Bacterial Skin Infections Practice Questions

Q: What condition is characterized by a malignant pustule?

Anthrax. **Explanation:** **Anthrax (Option D)** is the correct answer. The term **"Malignant Pustule"** is a clinical misnomer used to describe the cutaneous manifestation of infection by *Bacillus anthracis*. Despite the name, it is neither malignant (cancerous) nor a true pustule (as it lacks pus). It typically begins as a painless, pruritic papule that evolves into a vesicle and eventually forms a characteristic **painless, black necrotic eschar** surrounded by significant non-pitting edema. The lesion is "malignant" only in its historical potential to cause fatal septicemia if untreated. **Incorrect Options:** * **Melanoma (Option A):** While melanoma is a malignant skin cancer that can present as a dark or black lesion, it does not present as an acute "pustule" or eschar and follows different clinical progression (ABCDE criteria). * **Gas Gangrene (Option B):** Caused by *Clostridium perfringens*, this presents with crepitus (gas in tissues), foul-smelling discharge, and rapid muscle necrosis, rather than a localized black eschar. * **Ovarian Tumor (Option C):** This is a systemic malignancy and has no clinical association with the term "malignant pustule." **High-Yield Clinical Pearls for NEET-PG:** * **Causative Agent:** *Bacillus anthracis* (Gram-positive, spore-forming, aerobic rod). * **Pathogenesis:** Mediated by toxins—**Edema Factor** (increases cAMP) and **Lethal Factor** (zinc metalloprotease). * **Microscopy:** Large "box-car" shaped bacilli; colonies on agar show a **"Medusa head" appearance**. * **Occupational Hazard:** Also known as **Hide-porter’s disease** or **Wool-sorter’s disease** due to exposure to infected animal products. * **Drug of Choice:** Ciprofloxacin or Doxycycline.

Q: Ritter's disease is caused by which bacterium?

Staphylococcus aureus. **Explanation:** **Ritter’s disease**, also known as **Staphylococcal Scalded Skin Syndrome (SSSS)**, is caused by **Staphylococcus aureus**. The pathogenesis involves the production of **exfoliative toxins (ET-A and ET-B)** by specific phage group II strains of the bacteria. These toxins act as serine proteases that target and cleave **Desmoglein-1**, a cell-adhesion molecule located in the *stratum granulosum* of the epidermis. This leads to widespread blistering and denudation of the skin, typically in neonates and young children. **Analysis of Options:** * **Staphylococcus aureus (Correct):** The primary causative agent. It produces the epidermolytic toxins responsible for the characteristic "scalded" appearance. * **Staphylococcus epidermidis:** A common skin commensal. While it can cause infections related to prosthetic devices or catheters, it does not produce exfoliative toxins. * **Staphylococcus albus:** An older nomenclature for *S. epidermidis*; it is non-pathogenic in the context of Ritter’s disease. * **Staphylococcus saprophyticus:** Primarily associated with urinary tract infections (UTIs) in young, sexually active females ("honeymoon cystitis") and does not cause skin exfoliation. **High-Yield Clinical Pearls for NEET-PG:** * **Nikolsky Sign:** Positive (gentle pressure on the skin causes exfoliation). * **Site of Cleavage:** Subcorneal/Granular layer (unlike Pemphigus Vulgaris, which is suprabasal). * **Culture:** In SSSS, skin blisters are typically **sterile** because the damage is toxin-mediated from a distant site (e.g., nasopharynx or conjunctiva). * **Bullous Impetigo:** A localized form of SSSS where the bacteria are present in the blister fluid. * **Treatment:** Intravenous antibiotics (e.g., Cloxacillin/Nafcillin) and supportive fluid care.

Q: What is the recommended duration for the treatment of multibacillary leprosy?

12 months. **Explanation:** The treatment of Leprosy follows the World Health Organization (WHO) Multi-Drug Therapy (MDT) guidelines. The correct duration for **Multibacillary (MB) Leprosy** is **12 months**. **1. Why 12 months is correct:** In 1998, the WHO shortened the treatment duration for MB leprosy from 24 months to 12 months. This change was based on clinical trials showing that a 12-month regimen of Rifampicin, Clofazimine, and Dapsone was sufficient to achieve a cure and prevent relapse, while significantly improving patient compliance. **2. Analysis of Incorrect Options:** * **24 months (Option A):** This was the standard duration for MB leprosy prior to 1998. While some clinicians still consider it for patients with a very high Bacterial Index (BI >4+), it is no longer the standard WHO recommendation. * **18 months (Option B):** There is no standard WHO regimen for leprosy that lasts 18 months; this is a distractor. * **6 months (Option D):** This is the standard duration for **Paucibacillary (PB) Leprosy**, which involves fewer lesions and a lower bacterial load. **High-Yield Clinical Pearls for NEET-PG:** * **MB MDT Regimen:** Rifampicin (600mg once monthly, supervised), Clofazimine (300mg once monthly supervised + 50mg daily), and Dapsone (100mg daily). * **PB MDT Regimen:** Rifampicin (600mg once monthly) and Dapsone (100mg daily) for 6 months. * **Classification:** MB is defined by >5 skin lesions, >1 nerve involvement, or a positive skin smear. PB is 1–5 lesions and only 1 nerve involved. * **Accompanied MDT (A-MDT):** Providing the full course of treatment at the first visit to ensure completion in mobile populations.

Q: Hot tub folliculitis is caused by which organism?

Pseudomonas aeruginosa. **Explanation:** **Hot tub folliculitis** (also known as *Pseudomonas* folliculitis) is a skin infection of the hair follicles caused by **Pseudomonas aeruginosa**. This Gram-negative bacterium thrives in warm, alkaline environments, such as inadequately chlorinated hot tubs, whirlpools, or heated swimming pools. The organism penetrates the hair follicles, leading to an itchy, papulopustular eruption that typically appears 8 to 48 hours after exposure. The rash is most prominent in areas covered by swimwear, which traps the contaminated water against the skin. **Analysis of Incorrect Options:** * **B. Pityrosporum ovale (Malassezia):** This is a yeast that causes **Pityrosporum folliculitis**, characterized by monomorphic, itchy papulopustules on the back, chest, and shoulders. It is not associated with hot tubs. * **C. Aeromonas hydrophila:** This organism is typically associated with skin infections (like cellulitis or necrotizing fasciitis) following exposure to **freshwater** (lakes or rivers) or medicinal leeches. * **D. Vibrio vulnificans:** This is a halophilic (salt-loving) bacterium found in **marine environments**. It causes severe wound infections or septicemia, often following exposure to seawater or consumption of raw seafood. **Clinical Pearls for NEET-PG:** * **Self-limiting:** Most cases of hot tub folliculitis resolve spontaneously within 7–10 days without treatment. * **Treatment:** If severe or persistent, oral **Ciprofloxacin** (an anti-pseudomonal fluoroquinolone) is the drug of choice. * **Green Nail Syndrome:** Another dermatological manifestation of *Pseudomonas* is chloronychia (greenish discoloration of the nail plate). * **Ecthyma Gangrenosum:** A life-threatening *Pseudomonas* infection seen in immunocompromised/neutropenic patients, presenting as necrotic ulcers with a central black eschar.

Q: Coral-red fluorescence with Wood's light strongly suggests which diagnosis?

Erythrasma. ### Explanation **Correct Answer: D. Erythrasma** **Medical Concept:** Erythrasma is a superficial bacterial infection caused by **_Corynebacterium minutissimum_**. This organism produces **coproporphyrin III**, which accumulates in the stratum corneum. When exposed to **Wood’s light (365 nm)**, this porphyrin emits a pathognomonic **coral-red fluorescence**. Clinically, it presents as well-demarcated, reddish-brown, macerated plaques, typically in intertriginous areas like the axilla or groin. **Analysis of Incorrect Options:** * **A. Ash leaf macules:** These are hypopigmented macules seen in Tuberous Sclerosis. Under Wood’s light, they show **accentuation** (becoming more visible due to loss of melanin) but do not fluoresce. * **B. Acanthosis nigricans:** This is a metabolic/paraneoplastic marker characterized by velvety hyperpigmentation. It does not involve porphyrin-producing bacteria and shows no specific fluorescence. * **C. Erysipeloid:** Caused by *Erysipelothrix rhusiopathiae*, this is a deep-seated cellulitis-like infection (usually occupational). It does not produce surface porphyrins and is negative under Wood’s light. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of Choice:** Topical or oral **Erythromycin** (Clarithromycin is also highly effective). * **Wood’s Light Summary:** * **Golden Yellow:** Tinea versicolor (*Malassezia*). * **Bright Green:** Tinea capitis (*Microsporum*). * **Aqua Blue/White:** Pseudomonas (Pyoverdin). * **Pale White:** Vitiligo (shows total depigmentation). * **Differential Diagnosis:** Often confused with Tinea cruris; however, Erythrasma lacks a raised border and central clearing.

Q: Erythrasma is caused by which microorganism?

Corynebacterium. **Explanation:** **1. Why Corynebacterium is Correct:** Erythrasma is a superficial bacterial infection caused specifically by ***Corynebacterium minutissimum***, a Gram-positive, non-spore-forming bacillus. It thrives in warm, moist areas (intertriginous sites) like the axilla, groin, and toe webs. The hallmark of this condition is the production of **porphyrins** by the bacteria. When examined under **Wood’s lamp**, these porphyrins emit a characteristic **coral-red fluorescence**, which is a classic NEET-PG clinical finding. **2. Why Incorrect Options are Wrong:** * **Staphylococcus:** While *S. aureus* is the most common cause of pyodermas like impetigo, folliculitis, and furuncles, it does not cause the macular, reddish-brown lesions seen in erythrasma. * **Streptococci:** Group A Streptococci typically cause deeper or more inflammatory infections such as cellulitis, erysipelas, or ecthyma. * **Viruses:** Viral skin infections usually present as vesicles (Herpes), warts (HPV), or umbilicated papules (Molluscum), which are clinically distinct from the dry, scaly plaques of erythrasma. **3. Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Well-demarcated, reddish-brown, "cigarette-paper" wrinkled skin in intertriginous areas. * **Diagnostic Gold Standard:** Wood’s lamp examination (Coral-red fluorescence). * **Microscopy:** KOH mount is used to rule out Tinea cruris (Erythrasma will show no hyphae). * **Treatment of Choice:** Topical **Erythromycin** or Clindamycin. For extensive cases, oral Erythromycin or Clarithromycin is used. * **Differential Diagnosis:** Tinea cruris, Candidiasis, and Seborrheic dermatitis.

Q: In a diagnosed lepromatous leprosy patient, treatment was started. After intake of the drug, skin lesions and fever develop within a few days. Which type of hypersensitivity reaction leads to this manifestation?

Type 3. **Explanation:** The clinical scenario describes **Erythema Nodosum Leprosum (ENL)**, also known as a **Type 2 Lepra Reaction**. This typically occurs in patients with Lepromatous Leprosy (LL) or Borderline Lepromatous (BL) leprosy, often triggered by the initiation of multidrug therapy (MDT). **Why Type 3 Hypersensitivity is Correct:** ENL is a classic example of a **Type 3 (Immune-complex mediated) hypersensitivity reaction**. The rapid killing of a high load of *Mycobacterium leprae* bacilli by drugs releases a large amount of bacterial antigens into the circulation. these antigens combine with circulating antibodies to form **immune complexes**, which deposit in blood vessel walls, activating the complement system and leading to systemic vasculitis. This manifests clinically as painful erythematous nodules, high-grade fever, malaise, and occasionally organ involvement (neuritis, arthritis, or iridocyclitis). **Why Incorrect Options are Wrong:** * **Type 4 (Delayed-type):** This is the mechanism behind **Type 1 Lepra Reactions (Reversal Reactions)**, seen in borderline cases. It involves a cell-mediated immune response, not immune complexes. * **Type 2 (Antibody-dependent):** This involves antibodies directed against antigens on specific cell surfaces (e.g., hemolytic anemia), which is not the pathology of ENL. * **Type 1 (Immediate):** This is IgE-mediated (e.g., anaphylaxis/urticaria) and is not associated with lepra reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for ENL:** **Thalidomide** is the most effective treatment. Oral corticosteroids are used for milder cases or when thalidomide is contraindicated. * **Type 1 Reaction vs. Type 2 Reaction:** Type 1 occurs in paucibacillary/borderline cases (Type 4 hypersensitivity); Type 2 occurs in multibacillary cases (Type 3 hypersensitivity). * **Clofazimine:** This component of MDT has anti-inflammatory properties that help prevent and treat ENL.

Q: Type 2 lepra reaction occurs in which form of leprosy?

Multi bacillary leprosy. **Explanation:** **Type 2 Lepra Reaction**, also known as **Erythema Nodosum Leprosum (ENL)**, is a Type III hypersensitivity reaction (immune-complex mediated). It occurs due to the deposition of antigen-antibody complexes in tissues, leading to systemic inflammatory symptoms. **Why Option B is correct:** Type 2 reactions occur exclusively in patients with a high bacterial load, specifically those on the lepromatous end of the spectrum (**Lepromatous Leprosy (LL)** and **Borderline Lepromatous (BL)**). These forms are classified as **Multibacillary (MB) leprosy**. The high density of *Mycobacterium leprae* antigens reacts with circulating antibodies to form the immune complexes that trigger the reaction. **Why other options are incorrect:** * **Option A (Paucibacillary):** Paucibacillary leprosy (TT and BT) is characterized by high cell-mediated immunity and a very low bacterial load. Since there are insufficient antigens to form significant immune complexes, Type 2 reactions do not occur here. Instead, these patients are prone to **Type 1 reactions** (Type IV hypersensitivity). * **Option C & D:** These are incorrect as the reaction is specific to the bacterial load status of the patient. **NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Characterized by tender, evanescent, erythematous nodules, high-grade fever, malaise, and systemic involvement (iridocyclitis, neuritis, arthritis, and orchitis). * **Timing:** Usually occurs during or after the initiation of Multi-Drug Therapy (MDT), as killing the bacilli releases massive amounts of antigen. * **Drug of Choice:** **Thalidomide** is the most effective treatment for Type 2 reactions. Oral corticosteroids and Clofazimine are also used. * **Key Distinction:** Type 1 reaction = Delayed Hypersensitivity (Type IV); Type 2 reaction = Immune Complex Mediated (Type III).

Q: Pitted keratolysis affects which of the following areas?

Palm and soles. **Explanation:** **Pitted keratolysis** is a superficial bacterial infection of the stratum corneum, primarily caused by **Kytococcus sedentarius** (formerly *Micrococcus*), *Corynebacterium* species, or *Actinomyces*. 1. **Why Option A is correct:** The bacteria produce **extracellular serine proteases** that digest the keratin of the stratum corneum. This process requires a moist, occlusive environment, which is why it characteristically involves the **weight-bearing areas of the soles** (and occasionally the palms). The digestion of keratin results in the pathognomonic "punched-out" pits (1–7 mm) seen clinically. 2. **Why Options B and C are incorrect:** * **Face:** The facial skin is thinner and lacks the thick stratum corneum required for these specific bacteria to thrive and create deep pits. * **Nails:** This is an infection of the keratinized skin (stratum corneum), not the nail plate (onycho-). 3. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of Presentation:** Hyperhidrosis (excessive sweating), Bromhidrosis (foul odor due to sulfur compounds), and non-inflammatory punched-out pits. * **Risk Factors:** Occlusive footwear (boots), tropical climates, and prolonged immersion in water. * **Diagnosis:** Primarily clinical; Wood’s lamp may occasionally show coral-red fluorescence (if *Corynebacterium* is involved). * **Treatment:** Topical antibiotics like **Clindamycin, Erythromycin, or Mupirocin**, combined with measures to keep the feet dry (e.g., aluminum chloride hexahydrate).

Q: Blistering dactylitis is typically caused by which of the following?

Streptococcal infection. **Explanation:** **Blistering Dactylitis** is a localized superficial infection characterized by tense, fluid-filled blisters (bullae) over the volar fat pads of the distal phalanx of the fingers or toes. 1. **Why Option A is Correct:** The most common causative organism is **Group A Beta-hemolytic Streptococcus (Streptococcus pyogenes)**. Occasionally, *Staphylococcus aureus* may be co-isolated, but classic blistering dactylitis is traditionally associated with Streptococcus. The infection typically follows minor trauma or autoinoculation from the nasopharynx, leading to the formation of a characteristic oval bulla on an erythematous base. 2. **Why Other Options are Incorrect:** * **Option B (Staphylococcus):** While *S. aureus* can cause bullous impetigo, it is less frequently the primary isolate in the specific clinical presentation of volar dactylitis compared to Streptococcus. * **Option C (Tuberculosis):** Cutaneous TB (like Lupus Vulgaris) or TB of the bone (Spina Ventosa) can affect the digits, but they present as chronic nodules, ulcers, or "bottleneck" swelling, not acute superficial blisters. * **Option D (Sickle cell anaemia):** This is associated with **Hand-Foot Syndrome** (dactylitis) in infants, which is caused by microinfarction of the small bones, leading to painful, non-blistering inflammatory swelling. **Clinical Pearls for NEET-PG:** * **Target Population:** Most commonly seen in children (2–16 years). * **Clinical Feature:** Tense bullae containing seropurulent fluid over the **volar** aspect of the distal digit. * **Treatment:** Incision and drainage of the bulla followed by a course of oral antibiotics (e.g., Penicillinase-resistant penicillins or Cephalosporins). * **Differential Diagnosis:** Must be distinguished from herpetic whitlow (which presents with grouped vesicles and significant pain) and friction blisters.

Question 1

What condition is characterized by a malignant pustule?

Accepted Answer

Anthrax

Answer

Melanoma

Answer

Gas gangrene

Answer

Ovarian tumor

Question 2

Ritter's disease is caused by which bacterium?

Accepted Answer

Staphylococcus aureus

Answer

Staphylococcus epidermidis

Answer

Staphylococcus albus

Answer

Staphylococcus saprophyticus

Question 3

What is the recommended duration for the treatment of multibacillary leprosy?

Accepted Answer

12 months

Answer

24 months

Answer

18 months

Answer

6 months

Question 4

Hot tub folliculitis is caused by which organism?

Accepted Answer

Pseudomonas aeruginosa

Answer

Pityrosporum ovale

Answer

Aeromonas hydrophila

Answer

Vibrio vulnificans

Question 5

Coral-red fluorescence with Wood's light strongly suggests which diagnosis?

Accepted Answer

Erythrasma

Answer

Ash leaf macules

Answer

Acanthosis nigricans

Answer

Erysipeloid

Question 6

Erythrasma is caused by which microorganism?

Accepted Answer

Corynebacterium

Answer

Staphylococcus

Answer

Streptococci

Answer

Viruses

Question 7

In a diagnosed lepromatous leprosy patient, treatment was started. After intake of the drug, skin lesions and fever develop within a few days. Which type of hypersensitivity reaction leads to this manifestation?

Accepted Answer

Type 3

Answer

Type 4

Answer

Type 2

Answer

Type 1

Question 8

Type 2 lepra reaction occurs in which form of leprosy?

Accepted Answer

Multi bacillary leprosy

Answer

Pauci bacillary leprosy

Answer

Both of the above

Answer

None of the above

Question 9

Pitted keratolysis affects which of the following areas?

Accepted Answer

Palm and soles

Answer

Face

Answer

Nails

Answer

All of the above

Question 10

Blistering dactylitis is typically caused by which of the following?

Accepted Answer

Streptococcal infection

Answer

Staphylococcus

Answer

Tuberculosis

Answer

Sickle cell anaemia

Bacterial Skin Infections — MCQs

Bacterial Skin Infections — MCQs

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