in late **complement components** (C5-C9), part of the **membrane attack complex (MAC)**, primarily increase susceptibility to recurrent **Neisseria** infections (*N. meningitidis* and *N. gonorrhoeae*).
- These components are not directly involved in immunity against *Candida* infections.
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