Infectious Disease and Microbiology – Coxsackievirus Group

Overview

Coxsackieviruses are members of the enterovirus group and are divided mainly into coxsackievirus A and coxsackievirus B, each of which contains multiple serotypes.

They are common worldwide pathogens and are responsible for a wide range of clinical syndromes, including mucocutaneous disease, respiratory illness, myocarditis, meningitis, and neonatal disseminated infection.

Microbiologic Characteristics

Coxsackieviruses are:

• Single-stranded, positive-sense RNA viruses

• Nonenveloped (naked)

• Viruses with icosahedral symmetry

Because they are nonenveloped, they are relatively resistant to environmental conditions compared with enveloped viruses.

Epidemiology

Coxsackievirus infections occur worldwide and are a common cause of human illness.

Transmission is mainly through the fecal–oral route, although respiratory spread can also occur, particularly in syndromes involving the upper respiratory tract.

Children are commonly affected, but infection can occur at any age.

Hand-Foot-and-Mouth Disease

Coxsackievirus A is classically associated with hand-foot-and-mouth disease.

This syndrome is characterized by:

• Oral vesicles or ulcers

• Vesicular or papular lesions on the hands

• Lesions on the feet

• Fever

• Malaise

The mucosal lesions represent an enanthem, while the skin lesions represent an exanthem.

Herpangina

Herpangina is another classic coxsackievirus-associated syndrome.

It usually presents with:

• Fever

• Sore throat

• Painful vesicles or ulcers in the posterior oropharynx

• Difficulty swallowing

Coxsackievirus A is an important cause.

Upper Respiratory Tract Infection

Coxsackieviruses may produce nonspecific upper respiratory tract infections characterized by symptoms such as:

• Sore throat

• Rhinorrhea

• Cough

• Fever

• Malaise

Pleurodynia

Coxsackievirus B is classically associated with epidemic pleurodynia, also called Bornholm disease.

Patients may develop sudden episodes of:

• Severe chest pain

• Upper abdominal pain

• Fever

• Pain worsened by respiration or movement

The pain is related to inflammation of the chest wall and intercostal muscles.

Myopericarditis

Coxsackievirus B is an important viral cause of myocarditis and pericarditis.

Clinical manifestations may include:

• Chest pain

• Dyspnea

• Palpitations

• Arrhythmias

• Signs of heart failure

• Pericarditic pain

Severe myocarditis can occasionally result in substantial cardiac dysfunction.

Acute Hemorrhagic Conjunctivitis

Certain enteroviruses, including some coxsackievirus strains, may cause acute hemorrhagic conjunctivitis.

Patients may develop:

• Red eyes

• Eye discomfort

• Photophobia

• Conjunctival hemorrhage

• Excessive tearing

Central Nervous System Infection

Coxsackieviruses are important causes of aseptic meningitis.

They may also cause:

• Encephalitis

• Meningoencephalitis

• Rare paralytic syndromes

Neurologic infection may occur in both children and adults.

Chronic Meningoencephalitis

A particularly important complication can occur in severely immunocompromised patients, especially those with agammaglobulinemia.

These patients may develop chronic enteroviral meningoencephalitis because they lack adequate antibody-mediated immunity to control the infection.

Neonatal Disseminated Infection

Newborns can develop severe disseminated coxsackievirus infection.

This may involve multiple organs and can produce:

• Sepsis-like illness

• Myocarditis

• Hepatitis

• Meningoencephalitis

• Coagulopathy

• Shock

Neonatal disease may be rapidly progressive and life-threatening.

Diagnosis

Diagnosis can be established using:

• PCR

• Virologic culture

• Serologic testing

PCR is particularly useful for detecting enteroviral RNA in appropriate clinical specimens, including cerebrospinal fluid in suspected meningitis.

Treatment

Treatment is primarily supportive and symptomatic.

Management depends on the clinical syndrome and may include:

• Hydration

• Antipyretics and analgesics

• Cardiac monitoring for myocarditis

• Respiratory support when necessary

• Intensive supportive care in severe neonatal infection

Specific Antiviral Therapy

There is no routinely available specific antiviral treatment for most coxsackievirus infections.

Most uncomplicated infections resolve spontaneously.

Prevention

Prevention is based primarily on reducing transmission.

Important measures include:

• Careful hand hygiene

• Proper disposal of fecal material

• Avoiding close contact with infected secretions

• Enteric precautions during the contagious period

• Respiratory precautions when appropriate, such as during herpangina

Older recommendations include enteric isolation for approximately 1 week.

High-Yield Clinical Associations

Coxsackievirus A

→ Hand-foot-and-mouth disease

→ Herpangina

Coxsackievirus B

→ Pleurodynia

→ Myocarditis

→ Pericarditis

Both groups

→ Aseptic meningitis and other enteroviral syndromes

Exam Essentials

Group: Enterovirus

Genome: Positive-sense single-stranded RNA

Envelope: None

Capsid: Icosahedral

Distribution: Worldwide

Major syndromes: Hand-foot-and-mouth disease, herpangina, pleurodynia, myopericarditis, meningitis

Severe neonatal disease: Disseminated infection

High-risk chronic CNS disease: Agammaglobulinemia

Diagnosis: PCR, culture, serology

Treatment: Supportive

Specific antiviral: None routinely available

Prevention: Enteric and respiratory hygiene precautions

Key clinical pearl: The classic exam distinction is coxsackie A → hand-foot-and-mouth disease and herpangina, whereas coxsackie B → pleurodynia and myopericarditis.

Infectious Disease and Microbiology – Corynebacterium Species

Overview

Non-diphtherial Corynebacterium species are aerobic Gram-positive bacilli that are usually low-virulence organisms but can occasionally cause serious invasive disease. Important species include C. bovis, C. pilosum, C. pseudodiphtheriticum, C. striatum, and C. xerosis, among others.

These organisms are uncommon causes of infection, but they become more clinically significant in patients with neutropenia, prosthetic devices, or underlying cardiac disease.

Microbiologic Characteristics

Corynebacterium species are:

• Aerobic

• Gram-positive

• Bacillary organisms

Many species can colonize the skin or mucosal surfaces, which means that positive cultures must sometimes be interpreted carefully to distinguish true infection from contamination or colonization.

Epidemiology

These species are rare causes of human infection.

Clinically significant disease is more likely in patients with:

• Neutropenia

• Prosthetic heart valves

• Other implanted prosthetic material

• Severe underlying illness

• Prolonged hospitalization

Endocarditis

Non-diphtherial Corynebacterium species can cause infective endocarditis involving either:

• Native heart valves

• Prosthetic heart valves

Prosthetic valve infection is especially important because organisms may adhere to foreign material and become difficult to eradicate with antibiotics alone.

Septicemia

Septicemia is uncommon but occurs more frequently in neutropenic patients.

Patients may present with:

• Fever

• Chills

• Hypotension

• Persistent bacteremia

• Clinical evidence of sepsis

Repeated recovery of the same Corynebacterium species from blood cultures increases the likelihood that the isolate represents true infection rather than contamination.

Respiratory Tract Infections

These organisms can occasionally cause:

• Pneumonia

• Tracheitis

• Other respiratory tract infections

Respiratory disease is more likely in debilitated, hospitalized, or immunocompromised patients.

Prosthetic Material Infection

Corynebacterium species may infect implanted or prosthetic material.

Examples include:

• Prosthetic heart valves

• Vascular devices

• Orthopedic hardware

• Other implanted foreign bodies

Because biofilm formation and persistent colonization may occur, antimicrobial therapy alone may not always be sufficient.

Diagnosis

Diagnosis is made by culture from the appropriate clinical specimen.

Depending on the infection, samples may include:

• Blood cultures

• Respiratory specimens

• Tissue samples

• Prosthetic-device cultures

• Other sterile-site specimens

Clinical interpretation is important because some Corynebacterium species may be dismissed incorrectly as contaminants.

Treatment of Endocarditis

For severe endocarditis, a regimen described in the source is:

Vancomycin plus an aminoglycoside

This combination may be used initially in serious infection while awaiting susceptibility results.

Prosthetic Material Removal

When infection involves prosthetic material, removal of the infected device or prosthesis is frequently necessary.

Persistent infection despite apparently appropriate antimicrobial treatment should increase suspicion that the foreign material is acting as a continuing source.

Additional Antimicrobial Options

Therapy may need to be modified according to:

• Clinical response

• Site of infection

• Species identification

• In vitro susceptibility testing

Potential alternative agents include:

• Penicillin G

• Tetracycline

• Macrolides

• Rifampicin

• First-generation cephalosporins

• Teicoplanin

Treatment should be individualized because susceptibility patterns may vary among species.

High-Yield Clinical Pattern

Prosthetic valve or implanted device

• ●

Persistent bacteremia with a Corynebacterium species

• ●

Failure to clear infection with antibiotics alone

→ Consider true invasive Corynebacterium infection with infected prosthetic material

Exam Essentials

Genus: Corynebacterium

Type: Aerobic Gram-positive bacillus

Overall frequency: Rare cause of infection

Important syndromes: Endocarditis, septicemia, pneumonia, tracheitis, prosthetic-device infection

High-risk group for septicemia: Neutropenic patients

Diagnosis: Culture

Serious endocarditis treatment: Vancomycin plus an aminoglycoside

Important source-control measure: Removal of infected prosthetic material

Alternative agents: Penicillin G, tetracyclines, macrolides, rifampicin, first-generation cephalosporins, or teicoplanin

Key clinical pearl: When a non-diphtherial Corynebacterium species is repeatedly isolated from blood in a patient with a prosthetic valve, implanted device, or neutropenia, it should not automatically be dismissed as a contaminant.

Infectious Disease and Microbiology – Corynebacterium pseudotuberculosis

Overview

Corynebacterium pseudotuberculosis is an aerobic Gram-positive bacillus that primarily causes disease in animals and is only a rare cause of human infection. Human disease is usually associated with occupational or environmental exposure to infected animals.

The characteristic human manifestation is suppurative granulomatous lymphadenitis.

Microbiologic Characteristics

C. pseudotuberculosis is an aerobic, Gram-positive bacillus belonging to the genus Corynebacterium.

It is primarily an animal pathogen, with humans serving as accidental hosts following zoonotic exposure.

Epidemiology

Human infection is rare.

Most cases occur in people with significant contact with animals, particularly individuals whose occupations involve livestock or animal handling.

Potential exposure groups include:

• Farmers

• Veterinarians

• Abattoir workers

• Animal handlers

• Other individuals with close livestock exposure

Transmission

Human infection generally follows exposure to infected animals or contaminated animal material.

The organism may enter through breaks in the skin and subsequently spread through lymphatic channels to regional lymph nodes.

Suppurative Granulomatous Lymphadenitis

The classic human infection is suppurative granulomatous lymphadenitis.

Affected lymph nodes may become:

• Enlarged

• Painful or tender

• Inflamed

• Suppurative

• Chronically infected

The disease can resemble other causes of chronic granulomatous lymphadenopathy.

Differential Diagnosis

Important alternative causes of chronic or suppurative lymphadenitis include:

• Tuberculosis

• Nontuberculous mycobacterial infection

• Cat-scratch disease

• Tularemia

• Fungal infection

• Other bacterial lymphadenitis

A history of animal exposure provides an important clue to C. pseudotuberculosis infection.

Diagnosis

Definitive diagnosis is established by culture of material obtained from the infected lymph node or another appropriate specimen.

The organism can be cultured on:

Blood agar incubated with approximately 10% CO₂

Microbiologic identification is important because the clinical appearance can mimic several other causes of granulomatous lymphadenitis.

Treatment

Macrolide antibiotics may be used for C. pseudotuberculosis infection.

Treatment is often combined with appropriate management of the infected lymph nodes.

Surgical Management

Excision of infected lymph nodes may be necessary, particularly when lymphadenitis is persistent, suppurative, or inadequately responsive to antimicrobial therapy.

Thus, effective management may require both:

Antimicrobial therapy + surgical excision

Additional Treatment

Alternative antimicrobial agents include:

• Tetracyclines

• Penicillin G

Whenever possible, treatment of significant infection should be guided by culture and antimicrobial susceptibility results.

High-Yield Clinical Pattern

Animal or livestock exposure

• ●

Chronic enlarged lymph nodes

• ●

Suppurative granulomatous lymphadenitis

→ Think Corynebacterium pseudotuberculosis

Exam Essentials

Organism: Corynebacterium pseudotuberculosis

Type: Aerobic Gram-positive bacillus

Transmission: Zoonotic exposure, usually involving animals

Human infection: Rare

Classic manifestation: Suppurative granulomatous lymphadenitis

Diagnosis: Culture

Culture condition: Blood agar with approximately 10% CO₂

Treatment: Macrolide antibiotic

Source control: Excision of infected lymph nodes when indicated

Alternatives: Tetracycline or penicillin G

Key clinical pearl: The combination of animal exposure and chronic suppurative granulomatous lymphadenitis should raise suspicion for Corynebacterium pseudotuberculosis.

Infectious Disease and Microbiology – Corynebacterium minutissimum

Overview

Corynebacterium minutissimum is an aerobic Gram-positive bacillus best known as a common cause of erythrasma, a superficial skin infection that typically affects intertriginous areas. Although usually limited to the skin, the organism can rarely cause invasive disease such as bacteremia, sepsis, or endocarditis, particularly in immunocompromised patients.

Microbiologic Characteristics

C. minutissimum is an aerobic, Gram-positive bacillus belonging to the genus Corynebacterium.

It is primarily associated with superficial cutaneous infection, but under certain conditions it can invade deeper tissues or enter the bloodstream.

Epidemiology

C. minutissimum is a relatively common cause of superficial skin infection.

Erythrasma is especially associated with warm, moist areas of the body and is often seen in skin folds.

Erythrasma

The most characteristic infection caused by C. minutissimum is erythrasma.

It typically presents as:

• Well-demarcated reddish-brown patches

• Mild scaling

• Minimal inflammation

• Involvement of intertriginous areas such as the groin, axillae, or toe webs

The lesions may be asymptomatic or mildly pruritic.

Wood’s Lamp Examination

A classic diagnostic finding in erythrasma is coral-red fluorescence under a Wood’s lamp.

This occurs because C. minutissimum produces porphyrin compounds that fluoresce under ultraviolet light.

This finding is highly useful in distinguishing erythrasma from other intertriginous dermatoses.

Systemic Infection

Although uncommon, C. minutissimum can cause more serious invasive infections.

Reported manifestations include:

• Sepsis

• Endocarditis

• Bacteremia

• Subcutaneous tissue infection

These complications are more likely in patients with significant immunosuppression, particularly those with neutropenia.

Subcutaneous Tissue Infection

The organism may occasionally invade deeper tissues and produce localized subcutaneous infection.

Such cases should be evaluated carefully because they may indicate impaired host defenses or deeper tissue involvement.

Diagnosis

Diagnosis is based on:

• Culture of the organism from an appropriate clinical specimen

• Wood’s lamp examination in suspected erythrasma

The combination of a typical intertriginous rash and coral-red fluorescence strongly supports the diagnosis of erythrasma.

Treatment of Erythrasma

A classic systemic treatment regimen is:

Erythromycin 250 mg orally every 6 hours for 14 days

Local treatment with:

2% aqueous clindamycin

may also be effective.

Additional Treatment

Another option is:

Tetracycline 250 mg orally every 6 hours

Treatment choice may depend on severity, extent of disease, tolerance, and antimicrobial susceptibility where relevant.

Treatment of Systemic Infection

For serious systemic infection caused by C. minutissimum, such as sepsis or endocarditis:

Vancomycin is an important treatment option.

Management should also include evaluation for the source of infection and any underlying immunosuppressive condition.

High-Yield Clinical Pattern

Brown-red rash in a skin fold

• ●

Coral-red fluorescence with Wood’s lamp

→ Think Corynebacterium minutissimum causing erythrasma

Exam Essentials

Organism: Corynebacterium minutissimum

Type: Aerobic Gram-positive bacillus

Classic disease: Erythrasma

Typical site: Intertriginous skin folds

Key diagnostic clue: Coral-red fluorescence under Wood’s lamp

Other infections: Subcutaneous infection, sepsis, endocarditis

High-risk group for invasive disease: Neutropenic patients

Diagnosis: Culture and Wood’s lamp examination

Treatment of erythrasma: Erythromycin or topical clindamycin

Treatment of systemic infection: Vancomycin

Key clinical pearl: The classic association is erythrasma + coral-red Wood’s lamp fluorescence = Corynebacterium minutissimum.

Infectious Disease and Microbiology – Corynebacterium jeikeium

Overview

Corynebacterium jeikeium is an uncommon aerobic Gram-positive bacillus that acts mainly as an opportunistic pathogen. Infection is seen most often in patients with significant immunosuppression, particularly those with neutropenia or advanced HIV infection.

Microbiologic Characteristics

C. jeikeium is an aerobic, Gram-positive bacillus belonging to the genus Corynebacterium.

It is generally considered a low-frequency pathogen but can cause serious invasive disease in susceptible hosts.

Epidemiology

C. jeikeium infection is rare and occurs worldwide.

The organism is encountered primarily in hospitalized or immunocompromised patients, especially those with impaired host defenses or indwelling vascular devices.

Risk Groups

Clinically significant infection is most strongly associated with immunosuppression.

Important risk groups include:

• Patients with neutropenia

• Patients with advanced HIV infection

• Patients with prolonged hospitalization

• Patients with central venous catheters or other intravascular devices

Clinical Infections

C. jeikeium can cause several serious infections in vulnerable patients.

Sepsis

Bloodstream infection may progress to sepsis, particularly in severely immunocompromised patients.

Patients may present with fever, hypotension, systemic inflammatory findings, and other signs of invasive infection.

Endocarditis

C. jeikeium may cause infective endocarditis, especially in patients with underlying risk factors such as prosthetic material, prolonged bacteremia, or intravascular devices.

Central Venous Catheter-Associated Infection

Central venous catheters are an important potential source of infection.

Catheter-associated disease may present with:

• Persistent fever

• Positive blood cultures

• Local catheter-site inflammation

• Bacteremia or sepsis

Removal of an infected catheter may be required in addition to antimicrobial therapy.

Pneumonia

C. jeikeium can occasionally cause pneumonia, particularly in immunosuppressed patients.

Clinical manifestations may include fever, cough, dyspnea, hypoxemia, and pulmonary infiltrates.

Meningitis

Although uncommon, C. jeikeium can cause meningitis, particularly in patients with severe immune compromise.

This represents a serious invasive manifestation requiring prompt antimicrobial treatment.

Diagnosis

Diagnosis is made by culture from the appropriate clinical specimen.

Potential specimens include:

• Blood

• Catheter-related samples

• Cerebrospinal fluid

• Respiratory specimens

• Other normally sterile-site samples

Because corynebacteria may sometimes be dismissed as contaminants, repeated isolation of C. jeikeium in a compatible clinical setting should be taken seriously.

Treatment

Vancomycin is the principal treatment for serious C. jeikeium infection.

This is particularly important because the organism may show resistance to multiple other antimicrobial classes.

Additional Treatment

An alternative regimen described in older sources is:

Penicillin G combined with an antipseudomonal aminoglycoside

However, treatment should ideally be guided by antimicrobial susceptibility testing, especially in severe invasive disease.

High-Yield Clinical Pattern

Immunocompromised or neutropenic patient

• ●

Central venous catheter or prolonged hospitalization

• ●

Gram-positive bacillus in blood cultures

→ Consider Corynebacterium jeikeium

Exam Essentials

Organism: Corynebacterium jeikeium

Type: Aerobic Gram-positive bacillus

Epidemiology: Rare, worldwide infection

Major risk groups: Neutropenic and immunosuppressed patients

Important infections: Sepsis, endocarditis, catheter-associated infection, pneumonia, meningitis

Diagnosis: Culture

First-line treatment: Vancomycin

Alternative: Penicillin G plus an antipseudomonal aminoglycoside

Key clinical pearl: Corynebacterium jeikeium should not automatically be dismissed as a contaminant when isolated from a seriously immunocompromised patient, particularly when bacteremia or a central venous catheter infection is suspected.

Infectious Disease and Microbiology – Coronavirus Group

Overview

Coronaviruses are enveloped, positive-sense single-stranded RNA viruses capable of causing respiratory and gastrointestinal disease. Human coronaviruses range from viruses producing mild common-cold syndromes to novel coronaviruses capable of causing severe systemic and lower respiratory tract disease.

Microbiologic Characteristics

Coronaviruses are:

• Single-stranded, positive-sense RNA viruses
• Enveloped viruses

Their surface spike glycoproteins produce the characteristic crown-like appearance responsible for the name coronavirus.

Incubation Period

For the common respiratory coronaviruses described in the source material, the incubation period is generally approximately 2–4 days.

Incubation periods vary among individual coronavirus species and syndromes.

Epidemiology

Human coronavirus infections occur worldwide.

Common human coronaviruses circulate widely and are frequent causes of respiratory infections. Transmission occurs predominantly through respiratory secretions and close contact.

Upper Respiratory Tract Infection

Common human coronaviruses frequently produce relatively mild respiratory illnesses resembling the common cold.

Clinical manifestations may include:

• Rhinorrhea
• Nasal congestion
• Sore throat
• Cough
• Headache
• Malaise
• Fever

They may also be associated with other upper respiratory manifestations, including sinusitis.

Lower Respiratory Tract Infection

Although uncommon with traditional common-cold coronaviruses, infection may occasionally progress to pneumonia in children or adults.

Lower respiratory disease is more clinically important in vulnerable populations and with the highly pathogenic novel coronaviruses.

Severe Acute Respiratory Syndrome (SARS)

A novel coronavirus was identified as the cause of severe acute respiratory syndrome (SARS).

SARS demonstrated that members of the coronavirus family can emerge from animal reservoirs and produce severe human respiratory disease with substantial outbreak potential.

Subsequent decades also saw the emergence of other clinically important coronaviruses, including the viruses responsible for MERS and COVID-19.

Gastrointestinal Disease

Coronaviruses may also be associated with gastrointestinal manifestations, including diarrhea. The degree of gastrointestinal involvement varies according to the particular coronavirus and clinical syndrome.

Diagnosis

Specific viral identification is generally unnecessary in routine uncomplicated common-cold illness, because the result usually does not change management.

When specific identification is clinically or epidemiologically important, diagnostic approaches can include:

PCR: Molecular detection is an important method for identifying specific coronaviruses.

Antigen detection: Viral antigens can be detected using appropriate assays for certain coronavirus infections.

Electron microscopy: Coronaviruses can be visualized directly by electron microscopy, although this is primarily a specialized or historical diagnostic technique rather than a routine clinical test.

Treatment

For uncomplicated infections caused by common respiratory coronaviruses, treatment is primarily symptomatic and supportive.

Management may include adequate hydration, rest, fever control, and symptomatic treatment of respiratory complaints.

Treatment of severe disease caused by specific emerging coronaviruses differs substantially and should not be generalized from treatment recommendations for common-cold coronaviruses.

Prevention

General respiratory infection prevention measures include reducing exposure to infected individuals, appropriate hand hygiene, respiratory hygiene, and improving ventilation in crowded indoor environments.

The older recommendation to simply avoid crowded places during winter months reflects the increased circulation of many respiratory viruses during colder seasons but is not a coronavirus-specific preventive strategy.

High-Yield Clinical Pattern

Enveloped virus + positive-sense single-stranded RNA + respiratory infection → think coronavirus.

Common human coronaviruses

→ Common cold / upper respiratory infection

Novel highly pathogenic coronaviruses

→ Potential severe lower respiratory disease and outbreaks

Exam Essentials

Family/group: Coronavirus

Genome: Positive-sense single-stranded RNA

Envelope: Present

Distribution: Worldwide

Common presentation: Upper respiratory tract infection/common cold

Other manifestations: Sinusitis, pneumonia, diarrhea

Historical severe syndrome: SARS

Diagnosis when indicated: PCR or antigen testing

Routine common cold: Specific coronavirus testing usually unnecessary

Treatment of uncomplicated common coronavirus infection: Supportive/symptomatic

Key clinical pearl: Coronaviruses are enveloped, positive-sense single-stranded RNA viruses whose clinical spectrum extends from the ordinary common cold to severe emerging respiratory syndromes.

→ Common cold / upper respiratory infection Novel highly pathogenic coronaviruses

→ Potential severe lower respiratory disease and outbreaks Exam Essentials Family/group: Coronavirus

Genome: Positive-sense single-stranded RNA

Envelope: Present

Distribution: Worldwide

Common presentation: Upper respiratory tract infection/common cold

Other manifestations: Sinusitis, pneumonia, diarrhea

Historical severe syndrome: SARS

Diagnosis when indicated: PCR or antigen testing

Routine common cold: Specific coronavirus testing usually unnecessary

Treatment of uncomplicated common coronavirus infection: Supportive/symptomatic Key clinical pearl: Coronaviruses are enveloped, positive-sense single-stranded RNA viruses whose clinical spectrum extends from the ordinary common cold to severe emerging respiratory syndromes.

Infectious Disease and Microbiology – Conidiobolus Species

Overview

Conidiobolus coronatus is an uncommon filamentous fungus (mold) that primarily causes a chronic granulomatous infection of the nasal and facial subcutaneous tissues. The characteristic disease is called entomophthoromycosis conidiobolae, also known as conidiobolomycosis.

Microbiologic Characteristics

Conidiobolus coronatus is a filamentous fungus with broad hyphae containing relatively few septa. Infection typically produces a chronic granulomatous tissue response rather than the rapidly invasive necrosis characteristic of some other molds.

Epidemiology

The organism is primarily encountered in tropical regions, particularly:

• Central America
• Equatorial Africa
• India

Human infection is uncommon and generally occurs following environmental exposure.

Clinical Manifestations

Entomophthoromycosis Conidiobolae

The classic presentation is a slowly progressive granulomatous infection involving the nose, mouth, and surrounding facial tissues.

Patients may develop firm subcutaneous nodules and progressive swelling of the nasal and perinasal areas. Lesions can become extremely large and cause substantial facial disfigurement.

Rare manifestations include mediastinitis and pericarditis.

Diagnosis

Diagnosis is established by demonstrating fungal elements in a tissue biopsy and by obtaining a fungal culture.

Histopathologic examination is particularly useful when evaluating a chronic granulomatous facial mass.

Treatment

Because conidiobolomycosis is rare, evidence regarding optimal treatment is limited.

Saturated potassium iodide solution has traditionally been used for cutaneous and subcutaneous disease, either alone or with trimethoprim-sulfamethoxazole (TMP-SMX).

Azole antifungals such as fluconazole or ketoconazole have also historically been reported to produce improvement, particularly in more severe disease.

Large, persistent, or markedly disfiguring lesions may require surgical management, usually in conjunction with medical therapy.

High-Yield Clinical Pattern

Tropical exposure + slowly enlarging nodular nasal/perinasal mass + chronic granulomatous inflammation → consider Conidiobolus coronatus.

Key clinical pearl: Unlike rapidly invasive fungal infections, conidiobolomycosis classically produces a chronic, slowly progressive, disfiguring rhinofacial infection.

Infectious Disease and Microbiology – Coronavirus Group

Overview

Coronaviruses are enveloped, positive-sense single-stranded RNA viruses capable of causing respiratory and gastrointestinal disease. Human coronaviruses range from viruses producing mild common-cold syndromes to novel coronaviruses capable of causing severe systemic and lower respiratory tract disease.

Microbiologic Characteristics

Coronaviruses are:

• Single-stranded, positive-sense RNA viruses
• Enveloped viruses

Their surface spike glycoproteins produce the characteristic crown-like appearance responsible for the name coronavirus.

Incubation Period

For the common respiratory coronaviruses described in the source material, the incubation period is generally approximately 2–4 days.

Incubation periods vary among individual coronavirus species and syndromes.

Epidemiology

Human coronavirus infections occur worldwide.

Common human coronaviruses circulate widely and are frequent causes of respiratory infections. Transmission occurs predominantly through respiratory secretions and close contact.

Upper Respiratory Tract Infection

Common human coronaviruses frequently produce relatively mild respiratory illnesses resembling the common cold.

Clinical manifestations may include:

• Rhinorrhea
• Nasal congestion
• Sore throat
• Cough
• Headache
• Malaise
• Fever

They may also be associated with other upper respiratory manifestations, including sinusitis.

Lower Respiratory Tract Infection

Although uncommon with traditional common-cold coronaviruses, infection may occasionally progress to pneumonia in children or adults.

Lower respiratory disease is more clinically important in vulnerable populations and with the highly pathogenic novel coronaviruses.

Severe Acute Respiratory Syndrome (SARS)

A novel coronavirus was identified as the cause of severe acute respiratory syndrome (SARS).

SARS demonstrated that members of the coronavirus family can emerge from animal reservoirs and produce severe human respiratory disease with substantial outbreak potential.

Subsequent decades also saw the emergence of other clinically important coronaviruses, including the viruses responsible for MERS and COVID-19.

Gastrointestinal Disease

Coronaviruses may also be associated with gastrointestinal manifestations, including diarrhea. The degree of gastrointestinal involvement varies according to the particular coronavirus and clinical syndrome.

Diagnosis

Specific viral identification is generally unnecessary in routine uncomplicated common-cold illness, because the result usually does not change management.

When specific identification is clinically or epidemiologically important, diagnostic approaches can include:

PCR: Molecular detection is an important method for identifying specific coronaviruses.

Antigen detection: Viral antigens can be detected using appropriate assays for certain coronavirus infections.

Electron microscopy: Coronaviruses can be visualized directly by electron microscopy, although this is primarily a specialized or historical diagnostic technique rather than a routine clinical test.

Treatment

For uncomplicated infections caused by common respiratory coronaviruses, treatment is primarily symptomatic and supportive.

Management may include adequate hydration, rest, fever control, and symptomatic treatment of respiratory complaints.

Treatment of severe disease caused by specific emerging coronaviruses differs substantially and should not be generalized from treatment recommendations for common-cold coronaviruses.

Prevention

General respiratory infection prevention measures include reducing exposure to infected individuals, appropriate hand hygiene, respiratory hygiene, and improving ventilation in crowded indoor environments.

The older recommendation to simply avoid crowded places during winter months reflects the increased circulation of many respiratory viruses during colder seasons but is not a coronavirus-specific preventive strategy.

High-Yield Clinical Pattern

Enveloped virus + positive-sense single-stranded RNA + respiratory infection → think coronavirus.

Common human coronaviruses

→ Common cold / upper respiratory infection

Novel highly pathogenic coronaviruses

→ Potential severe lower respiratory disease and outbreaks

Exam Essentials

Family/group: Coronavirus

Genome: Positive-sense single-stranded RNA

Envelope: Present

Distribution: Worldwide

Common presentation: Upper respiratory tract infection/common cold

Other manifestations: Sinusitis, pneumonia, diarrhea

Historical severe syndrome: SARS

Diagnosis when indicated: PCR or antigen testing

Routine common cold: Specific coronavirus testing usually unnecessary

Treatment of uncomplicated common coronavirus infection: Supportive/symptomatic

Key clinical pearl: Coronaviruses are enveloped, positive-sense single-stranded RNA viruses whose clinical spectrum extends from the ordinary common cold to severe emerging respiratory syndromes.

Infectious Disease and Microbiology – Coronavirus Group Overview Coronaviruses are enveloped, positive-sense single-stranded RNA viruses capable of causing respiratory and gastrointestinal disease. Human coronaviruses range from viruses producing mild common-cold syndromes to novel coronaviruses capable of causing severe systemic and lower respiratory tract disease. Microbiologic Characteristics Coronaviruses are:  Single-stranded, positive-sense RNA viruses Enveloped viruses  Their surface spike glycoproteins produce the characteristic crown-like appearance responsible for the name coronavirus. Incubation Period For the common respiratory coronaviruses described in the source material, the incubation period is generally approximately 2–4 days. Incubation periods vary among individual coronavirus species and syndromes. Epidemiology Human coronavirus infections occur worldwide. Common human coronaviruses circulate widely and are frequent causes of respiratory infections. Transmission occurs predominantly through respiratory secretions and close contact. Upper Respiratory Tract Infection Common human coronaviruses frequently produce relatively mild respiratory illnesses resembling the common cold. Clinical manifestations may include:  Rhinorrhea Nasal congestion Sore throat Cough Headache Malaise Fever  They may also be associated with other upper respiratory manifestations, including sinusitis. Lower Respiratory Tract Infection Although uncommon with traditional common-cold coronaviruses, infection may occasionally progress to pneumonia in children or adults. Lower respiratory disease is more clinically important in vulnerable populations and with the highly pathogenic novel coronaviruses. Severe Acute Respiratory Syndrome (SARS) A novel coronavirus was identified as the cause of severe acute respiratory syndrome (SARS). SARS demonstrated that members of the coronavirus family can emerge from animal reservoirs and produce severe human respiratory disease with substantial outbreak potential. Subsequent decades also saw the emergence of other clinically important coronaviruses, including the viruses responsible for MERS and COVID-19. Gastrointestinal Disease Coronaviruses may also be associated with gastrointestinal manifestations, including diarrhea. The degree of gastrointestinal involvement varies according to the particular coronavirus and clinical syndrome. Diagnosis Specific viral identification is generally unnecessary in routine uncomplicated common-cold illness, because the result usually does not change management. When specific identification is clinically or epidemiologically important, diagnostic approaches can include: PCR: Molecular detection is an important method for identifying specific coronaviruses. Antigen detection: Viral antigens can be detected using appropriate assays for certain coronavirus infections. Electron microscopy: Coronaviruses can be visualized directly by electron microscopy, although this is primarily a specialized or historical diagnostic technique rather than a routine clinical test. Treatment For uncomplicated infections caused by common respiratory coronaviruses, treatment is primarily symptomatic and supportive. Management may include adequate hydration, rest, fever control, and symptomatic treatment of respiratory complaints. Treatment of severe disease caused by specific emerging coronaviruses differs substantially and should not be generalized from treatment recommendations for common-cold coronaviruses. Prevention General respiratory infection prevention measures include reducing exposure to infected individuals, appropriate hand hygiene, respiratory hygiene, and improving ventilation in crowded indoor environments. The older recommendation to simply avoid crowded places during winter months reflects the increased circulation of many respiratory viruses during colder seasons but is not a coronavirus-specific preventive strategy. High-Yield Clinical Pattern Enveloped virus + positive-sense single-stranded RNA + respiratory infection → think coronavirus. Common human coronaviruses

→ Common cold / upper respiratory infection Novel highly pathogenic coronaviruses

→ Potential severe lower respiratory disease and outbreaks Exam Essentials Family/group: Coronavirus

Genome: Positive-sense single-stranded RNA

Envelope: Present

Distribution: Worldwide

Common presentation: Upper respiratory tract infection/common cold

Other manifestations: Sinusitis, pneumonia, diarrhea

Historical severe syndrome: SARS

Diagnosis when indicated: PCR or antigen testing

Routine common cold: Specific coronavirus testing usually unnecessary

Treatment of uncomplicated common coronavirus infection: Supportive/symptomatic Key clinical pearl: Coronaviruses are enveloped, positive-sense single-stranded RNA viruses whose clinical spectrum extends from the ordinary common cold to severe emerging respiratory syndromes.

Infectious Disease and Microbiology – Conidiobolus Species

Overview

Conidiobolus coronatus is a rare filamentous fungal pathogen that mainly causes a chronic granulomatous infection of the nasal and facial subcutaneous tissues. The disease is classically known as entomophthoromycosis conidiobolae or conidiobolomycosis.

It most often affects people living in tropical regions and typically produces slowly progressive, firm, disfiguring swelling around the nose and adjacent facial structures.

Microbiologic Characteristics

Conidiobolus coronatus is a filamentous fungus (mold).

Its hyphae are relatively broad and contain few septa. In tissue, the organism can trigger a prominent granulomatous inflammatory response.

This fungus differs from the more aggressive Mucorales because conidiobolomycosis usually progresses slowly and tends to remain localized to subcutaneous facial tissues.

Epidemiology

The infection occurs mainly in tropical and subtropical regions, especially:

• Central America

• Equatorial Africa

• India

Human infection is uncommon.

The fungus is environmental, and acquisition is thought to occur after inhalation or traumatic inoculation of fungal material into nasal or adjacent tissues.

Clinical Manifestations

Entomophthoromycosis Conidiobolae

The classic manifestation is a chronic granulomatous infection of the nose and surrounding tissues.

Patients may develop:

• Firm nasal swelling

• Subcutaneous nodules

• Thickening of perinasal tissues

• Facial distortion

• Involvement of the upper lip or adjacent oral tissues

The lesions often enlarge slowly over time and may become markedly disfiguring.

Unlike many invasive molds, tissue necrosis and rapid vascular invasion are not usually the dominant features.

Nasal and Facial Disease

The disease often begins around the nasal mucosa and extends into nearby subcutaneous tissues.

As the infection progresses, patients may develop:

• Nasal obstruction

• Facial swelling

• Firm masses

• Distortion of the nose

• Extension into the mouth or surrounding facial structures

Large lesions may interfere with breathing, eating, or normal facial function.

Mediastinitis and Pericarditis

Rarely, Conidiobolus infection can extend beyond the usual facial and subcutaneous sites.

Reported severe manifestations include:

• Mediastinitis

• Pericarditis

These forms are unusual but potentially serious.

Diagnosis

Diagnosis depends on demonstrating the fungus in affected tissue and confirming the organism by culture.

Tissue Biopsy

Biopsy can show:

• Fungal hyphae

• Granulomatous inflammation

• Characteristic inflammatory reaction around the fungal elements

Histopathology is particularly important because chronic facial swelling has a broad differential diagnosis.

Culture

Fungal culture can confirm Conidiobolus coronatus and distinguish it from other molds causing chronic subcutaneous infection.

Differential Diagnosis

Important considerations include:

• Basidiobolomycosis

• Mucormycosis

• Sporotrichosis

• Chromoblastomycosis

• Phaeohyphomycosis

• Chronic bacterial or mycobacterial infection

• Granulomatous inflammatory disease

• Neoplastic facial masses

A slowly progressive, non-necrotizing nasal or perinasal mass in a patient from a tropical region should raise suspicion for conidiobolomycosis.

Treatment

Because the disease is rare, high-quality treatment data are limited.

Potassium Iodide

A traditional treatment for cutaneous and subcutaneous disease is:

Saturated potassium iodide solution

This may be used alone or in combination with other agents.

Trimethoprim-Sulfamethoxazole

Trimethoprim-sulfamethoxazole has also been used, sometimes together with potassium iodide.

Azole Antifungals

Azoles have been reported to produce clinical improvement.

Older regimens include:

• Fluconazole

• Ketoconazole

Other systemic azoles may also be considered depending on susceptibility and clinical circumstances.

Surgical Management

Surgery may be helpful for:

• Large disfiguring lesions

• Localized masses causing functional impairment

• Disease not adequately controlled with medical therapy

Debulking or excision is usually combined with antifungal treatment rather than relied upon alone.

Prognosis

The infection usually progresses slowly and remains localized, but untreated disease can cause substantial facial deformity.

Early diagnosis and prolonged medical therapy generally improve the chance of controlling the infection and limiting disfigurement.

High-Yield Clinical Pattern

Tropical-region patient

• ●

Slowly progressive firm nasal or perinasal swelling

• ●

Large non-necrotic granulomatous facial mass

→ Think conidiobolomycosis due to Conidiobolus coronatus

Exam Essentials

Organism: Conidiobolus coronatus

Type: Filamentous fungus

Hyphae: Few septa

Geography: Tropical regions, especially Central America, equatorial Africa, and India

Classic disease: Entomophthoromycosis conidiobolae

Typical site: Nose and perinasal subcutaneous tissues

Typical lesion: Chronic nodular or granulomatous facial swelling

Major consequence: Disfiguring facial masses

Rare complications: Mediastinitis and pericarditis

Diagnosis: Tissue biopsy + fungal culture

Traditional treatment: Saturated potassium iodide

Other therapies: TMP-SMX and systemic azoles

Surgery: Useful for large or disfiguring lesions

Key clinical pearl: Conidiobolus coronatus classically causes a slowly progressive, firm, disfiguring rhinofacial subcutaneous infection in patients from tropical regions.

Medicine – Cataracts

A cataract is an opacity or clouding of the normally transparent crystalline lens of the eye. The loss of lens transparency interferes with the passage and focusing of light onto the retina, producing progressive, painless impairment of vision.

Cataracts may be congenital or acquired. Ageing is by far the most common cause, but cataracts can also occur because of genetic disorders, congenital infections, ultraviolet exposure, medications, ocular inflammation, metabolic disease, and several systemic disorders.

1. Clinical Features of Cataract

The typical presentation is gradual, painless deterioration of vision.

Patients may complain of blurred or cloudy vision, glare from bright lights, difficulty driving at night, reduced contrast sensitivity, altered colour perception, or frequent changes in their spectacle prescription.

Some patients describe halos around lights, particularly at night.

2. Red Reflex

As the lens becomes increasingly opaque, the normal red reflex may become reduced or absent.

With advanced cataract, the pupil itself may appear grey or white because the opaque lens is visible behind it.

This is particularly important in children because a white pupil or abnormal red reflex requires urgent assessment to distinguish cataract from other serious causes of leukocoria, especially retinoblastoma.

3. Congenital Cataracts

Congenital cataracts are present at birth or develop during early infancy.

They may affect one or both eyes and can result from genetic abnormalities, congenital infections, metabolic disorders, or developmental abnormalities.

Congenital cataracts are especially important because a dense cataract can prevent normal visual development and cause deprivation amblyopia.

Early detection and treatment are therefore essential.

4. Autosomal Dominant Inheritance

Inherited congenital cataracts frequently show an autosomal dominant inheritance pattern, although autosomal recessive and X-linked forms also exist.

A positive family history of childhood cataracts may therefore provide an important diagnostic clue.

The exact appearance and severity of inherited cataracts vary according to the underlying genetic abnormality.

5. Maternal Rubella Infection

Congenital rubella syndrome is a classic cause of congenital cataracts.

Maternal rubella infection, particularly during early pregnancy, can interfere with fetal eye development.

The classic congenital rubella pattern includes:

Cataracts + sensorineural deafness + congenital heart disease.

Cardiac abnormalities classically include patent ductus arteriosus and pulmonary artery stenosis.

6. CMV and Toxoplasmosis

Congenital cytomegalovirus (CMV) and congenital toxoplasmosis can produce important ocular disease.

However, cataract is much more classically associated with congenital rubella.

Congenital toxoplasmosis is particularly associated with chorioretinitis, while congenital CMV commonly causes chorioretinitis and neurological abnormalities.

Therefore, although these infections can be considered in congenital ocular disease, remember:

Rubella → classic congenital cataract association.

7. Down Syndrome

Children and adults with Down syndrome have an increased risk of several ocular abnormalities, including cataracts.

Cataracts may develop at a younger age than in the general population.

Other associated ocular problems include refractive errors, strabismus and keratoconus.

8. Age-Related Cataract

Age-related cataract, historically called senile cataract, is the most common form of cataract.

With increasing age, lens proteins undergo progressive structural and biochemical changes that reduce lens transparency.

The process is usually gradual and bilateral, although the severity may differ between the two eyes.

The modern term age-related cataract is preferred to “senile cataract.”

9. Types of Age-Related Cataract

Age-related cataracts can be classified according to the part of the lens predominantly affected.

Important patterns include:

Nuclear sclerotic cataract.

Cortical cataract.

Posterior subcapsular cataract.

Different patterns can coexist in the same patient.

10. Ultraviolet Light

Long-term exposure to ultraviolet radiation, particularly UV-B, is associated with an increased risk of cataract formation.

Chronic UV exposure contributes to oxidative and structural damage within the lens.

Appropriate UV-protective eyewear may therefore help reduce cumulative ocular ultraviolet exposure.

11. Corticosteroids

Long-term corticosteroid therapy is an important drug-related cause of cataract.

The classic pattern is a posterior subcapsular cataract.

The risk generally increases with greater cumulative steroid exposure, although susceptibility varies between individuals.

Steroids may also increase intraocular pressure and contribute to glaucoma in susceptible patients.

12. Other Drugs

Although corticosteroids are the classic examination association, several other medications can occasionally contribute to lens abnormalities.

A medication history should therefore form part of the assessment of unusually early or rapidly developing cataracts.

13. Uveitis

Chronic or recurrent uveitis can cause secondary cataract formation because persistent intraocular inflammation damages the lens environment.

The risk may be further increased because patients with significant uveitis often require prolonged corticosteroid treatment.

Therefore, cataract formation in uveitis may result from both:

Chronic inflammation + corticosteroid exposure.

14. High Myopia

High myopia is associated with an increased risk of developing cataracts and may lead to cataract formation at a younger age.

Highly myopic patients also have increased risks of other ocular complications, particularly retinal abnormalities.

15. Diabetes Mellitus

Diabetes mellitus is an important metabolic risk factor for cataract formation.

Chronic hyperglycaemia alters glucose metabolism within the lens, causing osmotic and oxidative changes that promote lens opacity.

Diabetic patients may therefore develop cataracts earlier and more rapidly than non-diabetic individuals.

16. Cushing Syndrome

Cushing syndrome can be associated with cataract formation, particularly in the context of prolonged glucocorticoid excess.

The relationship is especially relevant because exogenous corticosteroid therapy is itself a major cause of posterior subcapsular cataract.

17. Hypocalcaemia

Chronic hypocalcaemia can be associated with cataract formation.

This may occur in disorders such as hypoparathyroidism, where persistent low serum calcium contributes to abnormal lens metabolism.

Therefore:

Hypoparathyroidism → hypocalcaemia → cataracts is a useful clinical association.

18. Myotonic Dystrophy

Myotonic dystrophy has a strong association with cataracts.

The characteristic cataracts may have a distinctive multicoloured or “Christmas-tree” appearance on slit-lamp examination.

They can occur relatively early in life.

Other clues to myotonic dystrophy include myotonia, muscle weakness, frontal balding, cardiac conduction abnormalities, and endocrine manifestations.

19. Retinitis Pigmentosa

Retinitis pigmentosa is also associated with cataract formation.

The typical cataract associated with retinitis pigmentosa is a posterior subcapsular cataract.

Because RP itself progressively impairs retinal function, cataract formation can further reduce the patient’s remaining useful vision.

20. Diagnosis

Cataracts are diagnosed primarily by ophthalmological examination, particularly slit-lamp examination of the lens.

Visual acuity testing establishes the functional effect of the cataract.

The retina and optic nerve should also be assessed whenever possible because visual impairment may have more than one cause.

21. Treatment

The definitive treatment for a visually significant cataract is surgical removal of the opaque lens.

Modern cataract surgery commonly uses phacoemulsification, in which ultrasound energy fragments the cataractous lens so that it can be removed through a small incision.

An artificial intraocular lens (IOL) is then implanted to replace the focusing power of the natural lens.

22. When Is Surgery Required?

The presence of a cataract alone does not automatically require surgery.

Surgery is generally considered when the cataract causes sufficient visual impairment to interfere with daily activities, work, driving, reading, or quality of life, or when removal is necessary for another ophthalmological reason.

In children with dense congenital cataracts, treatment may need to occur urgently to allow normal visual development and prevent amblyopia.

23. Cataracts – Causes in Note Form

Congenital: inherited or developmental cataracts occurring at or shortly after birth.

Autosomal dominant: common inheritance pattern among familial congenital cataracts, although other inheritance patterns exist.

Congenital rubella: classic maternal infection associated with congenital cataracts.

CMV and toxoplasmosis: important congenital infections causing ocular disease, although cataract is much more classically associated with rubella.

Down syndrome: increased risk of cataract formation.

Ageing: the most common overall cause; modern terminology is age-related cataract.

Ultraviolet radiation: chronic exposure increases cataract risk.

Corticosteroids: classic drug association, particularly with posterior subcapsular cataracts.

Uveitis: chronic ocular inflammation can cause secondary cataracts; steroid treatment may contribute further.

High myopia: associated with increased and earlier cataract formation.

Diabetes mellitus: cataracts may develop earlier and progress more rapidly.

Cushing syndrome: glucocorticoid excess can contribute to cataract formation.

Hypocalcaemia: chronic hypocalcaemia, particularly from hypoparathyroidism, can cause cataracts.

Myotonic dystrophy: classically associated with Christmas-tree cataracts.

Retinitis pigmentosa: associated particularly with posterior subcapsular cataracts.

Key Clinical Pattern

Remember cataract as:

Progressive + painless + cloudy/blurred vision + glare + reduced red reflex.

Important examination associations are:

Congenital rubella → congenital cataracts.

Steroids → posterior subcapsular cataracts.

Diabetes → earlier cataract formation.

Uveitis → secondary cataracts.

Myotonic dystrophy → Christmas-tree cataracts.

Retinitis pigmentosa → posterior subcapsular cataracts.

And the definitive treatment for a visually significant cataract is:

Cataract extraction + intraocular lens implantation.

Medicine – Uveitis

Uveitis is inflammation involving the uveal tract of the eye, which consists of the iris, ciliary body, and choroid. Inflammation may be limited to one anatomical region or involve several parts of the eye.

Uveitis is clinically important because recurrent or severe inflammation can cause permanent visual impairment through complications such as cataract, glaucoma, macular oedema, retinal damage, or optic nerve involvement.

1. Classification of Uveitis

Uveitis is classified according to the main anatomical site of inflammation.

Anterior uveitis mainly affects the iris and anterior ciliary body and is the most common form.

Intermediate uveitis predominantly affects the vitreous and peripheral retina.

Posterior uveitis primarily involves the choroid and/or retina.

Panuveitis involves the anterior chamber, vitreous, and retina or choroid.

The underlying causes differ somewhat according to the anatomical pattern.

2. Anterior Uveitis

Anterior uveitis is often called iritis when inflammation primarily affects the iris or iridocyclitis when both the iris and ciliary body are involved.

The typical presentation is:

Painful red eye + photophobia + blurred vision.

The redness is often most prominent around the cornea, producing ciliary or circumcorneal injection.

3. Clinical Features

Patients with acute anterior uveitis commonly experience ocular pain, redness, photophobia, excessive tearing, and reduced or blurred vision.

Photophobia can be particularly prominent because movement of the inflamed iris and ciliary body causes discomfort.

Unlike acute angle-closure glaucoma, the pupil in anterior uveitis is often small or irregular, rather than fixed and mid-dilated.

4. Cells and Flare

Slit-lamp examination may demonstrate cells and flare in the anterior chamber.

Cells represent inflammatory cells circulating within the aqueous humour.

Flare results from increased protein entering the aqueous because inflammation disrupts the blood-aqueous barrier.

Therefore:

Anterior chamber cells + flare → characteristic evidence of anterior uveitis.

5. Posterior Synechiae

Inflammation can cause the posterior surface of the iris to adhere to the anterior lens capsule.

These adhesions are called posterior synechiae.

They can produce an irregular pupil and, when extensive, interfere with normal aqueous humour circulation.

This is one reason why cycloplegic/mydriatic drops are often used in anterior uveitis.

Causes of Uveitis

Uveitis has a very broad differential diagnosis. Causes include idiopathic disease, immune-mediated systemic disorders, infection, trauma, and ocular-specific inflammatory conditions.

6. Idiopathic Uveitis

A substantial proportion of patients have no identifiable systemic or infectious cause, even after appropriate investigation.

These cases are classified as idiopathic uveitis.

The extent of investigation depends on the patient’s age, anatomical type of uveitis, whether disease is unilateral or bilateral, recurrence, severity, and associated systemic features.

7. Ankylosing Spondylitis

Ankylosing spondylitis is one of the classic systemic associations with acute anterior uveitis.

The uveitis is often:

Acute + unilateral + painful + recurrent.

It is strongly associated with HLA-B27.

Some patients presenting with recurrent anterior uveitis may have previously unrecognised axial spondyloarthritis.

8. Reactive Arthritis

Reactive arthritis, formerly called Reiter syndrome, is another HLA-B27-associated spondyloarthritis that may cause ocular inflammation.

Patients may develop conjunctivitis or acute anterior uveitis.

Other features can include arthritis and urethritis or cervicitis following an appropriate gastrointestinal or genitourinary infection.

The modern term reactive arthritis is preferred over Reiter syndrome.

9. Psoriatic Disease

Psoriatic arthritis and other forms of psoriatic spondyloarthritis can be associated with uveitis.

Anterior uveitis is particularly relevant in patients with psoriatic disease who also have features of axial or HLA-B27-associated spondyloarthritis.

10. Inflammatory Bowel Disease

Both Crohn disease and ulcerative colitis can have extraintestinal ocular manifestations.

These include:

Episcleritis.

Anterior uveitis.

Uveitis does not necessarily parallel intestinal disease activity and may occasionally occur independently of a gastrointestinal flare.

11. The Spondyloarthritis Connection

An important examination pattern is the relationship between HLA-B27 spondyloarthritis and acute anterior uveitis.

Remember:

Ankylosing spondylitis → anterior uveitis.

Reactive arthritis → anterior uveitis/conjunctivitis.

Psoriatic arthritis → anterior uveitis.

IBD-associated arthritis → anterior uveitis.

These disorders belong to the broader seronegative spondyloarthritis family.

12. Sarcoidosis

Sarcoidosis is an important systemic cause of uveitis.

It can produce anterior, intermediate, posterior, or panuveitis, and ocular disease may be unilateral or bilateral.

Other clues to sarcoidosis may include pulmonary disease, bilateral hilar lymphadenopathy, erythema nodosum, lupus pernio, or other systemic manifestations.

Therefore:

Sarcoidosis + eye inflammation → think uveitis.

13. Juvenile Idiopathic Arthritis

The older term juvenile chronic arthritis has largely been replaced by juvenile idiopathic arthritis (JIA).

JIA is an important cause of chronic anterior uveitis in children.

Unlike the painful red eye of typical HLA-B27-associated acute uveitis, JIA-associated uveitis may be silent and asymptomatic, particularly early in the disease.

For this reason, children in relevant JIA risk groups require regular slit-lamp screening, even when they have no ocular symptoms.

14. Trauma

Ocular trauma can produce anterior uveal inflammation known as traumatic iritis.

It may develop following blunt trauma to the eye and cause:

Pain + photophobia + redness + blurred vision.

A history of recent ocular injury is therefore an important clue.

Infectious Causes

Infectious uveitis is particularly important to recognise because inappropriate immunosuppression without treating the infection can allow the underlying infection to worsen.

15. Tuberculosis

Tuberculosis can produce several patterns of intraocular inflammation, including posterior uveitis and choroidal disease.

Ocular TB may occur with or without obvious active pulmonary tuberculosis.

Diagnosis can be difficult and generally requires interpretation of ocular findings alongside systemic investigation and evidence of TB infection.

16. Herpes Simplex Virus

Herpes simplex virus (HSV) can cause anterior uveitis, sometimes in association with keratitis.

Herpetic anterior uveitis may be unilateral and can be associated with raised intraocular pressure.

Varicella-zoster virus is another important herpesvirus capable of producing similar ocular inflammation.

17. Toxoplasmosis

Toxoplasma gondii is a particularly important cause of posterior uveitis, specifically retinochoroiditis.

Patients may present with floaters and reduced or blurred vision.

Fundoscopy classically demonstrates an area of active retinal inflammation, sometimes adjacent to an old pigmented scar.

Therefore:

Toxoplasmosis → think posterior uveitis / retinochoroiditis.

18. Toxocariasis

Toxocara infection can cause ocular disease, particularly in children and young people.

Ocular toxocariasis can produce posterior segment inflammation and retinal granulomas, sometimes causing significant unilateral visual impairment.

It is an important infectious differential diagnosis of posterior ocular inflammation.

19. Other Important Infectious Causes

The original list is not exhaustive.

Depending on the patient’s immune status and clinical presentation, other important infectious causes include varicella-zoster virus, cytomegalovirus, syphilis, and other bacterial, viral, fungal, or parasitic infections.

CMV retinitis is particularly important in patients with severe immunosuppression.

Treatment

20. Treatment Depends on the Cause

Management depends heavily on whether the uveitis is infectious or non-infectious and on which part of the eye is involved.

For non-infectious anterior uveitis, treatment commonly includes topical corticosteroids to suppress inflammation.

21. Cycloplegic and Mydriatic Drops

Cycloplegic/mydriatic agents are often given in anterior uveitis.

They help:

Relieve pain from ciliary muscle spasm.

Prevent or break posterior synechiae.

This is an important difference from some other causes of a painful red eye.

22. Systemic Treatment

Severe, posterior, bilateral, recurrent, or systemic inflammatory uveitis may require systemic corticosteroids or steroid-sparing immunosuppressive/biologic treatment under specialist supervision.

When an underlying systemic inflammatory disease is present, treating that disease is an important part of controlling the ocular inflammation.

23. Infectious Uveitis

When uveitis is caused by infection, the underlying pathogen requires specific antimicrobial therapy.

For example, management may require anti-tuberculous therapy, antiviral therapy, or anti-Toxoplasma treatment depending on the diagnosis.

This distinction is crucial because corticosteroid treatment without appropriate antimicrobial coverage can be dangerous in some infectious forms.

24. Complications

Uveitis can cause several important complications:

Posterior synechiae.

Cataract.

Secondary glaucoma.

Cystoid macular oedema.

Retinal damage.

Optic nerve damage.

Permanent visual impairment.

Early diagnosis and adequate control of inflammation therefore matter greatly.

25. Uveitis – Causes in Note Form

Idiopathic: no underlying cause identified.

Ankylosing spondylitis: classic association with recurrent acute anterior uveitis; often HLA-B27 related.

Reactive arthritis: formerly Reiter syndrome; may cause anterior uveitis or conjunctivitis.

Psoriatic arthritis: can be associated with anterior uveitis, especially with spondyloarthritis features.

Inflammatory bowel disease: Crohn disease and ulcerative colitis can cause anterior uveitis.

Sarcoidosis: important systemic cause; can affect anterior and posterior portions of the eye.

Juvenile idiopathic arthritis: chronic anterior uveitis that may be completely asymptomatic in children.

Trauma: blunt ocular injury may produce traumatic anterior uveitis/iritis.

Tuberculosis: may cause various forms of uveitis, including posterior involvement.

HSV: may cause unilateral anterior uveitis, sometimes with keratitis and raised IOP.

Toxoplasmosis: classic infectious cause of posterior uveitis/retinochoroiditis.

Toxocariasis: may cause posterior ocular inflammation and retinal granuloma.

Key Clinical Pattern

For examination purposes, remember:

Painful red eye + photophobia + small/irregular pupil + cells and flare → anterior uveitis.

The major systemic association is:

HLA-B27 spondyloarthritis → acute anterior uveitis.

This includes:

Ankylosing spondylitis + reactive arthritis + psoriatic arthritis + IBD-associated spondyloarthritis.

Also remember:

JIA → chronic anterior uveitis that may be asymptomatic.

Sarcoidosis → uveitis.

Toxoplasmosis → posterior uveitis/retinochoroiditis.

And a useful painful-red-eye distinction:

Uveitis → photophobia + small/irregular pupil.

Acute angle-closure glaucoma → hazy cornea + mid-dilated fixed pupil + markedly raised IOP.

Scleritis → severe deep boring pain + deep violaceous scleral redness.