Infectious Disease and Microbiology - Basidiobolus ranarum

Basics

Basidiobolus ranarum is a rare filamentous fungus that causes a chronic form of subcutaneous fungal infection. Disease is usually localized and slowly progressive rather than rapidly invasive.

The organism most often produces firm, painless or minimally tender nodules within the subcutaneous tissues.

Microbiologic Characteristics

Basidiobolus ranarum is a filamentous fungus, or mold.

It belongs to a group of fungi capable of producing chronic subcutaneous disease after environmental inoculation.

Epidemiology

Infection is rare but occurs worldwide.

Cases are reported more commonly from:

• India

• Indonesia

• Africa

The infection is generally associated with environmental exposure and traumatic inoculation into the skin or subcutaneous tissues.

Clinical Manifestations

The classic presentation is a chronic, nonulcerating subcutaneous lesion.

Lesions most often occur on:

• Chest

• Back

• Buttocks

• Extremities

They are usually:

• Nodular

• Firm

• Slowly enlarging

• Nonulcerating

• Located beneath the skin

Because the disease progresses slowly, it may initially be mistaken for a tumor, inflammatory lesion, or other chronic fungal infection.

Diagnosis

Diagnosis is based on:

• Fungal culture

• Histopathologic examination of tissue biopsy

Biopsy is especially helpful because it can demonstrate fungal elements within the inflammatory tissue and exclude other causes of a chronic subcutaneous mass.

Differential Diagnosis

Important considerations include:

• Sporotrichosis

• Phaeohyphomycosis

• Mycetoma

• Cutaneous tuberculosis

• Nontuberculous mycobacterial infection

• Subcutaneous tumors

• Other chronic fungal infections

Treatment

Potassium Iodide

A traditional treatment is saturated potassium iodide solution.

The source regimen describes approximately:

30 mg/kg/day for 6–12 months

Treatment is usually prolonged because of the chronic nature of the infection.

Other Antimicrobial Options

Alternative therapies that have been used include:

• Trimethoprim-sulfamethoxazole

• Ketoconazole

• Amphotericin B

The optimal regimen varies, and treatment response should be monitored clinically.

Surgical Management

Surgical excision or debridement may be helpful when lesions are:

• Localized

• Resistant to medical therapy

• Large or functionally problematic

Surgery is generally combined with antifungal treatment rather than used as the sole therapy.

Prognosis

The course is usually chronic but localized.

Spontaneous resolution has occasionally been reported, although most symptomatic cases are treated.

The prognosis is generally favorable when infection remains confined to the subcutaneous tissues.

Exam Essentials

Organism:

→ Basidiobolus ranarum

Type:

→ Filamentous fungus

Geographic association:

→ India, Indonesia, and Africa

Classic manifestation:

→ Chronic nonulcerating subcutaneous nodules

Common sites:

→ Chest, back, buttocks, extremities

Diagnosis:

→ Culture + tissue biopsy

Traditional treatment:

→ Prolonged potassium iodide

Other options:

→ TMP-SMX, ketoconazole, amphotericin B

Additional management:

→ Surgical excision for difficult localized disease

Key clinical pearl: A slowly enlarging, nonulcerating subcutaneous mass in a patient from a tropical region should raise consideration of Basidiobolus ranarum.

Infectious Disease and Microbiology - Baylisascaris procyonis

Basics

Baylisascaris procyonis is a nematode parasite, or roundworm, whose normal definitive host is the raccoon.

Humans are accidental hosts. Infection occurs after ingestion of embryonated eggs from soil or objects contaminated with raccoon feces.

Unlike ordinary intestinal helminths, the larvae do not mature normally in humans. Instead, they migrate through tissues and can cause severe visceral, ocular, and neurologic disease.

Microbiologic Characteristics

Baylisascaris procyonis is a nematode helminth.

The adult worm normally lives in the raccoon intestine, where eggs are produced and passed in feces.

After environmental maturation, these eggs become infective.

Epidemiology

Human infection is rare but is particularly recognized in North America, including the United States.

Risk is greatest where raccoons commonly contaminate:

• Soil

• Sandboxes

• Yards

• Woodpiles

• Outdoor play areas

• Raccoon latrines

Children are at particular risk because of hand-to-mouth behavior and possible ingestion of contaminated soil.

Transmission

Humans become infected by swallowing infective eggs.

The sequence is:

Raccoon feces

→ Eggs contaminate soil

→ Eggs embryonate

→ Human ingests eggs

→ Larvae hatch

→ Larvae migrate through tissues

Because humans are accidental hosts, the larvae can migrate widely rather than remaining in the intestinal lumen.

Visceral Larva Migrans

One major manifestation is visceral larva migrans.

Larvae may migrate through:

• Liver

• Lungs

• Other internal organs

Patients may develop:

• Fever

• Malaise

• Hepatomegaly

• Pulmonary symptoms

• Marked eosinophilia

The severity depends on the number of larvae ingested and the tissues involved.

Neural Larva Migrans

The most serious complication is migration into the central nervous system.

This can cause:

Eosinophilic meningoencephalitis

Possible manifestations include:

• Altered mental status

• Irritability

• Ataxia

• Weakness

• Cranial nerve abnormalities

• Seizures

• Progressive neurologic deterioration

Severe neurologic injury may be permanent.

High-Yield Pattern

Young child

• ●

Raccoon exposure

• ●

Marked eosinophilia

• ●

Progressive encephalopathy

→ Think Baylisascaris procyonis.

Ocular Larva Migrans

Larvae can also migrate into the eye.

Possible manifestations include:

• Visual loss

• Retinal inflammation

• Ocular larval lesions

• Unilateral visual disturbance

Ocular disease may be mistaken for toxocariasis or other causes of ocular larva migrans.

Diagnosis

Definitive diagnosis may be difficult.

The source emphasizes histologic identification of larvae in surgically obtained tissue.

Evaluation may also involve:

• Peripheral eosinophil count

• Neuroimaging

• Ophthalmologic examination

• Specialized serologic testing where available

Because larvae are migrating through tissues, routine stool examination is generally not useful for diagnosing human infection.

Histopathology

Larvae may be identified within involved tissue.

This can establish the diagnosis, although biopsy is often impractical in CNS disease.

Treatment

Corticosteroids

Corticosteroids may be used to reduce the inflammatory response caused by migrating or dying larvae, especially in CNS or ocular disease.

They are usually used as adjunctive therapy rather than as the sole treatment.

Anthelmintic Therapy

The older source mentions diethylcarbamazine or ivermectin as possible therapies.

In contemporary practice, early albendazole is generally regarded as the preferred antiparasitic treatment when neural or visceral baylisascariasis is suspected, often together with corticosteroids.

Treatment is most likely to be beneficial when started early, before extensive neurologic damage occurs.

Ocular Disease

For localized ocular infection, treatment may include:

• Ophthalmologic procedures

• Laser photocoagulation when the larva can be localized

• Corticosteroids

• Systemic antiparasitic therapy in selected cases

Management should involve an ophthalmologist.

Prognosis

Visceral disease can range from mild to severe.

Neurologic baylisascariasis is much more serious. Once extensive CNS injury has occurred, recovery may be incomplete despite eradication of the parasite.

Therefore, early recognition and treatment are especially important.

Prevention

The most important preventive measure is avoiding contact with raccoon feces and contaminated soil.

Important measures include:

• Keep children away from raccoon latrines.

• Prevent raccoons from nesting near homes.

• Do not handle raccoon feces with bare hands.

• Use gloves when cleaning contaminated areas.

• Wash hands thoroughly afterward.

• Prevent children from eating soil or placing contaminated objects in their mouths.

Raccoon feces should be removed carefully because the eggs are environmentally resistant.

High-Yield Comparison

Baylisascaris procyonis

Definitive host:

→ Raccoon

Human infection:

→ Accidental ingestion of eggs

Major syndromes:

→ Visceral, neural, and ocular larva migrans

Key lab clue:

→ Eosinophilia

Worst complication:

→ Severe meningoencephalitis

Diagnosis:

→ Histology or specialized testing

Treatment:

→ Early antiparasitic therapy + corticosteroids

Exam Essentials

Organism:

→ Baylisascaris procyonis

Type:

→ Nematode helminth

Definitive host:

→ Raccoon

Transmission:

→ Ingestion of infective eggs from contaminated soil

Major syndromes:

→ Visceral larva migrans, neural larva migrans, ocular larva migrans

Classic high-risk patient:

→ Young child with soil exposure

Important laboratory clue:

→ Marked eosinophilia

Severe neurologic manifestation:

→ Eosinophilic meningoencephalitis

Diagnosis:

→ Tissue identification or specialized testing

Important treatment principle:

→ Start antiparasitic therapy early when suspected

Adjunct:

→ Corticosteroids

Ocular management:

→ Ophthalmologic intervention, sometimes laser therapy

Key clinical pearl: Raccoon exposure plus eosinophilia and progressive neurologic disease is a classic warning pattern for Baylisascaris procyonis.