154: Gram-Negative Coccal and Bacillary Infections Flashcards
What is the primary virulence factor of Neisseria meningitidis that allows differentiation into serogroups?
The primary virulence factor is the capsule, which is based on capsule polysaccharides and allows differentiation into serogroups A, C, W-135, X, and Y.
What are the common culture media used for isolating Neisseria meningitidis?
Common culture media include:
- Blood agar
- Trypticase-soy agar
- Chocolate agar
- Modified Thayer Martin agar
On blood agar, colonies appear as light gray, non-hemolytic, round, and glistening with a clear defined edge.
What is the significance of the Factor H binding protein in Neisseria meningitidis?
The Factor H binding protein binds factor H, which downregulates the alternative complement pathway and degrades C3, playing a crucial role in evading the host’s immune response.
What is the relationship between lipooligosaccharide levels and the severity of meningococcal infection?
There is a direct correlation between the levels of lipooligosaccharide and the severity of meningococcal infection; high levels are associated with poor prognosis.
Who is the exclusive host for Neisseria meningitidis and what is a common factor affecting infection rates in young children?
Humans are the exclusive host for Neisseria meningitidis, primarily through nasopharyngeal carriage. Young children experience sporadic infections due to waning levels of protective maternal antibodies.
What is the causative agent of meningococcal infections worldwide?
Neisseria meningitidis is responsible for 1.2 million cases of infection and 135,000 deaths annually.
What are the common presentations of disseminated meningococcal infection?
It may present as meningitis alone, acute meningococcemia, or chronic meningococcemia.
What is the gold standard for diagnosing Neisseria meningitidis infections?
Culture isolation of N. meningitidis from blood, cerebrospinal fluid, or other bodily fluids.
What is the most important factor in the treatment of acute meningococcal infection?
Early initiation of antibiotics is crucial.
What is the recommended vaccination schedule for Neisseria meningitidis?
Vaccination against serogroups A, C, W-135, and Y is recommended for all patients at 11 or 12 years of age with a booster at age 16 years.
What virulence factor allows differentiation into serogroups for Neisseria meningitidis?
The capsule is a virulence factor that allows differentiation based on capsule polysaccharides.
What role do pili play in Neisseria meningitidis infections?
Pili promote adherence to host cells and tissues and undergo phase and antigenic variation.
What is the significance of lipooligosaccharide in Neisseria meningitidis?
It triggers the production of pro-inflammatory cytokines and correlates with the severity of meningococcal infection.
Who is the exclusive host for Neisseria meningitidis?
Humans are the exclusive host, primarily through nasopharyngeal carriage.
Why are young children at risk for sporadic infections of Neisseria meningitidis?
Due to waning levels of protective maternal antibodies.
What are the primary virulence factors of Neisseria meningitidis and their roles in infection?
The primary virulence factors of Neisseria meningitidis include:
| Virulence Factor | Role |
|——————|——|
| Capsule | Allows differentiation into serogroups based on polysaccharides; important for immune evasion. |
| Pili | Promotes adherence to host cells and tissues; undergoes phase and antigenic variation. |
| Opa proteins | Found on the outer membrane; enhances adherence to nasopharyngeal epithelium. |
| Factor H binding protein | Binds factor H, downregulating the alternative complement pathway, aiding in immune evasion. |
| Lipooligosaccharide | Triggers pro-inflammatory cytokine production and activates complement pathways; correlates with infection severity.
How does the epidemiology of Neisseria meningitidis infections differ in young children compared to adults?
In the epidemiology of Neisseria meningitidis infections:
- Young children are at higher risk due to:
- Sporadic infections resulting from waning levels of protective maternal antibodies.
- Adults typically have a lower incidence of infection, as they may have developed immunity through previous exposure or vaccination.
What is the significance of the capsule in Neisseria meningitidis regarding vaccination challenges?
The capsule of Neisseria meningitidis is significant because:
- It serves as a virulence factor, allowing differentiation into serogroups (A, C, W-135, X, Y).
- The B serogroup demonstrates molecular mimicry, resembling human neuronal cells, which makes it poorly immunogenic and presents challenges for effective vaccination.
What are the clinical implications of high levels of lipooligosaccharide in Neisseria meningitidis infections?
High levels of lipooligosaccharide in Neisseria meningitidis infections have clinical implications such as:
- Triggering the production of pro-inflammatory cytokines, which can lead to severe inflammatory responses.
- Activating complement pathways, which can result in simultaneous activation and inhibition of coagulation pathways.
- A direct correlation exists between high levels of lipooligosaccharide and poor prognosis in meningococcal infections.
What are the common cutaneous findings associated with acute meningococcemia?
- Fever + petechial rash that progresses to fulminant septicemia within hours.
-
Petechial rash:
- Hallmark (not always present); small, irregular with smudged appearance.
- Common in children aged 1-18 more than in infants and adults.
- Most common location: extremities; can occur on palms, soles, mucous membranes, and conjunctiva.
- Rapid increase in number and size indicates fulminant disease progression.
-
Purpura fulminans:
- Retiform purpura and skin necrosis; may occur with DIC; caused by sepsis.
- DIC + purpura fulminans = Low Protein C levels.
What are the risk factors associated with N. meningitidis infections?
-
Lack of bactericidal antibodies:
- Anatomic/functional asplenia, HIV, defects of terminal alternative complement pathways.
- Deficiency of properdin: Positive regulator of alternative complement pathway.
- Crowded living conditions: Adolescents and young adults living in crowded environments are at higher risk.
What are the non-cutaneous findings associated with meningococcemia?
- Myalgias
- Arthralgias
- Cold or discolored extremities
- Hypotension
- Altered mental status
- Renal failure
- Acute Respiratory Distress Syndrome (ARDS)
- DIC (Disseminated Intravascular Coagulation)
- Waterhouse-Friedrichsen syndrome
What is the transmission method of N. meningitidis?
- Transmission occurs via respiratory droplets, direct contact, or kissing.
- The bacteria reside in the nasopharynx of healthy individuals and can arise within 2 weeks of acquisition.
A college student living in a dormitory develops meningococcal meningitis. What are the risk factors associated with this condition?
Crowded living conditions, lack of bactericidal antibodies, and deficiencies in the alternative complement pathway (e.g., properdin deficiency).
What is the primary risk factor for higher infection rates of N. meningitidis in older children?
Close living conditions such as in colleges and dormitories.
What are the common serogroups of N. meningitidis associated with different regions?
A, W-135, X in sub-Saharan Africa; B and C in developed countries; Y associated with meningococcal pneumonia in adults.
How is N. meningitidis transmitted?
Through respiratory droplets, direct contact, or kissing.
What is a hallmark clinical feature of acute meningococcemia?
Petechial rash, which may progress to fulminant septicemia.
What is the most common location for petechial rash in children with meningococcemia?
Extremities, but it can occur all over the body including palms, soles, mucous membranes, and conjunctiva.
What condition may occur with purpura fulminans in meningococcemia?
Disseminated intravascular coagulation (DIC).
What are some non-cutaneous findings associated with meningococcemia?
Myalgias, arthralgias, cold or discolored extremities, hypotension, altered mental status, renal failure, ARDS, and DIC.
What syndrome is associated with severe meningococcal infections?
Waterhouse-Friedrichsen syndrome.
What is the significance of properdin deficiency in relation to N. meningitidis infections?
It is a positive regulator of the alternative complement pathway, and its deficiency increases the risk of infection.
What are the key risk factors for N. meningitidis infections in adolescents and young adults living in crowded conditions?
Key risk factors include:
- Lack of bactericidal antibodies due to:
- Anatomic/functional asplenia
- HIV
- Defects of terminal alternative complement pathways
- Deficiency of properdin, a positive regulator of the alternative complement pathway.
How does acute meningococcemia present clinically, and what are the implications of a petechial rash?
Acute meningococcemia presents with:
- Fever and a petechial rash that can progress to fulminant septicemia within hours.
- The petechial rash is a hallmark sign, often small and irregular with a smudged appearance.
- It is more common in children aged 1-18 than in infants and adults, and its rapid increase in number and size indicates fulminant disease progression.
What are the differences in cutaneous findings between acute and chronic meningococcemia?
Feature | Acute Meningococcemia | Chronic Meningococcemia |
|—————————–|————————————————|————————————————–|
| Rash | Petechial rash, hallmark sign | Polymorphic rash, fades and recurs |
| Appearance | Small, irregular, smudged | Rose-colored papules/macules |
| Progression | Rapid increase in number and size | Weeks to months of recurrent fevers |
| Other findings | Purpura fulminans, skin necrosis | Erythema nodosum-like nodules, petechiae |
What non-cutaneous findings are associated with severe meningococcal infections?
Non-cutaneous findings include:
- Myalgias and arthralgias
- Cold or discolored extremities
- Hypotension
- Altered mental status
- Renal failure
- Acute Respiratory Distress Syndrome (ARDS)
- Waterhouse-Friedrichsen syndrome, which is characterized by adrenal hemorrhage and can lead to adrenal insufficiency.
What are the common clinical features of meningococcal meningitis?
Common clinical features include:
1. Nuchal rigidity
2. Headache
3. Photophobia
4. Fever
5. Altered mental status
6. Positive Kernig and Brudzinski signs
7. Potential for septic foci in other locations (e.g., septic arthritis, purulent pericarditis, bacterial endocarditis).
What are the complications associated with meningococcal infections?
Complications include:
1. Purpura fulminans – can lead to amputation.
2. Meningitis – may result in sensorineural hearing loss/deafness, seizures, hydrocephalus, mental retardation, and cognitive/behavioral problems.
3. Chronic meningococcemia – can lead to acute meningococcemia, meningitis, and carditis.
What laboratory tests are considered the gold standard for diagnosing acute meningococcemia?
The gold standard laboratory tests for diagnosing acute meningococcemia include:
- Culture of:
- Blood
- CSF (Cerebrospinal fluid)
- Synovial fluid
- Pleural fluid
- Pericardial fluid
- Skin biopsy
- PCR (Polymerase Chain Reaction) if there is high suspicion but negative workup.
What are the advantages and disadvantages of using PCR for diagnosing meningococcal infections?
Advantages of PCR:
1. Highly sensitive and specific
2. Sensitivity not diminished
3. Fast results
4. More helpful in chronic meningococcemia due to difficulties in obtaining cultures.
Disadvantages of PCR:
1. Cannot determine antibiotic sensitivity
2. No widespread availability
What histopathological findings are associated with chronic meningococcemia?
Histopathological findings in chronic meningococcemia include:
- Perivascular infiltrates of lymphocytes and neutrophils.
- Leukocytoclastic vasculitis in petechial lesions.
A 5-year-old child presents with fever, petechial rash, and altered mental status. What diagnostic tests should be prioritized to confirm acute meningococcemia?
Blood culture (40-80% sensitivity), CSF culture, and PCR for high sensitivity and specificity. Skin biopsy may also be used if antibiotics have already been administered.
A patient recovering from meningococcal meningitis develops sterile arthritis and vasculitis. What is the likely underlying mechanism?
Delayed immune complex-mediated syndrome, which occurs during recovery and manifests as sterile arthritis, vasculitis, pleuritis, pericarditis, or episcleritis.
A patient with chronic meningococcemia presents with rose-colored macules and migratory arthralgia. What is the recommended diagnostic approach?
Perform blood culture, PCR for high sensitivity, and skin biopsy to identify perivascular infiltrates of lymphocytes and neutrophils.
A patient with suspected meningococcal infection has a negative culture but high clinical suspicion. What diagnostic test can confirm the infection?
PCR, as it is highly sensitive and specific, and its sensitivity is not diminished by prior antibiotic use.
A patient presents with necrotizing vasculitis and microvascular thrombosis. What histopathological findings are expected in meningococcal infection?
Necrotizing vasculitis, perivascular infiltrates of neutrophils and monocytes, microvascular thrombosis, and perivascular hemorrhage.
A patient with meningococcal meningitis develops sensorineural hearing loss. What is the underlying complication?
Sensorineural hearing loss is the most common sequelae of meningitis, along with seizures, hydrocephalus, and cognitive or behavioral problems.
A patient with a history of meningococcal infection presents with purulent pericarditis. What is the likely pathogenesis?
Meningococcal meningitis can lead to septic foci in other locations, including purulent pericarditis, due to the breach of the blood-brain barrier.
What are the common symptoms of meningococcal meningitis?
Nuchal rigidity, headache, photophobia, fever, altered mental status, and positive Kernig and Brudzinski signs.
What is a life-threatening complication associated with adrenal hemorrhage in meningococcal infections?
Purpura fulminans.
What is the likely pathogenesis of purulent pericarditis in meningococcal infection?
Meningococcal meningitis can lead to septic foci in other locations, including purulent pericarditis, due to the breach of the blood-brain barrier.
What are the common sequelae of meningitis?
Sensorineural hearing loss, seizures, hydrocephalus, mental retardation, and cognitive behavioral problems.
What is the gold standard for diagnosing acute meningococcemia?
Culture of blood, CSF, synovial fluid, pleural fluid, pericardial fluid, or skin biopsy.
What are the advantages of using PCR in diagnosing meningococcemia?
Highly sensitive and specific, sensitivity not diminished, fast results, and more helpful in chronic meningococcemia.
What are the disadvantages of PCR testing for meningococcemia?
Cannot determine antibiotic sensitivity and no widespread availability.
What histopathological findings are associated with chronic meningococcemia?
Perivascular infiltrates of lymphocytes and neutrophils, and leukocytoclastic vasculitis in petechial lesions.
What is a delayed immune complex mediated syndrome in the context of meningococcal infections?
It occurs while patients are in recovery and manifests as sterile arthritis, vasculitis, pleuritis, pericarditis, and episcleritis.
What are the clinical features of meningococcal meningitis and how do they relate to the breach of the blood-brain barrier?
Clinical features include nuchal rigidity, headache, photophobia, fever, altered mental status, and positive Kernig and Brudzinski signs. These symptoms arise due to inflammation and irritation of the meninges, which can occur when the blood-brain barrier is breached.
What are the potential complications of meningococcal infections and their clinical implications?
Potential complications include purpura fulminans, sensorineural hearing loss, seizures, hydrocephalus, and chronic meningococcemia. These highlight the importance of early diagnosis and treatment to prevent long-term morbidity.
What are the advantages and disadvantages of using PCR for diagnosing meningococcal infections?
Advantages include high sensitivity and specificity, sensitivity not diminished after antibiotic initiation, fast results, and usefulness in chronic meningococcemia. Disadvantages include inability to determine antibiotic sensitivity and limited availability.
What histopathological findings are associated with chronic meningococcemia?
Necrotizing vasculitis, gram-negative cocci on gram stain, and perivascular infiltrates of lymphocytes and neutrophils.
What is the single most important factor in the treatment of meningococcemia?
Early initiation of antibiotics (not less than 30 minutes between diagnosis and administration of IV antibiotics).
What is the standard duration of antibiotic treatment for meningococcemia?
The standard antibiotic duration is 7 days.
What are the recommended antibiotics for empiric treatment of meningococcemia?
Third generation cephalosporins (Ceftriaxone, Cefotaxime) are recommended for empiric treatment.
What vaccination is recommended for patients aged 11-12 years for meningococcal prevention?
The conjugate quadrivalent vaccine is recommended, with a booster at 12-16 years old.
What is the recommendation for the serogroup B meningococcal vaccine?
It is recommended for certain high-risk patients over 10 years old and for elective administration in patients aged 16-23 years, preferably between 16-18 years.
A patient presents with purpura fulminans and low Protein C levels. What is the immediate treatment approach?
Early initiation of IV antibiotics (e.g., third-generation cephalosporins) and administration of Protein C concentrate.
A 12-year-old is due for meningococcal vaccination. What vaccine schedule should be followed?
Administer the conjugate quadrivalent vaccine at 11-12 years old with a booster at 16 years old. If the first dose is given after 16 years, a booster is not needed.
What is the significance of early initiation of antibiotics in the treatment of meningococcemia?
Early initiation of antibiotics (within 30 minutes of diagnosis) is the single most important factor in the treatment of meningococcemia, as it significantly improves patient outcomes and reduces the risk of severe complications.
What are the standard antibiotic treatments for acute meningococcemia and their duration?
The standard antibiotic treatment for acute meningococcemia is a duration of 7 days, typically involving third generation cephalosporins, Penicillin G or Ampicillin if MIC is <0.1 µg/mL, Chloramphenicol if there is an allergy, and Protein C concentrate for purpura fulminans.
What vaccination recommendations are made for preventing meningococcal infections in adolescents?
Vaccination recommendations include the conjugate quadrivalent vaccine for patients aged 11-12 years with a booster at 12-16 years, and the serogroup B meningococcal vaccine for high-risk patients over 10 years old.
What is the definition of close contact for antibiotic prophylaxis in meningococcal infections?
Close contact is defined as prolonged contact >8 hours, close proximity <3 feet, and direct exposure to patients’ oral secretions from 7 days before symptom onset until 24 hours following initiation of treatment.
What are the recommended antibiotics for prophylaxis in close contacts of meningococcal infections?
The recommended antibiotics for prophylaxis are Rifampin (4 doses over 2 days), Ciprofloxacin (single dose), and Ceftriaxone (single IM dose; use in pregnancy).
What is the prognosis for acute meningococcal infection?
Acute meningococcal infection is often fatal, leading to shock and multiple organ failure.
What is the prognosis for chronic meningococcemia without treatment?
Without treatment, chronic meningococcemia is more likely to worsen and progress to affect vital function, leading to death. However, if treated, the prognosis is excellent.
When should antibiotic prophylaxis be initiated after identifying an index patient?
Within 24 hours of identification of the index patient.
What are the criteria for defining close contact in the context of antibiotic prophylaxis for meningococcal infections?
The criteria for defining close contact include prolonged contact >8 hours, close proximity <3 feet, and direct exposure to patients’ oral secretions from 7 days before symptom onset until 24 hours following initiation of treatment.
What are the treatment options for antibiotic prophylaxis in close contacts of meningococcal infections?
The treatment options include Rifampin (4 doses over 2 days), Ciprofloxacin (single dose), and Ceftriaxone (single IM dose; use in pregnancy).
What are the potential outcomes of acute meningococcal infection if left untreated?
Acute meningococcal infection can be fatal, leading to shock and multiple organ failure if left untreated.
What is the prognosis for chronic meningococcemia if treated versus untreated?
Without treatment, chronic meningococcemia is more likely to worsen and progress to affect vital function, leading to death. If treated, the prognosis is excellent, with some patients spontaneously recovering.
What are the key characteristics of Pseudomonas aeruginosa?
Gram-negative rod with a sweet, grape-like odor and blue-green color due to pyocyanin pigment. Oxidase positive, non-lactose fermenting, and obligately aerobic.
What are the common cutaneous infections caused by Pseudomonas aeruginosa?
Green nail syndrome, toe web infection, folliculitis, hot-foot syndrome, external otitis, and perichondritis.
What are the virulence factors of Pseudomonas aeruginosa?
ExoS, ExoT, ExoU, ExoY, Exotoxin A, Lipooligosaccharide, Pyocyanin, Pyoverdin & Pyochelin, and Alginate.
What are the drug resistance mechanisms of Pseudomonas aeruginosa?
Biofilms, efflux pumps, beta-lactamases, and porin downregulation.
A patient presents with a grape-like odor and blue-green pus from a wound. What is the likely causative organism?
Pseudomonas aeruginosa, which produces pyocyanin and pyoverdin pigments.
What type of organism is Pseudomonas aeruginosa?
A ubiquitous Gram-negative rod.
What is a characteristic color and odor of Pseudomonas aeruginosa?
Blue-green color and grape-like odor.
What are common infections caused by Pseudomonas aeruginosa?
Nosocomial pneumonia, cystic fibrosis lung infections, and skin infections.
What is the role of exoenzymes produced by Pseudomonas aeruginosa?
They interact with TLRs to induce TNF-a production and damage host tissues.
What is the significance of pyocyanin in Pseudomonas aeruginosa infections?
It is a pigment specific to Pseudomonas and contributes to its pathogenicity.
What is the clinical implication of Pseudomonas aeruginosa in hospitalized patients?
It can cause severe infections, especially in immunocompromised hosts, with high mortality rates.
What is the relationship between skin integrity and Pseudomonas aeruginosa infections?
A breach in skin integrity is typically required for invasion.
Why is skin integrity necessary?
Skin integrity is necessary for invasion and infection.
What are the primary cutaneous infections associated with Pseudomonas aeruginosa?
Primary cutaneous infections include:
- Green nail syndrome
- Toe web infection
- Folliculitis
- Hot-foot syndrome
- External otitis
- Perichondritis
What conditions typically necessitate a breach in skin integrity?
Conditions that necessitate a breach in skin integrity include:
- Trauma or burns
- Indwelling catheters
- Maceration of skin
- Dermatophyte infections
What are the virulence factors of Pseudomonas aeruginosa?
Virulence factors of Pseudomonas aeruginosa include:
Factor | Role in Infection |
| - - - - - - - - - | - - - - - - - - - - - - - - - - - - - |
| Exoenzymes | Interact with host immune responses; damage host tissues |
| Exotoxin A | Induces septic shock; inhibits protein synthesis |
| Lipooligosaccharide | Mediates septic shock; activates TLR4 |
| Pyocyanin | Contributes to oxidative stress; impairs immune response |
| Alginate | Forms biofilms; protects against phagocytosis |
How do virulence factors enhance the bacterium’s ability to invade tissues?
These factors enhance the bacterium’s ability to invade tissues, evade the immune system, and establish persistent infections.
What are the drug resistance mechanisms employed by Pseudomonas aeruginosa?
Drug resistance mechanisms of Pseudomonas aeruginosa include:
Mechanism | Description |
| - - - - - - - - - - - - | - - - - - - - - - - - - - - - - - - - |
| Biofilms | Protect bacteria from antibiotics and immune response |
| Efflux pumps | Actively expel antibiotics from bacterial cells |
What are lux pumps?
Actively expel antibiotics from bacterial cells.
What are beta-lactamases?
Enzymes that degrade beta-lactam antibiotics.
What is porin downregulation?
Reduces permeability of the outer membrane to antibiotics.
What do these mechanisms complicate?
They complicate treatment options and necessitate the use of combination therapies or alternative antibiotics.
What are the primary sources of Pseudomonas aeruginosa infections in healthy patients?
- Conjunctival microflora
- Feces of healthy patients
- Water reservoir systems
What are the risk factors associated with green nail syndrome caused by Pseudomonas aeruginosa?
- Prolonged submersion in fresh water, soap, and detergents
- Onycholysis
- Chronic paronychia
- Nail disorders
What are the common risk factors for developing folliculitis and hot foot syndrome?
- Recreational use of hot tubs, whirlpools, or pools that lack adequate halogenation
- Heated water above 38 degrees, with increased infection risk correlating with the duration of bathing.
What are the primary sites of infection associated with bacteremia from Pseudomonas aeruginosa?
- Lungs
- Urinary tract
- Gastrointestinal tract
- Skin and soft tissues (wound infection)
What are the risk factors for developing malignant otitis externa (OE) due to Pseudomonas aeruginosa?
Risk factors include conditions that compromise the immune system or skin integrity.
What are the risk factors for developing malignant otitis externa (OE)?
- Swimmers
- Excessive ear scratching/cleaning
- Ear occluding devices
- Presence of dermatologic conditions that promote breakdown of skin cerumen barrier
- Microangiopathy of ear canal
- Increased pH of diabetic cerumen
What is the most likely causative organism for a patient with a history of burns who develops sepsis?
Pseudomonas aeruginosa, which is frequently isolated from burn wounds.
What is the likely causative organism for a patient with a catheter-associated UTI who develops bacteremia?
Pseudomonas aeruginosa, the third most common cause of catheter-associated UTIs.
What is the likely causative organism and risk factors for a patient with a history of prolonged antibiotic use who develops sepsis?
Pseudomonas aeruginosa. Risk factors include hospitalization, neutropenia, hematologic malignancy, and recent antibiotic use.
What is a common source of infection in immunocompromised patients according to the epidemiology section?
Conjunctival microflora and feces of healthy patients, and water reservoir systems.
What is the most common pathogen for lung infections among ventilator-dependent patients?
Pseudomonas aeruginosa.
What are the risk factors for green nail syndrome?
Prolonged submersion in fresh water, soap, and detergents; onycholysis, chronic paronychia, nail disorders.
What is chronic paronychia?
Chronic paronychia is a nail disorder.
What is the primary risk factor for toe web infections?
Persistently wet feet, closed toe shoes, tight fitting shoes, occupational or recreational exertion, and/or warm humid weather.
What increases the risk of folliculitis and hot foot syndrome?
Recreational use of hot tubs, whirlpools, and heated water above 38 degrees.
What are the risk factors for external otitis?
Swimmers, excessive ear scratching/cleaning, ear occluding devices, and presence of dermatologic conditions.
What is a common cause of malignant otitis externa in HIV patients?
Pseudomonas and Aspergillus.
What are the primary sites of infection in bacteremia?
Lungs, urinary tract, gastrointestinal tract, skin, and soft tissues (wound infection).
What are the risk factors for bacteremia?
Hospitalization, neutropenia, hematologic malignancy, CD4 < 50, immunocompromised status, recent courses of antibiotics/chemo, and invasive devices.
What are the primary risk factors associated with green nail syndrome and how does it develop?
Green nail syndrome develops due to prolonged submersion in fresh water, soap, and detergents. The primary risk factors include:
- Onycholysis
- Chronic paronychia
- Nail disorders.
What are the common risk factors for toe web infections and how can they be prevented?
Toe web infections are commonly associated with the following risk factors:
- Persistently wet feet
- Closed toe shoes
- Tight fitting shoes
- Occupational or recreational exertion in warm humid weather.
Prevention strategies include:
- Keeping feet dry
- Wearing breathable footwear
- Avoiding prolonged exposure to wet conditions.
What factors increase the risk of folliculitis and hot foot syndrome, particularly in recreational settings?
The risk of folliculitis and hot foot syndrome increases due to:
1. Recreational use of hot tubs, whirlpools, and pools lacking adequate halogenation.
2. Bathing in heated water above 38 degrees Celsius.
3. Prolonged duration of bathing.
What does prevention include for folliculitis and hot foot syndrome?
Prevention includes ensuring proper water sanitation and limiting time spent in hot water.
What are the risk factors for malignant otitis externa and its common causative agents in immunocompromised patients?
Malignant otitis externa is characterized by:
1. Invasion of soft tissues at the cartilaginous junction of the external auditory canal.
2. Risk factors include:
- Microangiopathy of the ear canal.
- Increased pH of diabetic cerumen.
- Common in elderly and immunocompromised individuals.
What are the common causative agents of malignant otitis externa?
Common causative agents include:
- Pseudomonas aeruginosa.
- Aspergillus species.
What are the primary sites of infection in bacteremia associated with Pseudomonas aeruginosa?
In bacteremia associated with Pseudomonas aeruginosa, the primary sites of infection include:
1. Lungs.
2. Urinary tract.
3. Gastrointestinal tract.
4. Skin and soft tissues (wound infections).
What are the risk factors for developing bacteremia?
Risk factors for developing bacteremia include:
- Hospitalization.
- Neutropenia.
- Hematologic malignancy.
- CD4 count < 50.
- Immunocompromised status.
- Recent courses of antibiotics or chemotherapy.
- Use of invasive devices.
What are the clinical features of Green nail syndrome?
Nail dyspigmentation: Greenish-yellow/brown/black due to accumulation of debris.
What is Green nail syndrome?
A condition characterized by greenish-yellow/brown/black due to accumulation of debris and pyocyanin.
What digits are typically affected by Green nail syndrome?
Typically limited to one or two digits; may affect the entire or partial nail.
What is the triad of symptoms associated with Green nail syndrome?
Dyspigmentation, Onycholysis, Paronychia.
What are the common cutaneous infections associated with direct inoculation?
- Green nail syndrome
- Toe web infection
- Folliculitis
- Hot foot syndrome
- External otitis
- Perichondritis
What are the characteristics of Toe web infection?
Appearance: Thickened, macerated skin with a characteristic moth-eaten appearance and yellow-green pustules.
Affected areas: Affects the toe web spaces and sole of the foot; may be accompanied by burning and pain.
What is Hot foot syndrome and its common presentation?
Common in children. Symptoms: Acute painful erythematous, warm, plantar nodules after immersion in contaminated wading pools or hot tubs.
What are the symptoms of External otitis/Swimmer’s ear?
Onset: Acute onset of edema and erythema or discoloration of the external auditory canal (EAC) sometimes with maceration, discharge, and regional lymphadenopathy (LAD).
Symptoms: (+) tragal tenderness, pruritus. Most common in children aged 5-14 years.
What is the clinical significance of malignant otitis externa?
Onset: Insidious onset with edema, erythema, and persistent discharge from the ear canal.
Pain: Severe pain disproportionate to examination findings. Risk groups: More common in elderly patients and diabetics.
What are the complications of malignant otitis externa?
Life-threatening; can lead to skull base osteomyelitis.
What is the likely diagnosis for a diabetic patient with external otitis and severe pain disproportionate to examination findings?
Malignant otitis externa, which involves soft tissue invasion and can lead to skull base osteomyelitis.
What is the likely diagnosis and causative organism for a patient with a history of hot tub use presenting with follicular papules and pustules?
Hot tub folliculitis caused by Pseudomonas aeruginosa, typically presenting 24 hours after exposure.
What is the likely diagnosis and causative organism for a patient presenting with a painful, erythematous plantar nodule after using a wading pool?
Hot foot syndrome caused by Pseudomonas aeruginosa, commonly seen in children.
What is the likely diagnosis and causative organism for a patient with a history of ear scratching presenting with tragal tenderness and discharge?
External otitis (swimmer’s ear) caused by Pseudomonas aeruginosa.
What is the likely diagnosis and causative organism for a patient with a history of water irrigation of the ear developing severe pain and discharge?
Malignant otitis externa caused by Pseudomonas aeruginosa, often following water irrigation in diabetic or immunocompromised patients.
What is the likely diagnosis and causative organism for a patient with a history of swimming in a poorly chlorinated pool developing pruritic follicular papules?
Hot tub folliculitis caused by Pseudomonas aeruginosa.
What is the likely diagnosis and causative organism for a patient with a history of hot tub use presenting with painful plantar nodules?
Hot foot syndrome caused by Pseudomonas aeruginosa.
What is the likely diagnosis for a patient with a history of ear cleaning presenting with tragal tenderness?
External otitis (swimmer’s ear) caused by Pseudomonas aeruginosa.
What is the likely diagnosis and causative organism for ear cleaning history presenting with tragal tenderness and erythema?
External otitis (swimmer’s ear) caused by Pseudomonas aeruginosa.
What is a common skin infection caused by direct inoculation that affects the nails?
Green nail syndrome.
What skin condition is characterized by thickened, macerated skin with a moth-eaten appearance?
Toe web infection.
What is the typical onset time for folliculitis associated with hot tubs?
24 hours following exposure to contaminated hot tubs.
What are the common symptoms of external otitis, also known as swimmer’s ear?
Acute onset of edema, erythema, and discharge from the ear canal.
What is the triad of symptoms associated with green nail syndrome?
Dyspigmentation, Onycholysis, Paronychia.
What is a serious complication of malignant otitis externa?
Skull base osteomyelitis.
What type of skin infection can lead to bacteremia in immunocompromised patients?
Localized skin infections in immunocompetent patients.
What is the common presentation of hot foot syndrome in children?
Acute painful erythematous, warm, plantar nodules after immersion in contaminated water.
What are the clinical features associated with Green nail syndrome and how does it present?
Green nail syndrome is characterized by:
- Nail dyspigmentation: greenish-yellow/brown/black due to debris and pyocyanin accumulation.
- Typically affects one or two digits, but can involve the entire or partial nail.
- Triad of symptoms: Dyspigmentation, Onycholysis, Paronychia.
Describe the presentation and common causes of Folliculitis/Hot tub folliculitis in adults.
Folliculitis is characterized by inflammation of hair follicles, often caused by bacteria or fungi, particularly in warm, moist environments like hot tubs.
What is Hot tub folliculitis?
Hot tub folliculitis presents with discrete follicular papules and pustules that heal with fine desquamation and hyperpigmented macules.
What is the onset time for symptoms of Hot tub folliculitis?
Sudden onset occurring 24 hours after exposure to contaminated hot tubs, often associated with pruritus or pain.
Which areas are commonly affected by Hot tub folliculitis?
Commonly affects areas covered by bathing suits, such as the upper trunk, axillary folds, hips, and buttocks.
What are the key clinical features of External otitis/Swimmer’s ear?
External otitis/Swimmer’s ear is characterized by acute onset of edema and erythema or discoloration of the external auditory canal (EAC), sometimes with maceration and discharge.
What symptoms are associated with External otitis/Swimmer’s ear?
Symptoms include tragal tenderness and pruritus.
Which age group is most commonly affected by External otitis/Swimmer’s ear?
Most common in children aged 5-14 years.
What is Malignant otitis externa?
Malignant otitis externa can occur, presenting with:
- Insidious onset with severe pain disproportionate to examination findings.
- Higher risk in elderly patients and diabetics.
- Can be life-threatening, leading to skull base osteomyelitis.
What are the clinical implications of localized skin infections in immunocompetent patients?
Localized skin infections in immunocompetent patients can become a source of bacteremia in immunocompromised patients. This highlights the importance of early identification and management of skin infections to prevent potential systemic complications, especially in vulnerable populations.
What are the classic findings associated with perichondritis following commercial piercings?
Classic findings include granulatin tissue.
What are classic findings in aural piercings?
Granulation tissue in the floor of the external auditory canal (EAC) and bony cartilaginous junction blocking the tympanic membrane (TM).
What are the characteristics of SQ nodules associated with bacteremia?
SQ nodules are warm, erythematous, indurated, usually non-fluctuant, and can be painful or less painful. They typically affect the face, neck, chest, abdomen, back, and extremities.
Describe the progression and appearance of ecthyma gangrenosum in patients with P. aeruginosa bacteremia.
Ecthyma gangrenosum begins as a painless, infarcted gunmetal gray macule or papule with surrounding erythema. It becomes indurated, and hemorrhagic bullae may develop. Over 12-18 hours, it progresses to a necrotic, ulcerative eschar with a halo of tender erythema. Common locations include anogenital, extremities, trunk, and face.
What non-cutaneous findings may be present in cases of bacteremia?
Non-cutaneous findings include fever and malaise, even in the absence of bacteremia or mild infections, and sepsis with systemic symptoms. Additionally, otitis externa (OE) may lead to conductive hearing loss and cranial nerve palsies (most commonly the facial nerve), as well as trismus and lockjaw.
What laboratory tests are recommended for diagnosing perichondritis?
For diagnosing perichondritis, otoscopy and cultures should be performed. Additionally, perichondritis should be cultured following incision and drainage (I and D).
What imaging technique is used to assess malignant otitis externa (OE) and what is its purpose?
CT/MRI is used to assess malignant otitis externa (OE) to evaluate the extent of the disease.
What is external otitis (OE) and what is its purpose?
CT/MRI is used to detect extension into the bony structures in cases of malignant otitis externa (OE). It helps differentiate from other conditions, such as squamous cell carcinoma (SCC).
What histopathological findings are associated with hot foot syndrome?
Histopathological findings in hot foot syndrome include perivascular, interstitial, and peri-adnexal neutrophils that extend to the lobules of subcutaneous fat and may include deep dermal or subcutaneous abscess.
What is the likely diagnosis and causative organism for a patient with a painless, infarcted gunmetal gray macule surrounded by erythema?
Ecthyma gangrenosum caused by Pseudomonas aeruginosa, commonly seen in neutropenic patients.
What is the likely diagnosis and causative organism for a patient with neutropenia presenting with fever, malaise, and necrotic skin lesions?
Bacteremia with ecthyma gangrenosum caused by.
What is the likely diagnosis and causative organism for a patient with diabetes presenting with necrotic cartilage following ear trauma?
Perichondritis caused by Pseudomonas aeruginosa, often following trauma or contaminated cleaning agents.
What is the likely diagnosis and causative organism for a patient with a history of chemotherapy presenting with fever and subcutaneous nodules?
Bacteremia with subcutaneous nodules caused by Pseudomonas aeruginosa, commonly seen in immunocompromised patients.
What is the likely diagnosis and causative organism for a patient presenting with a necrotic ulcerative eschar surrounded by tender erythema?
Ecthyma gangrenosum caused by Pseudomonas aeruginosa, commonly seen in neutropenic patients.
What is the likely diagnosis and causative organism for a patient with a history of burns developing a necrotic skin lesion with a gunmetal gray center?
Ecthyma gangrenosum caused by Pseudomonas aeruginosa.
What is the likely diagnosis and causative organism for a patient with neutropenia presenting with fever and necrotic skin lesions?
Bacteremia with ecthyma gangrenosum caused by Pseudomonas aeruginosa.
What is commonly seen in immunocompromised patients?
Infections caused by Pseudomonas aeruginosa.
What are the classic findings associated with external auditory canal (EAC) infections?
Granulation tissue in the floor of EAC and bony cartilaginous junction blocking the tympanic membrane (TM).
What is perichondritis and what can cause it?
An infection following commercial piercings due to contaminated cleansing agents, trauma, or acupuncture, leading to rapid cartilage necrosis.
What are SQ nodules and their characteristics in the context of bacteremia?
Warm, erythematous, indurated, usually non-fluctuant, and painful/less, affecting the face, neck, chest, abdomen, back, and extremities.
What is ecthyma gangrenosum and how does it present?
Necrotic lesions associated with P. aeruginosa bacteremia, beginning as a painless, infarcted gray macule or papule with surrounding erythema, which can develop into a necrotic ulcerative eschar.
What non-cutaneous findings can occur with Pseudomonas infections?
Fever and malaise, sepsis with systemic symptoms, and conductive hearing loss with cranial nerve palsies.
