Infectious Disease and Microbiology – Endolimax nana

Overview

Endolimax nana is an intestinal protozoan with a worldwide distribution. It is generally regarded as a nonpathogenic commensal organism rather than a cause of gastrointestinal disease.

Its presence in stool usually reflects colonization rather than clinically significant infection.

Microbiologic Characteristics

Endolimax nana is a protozoan parasite that can inhabit the human intestinal tract.

Unlike pathogenic intestinal protozoa such as Entamoeba histolytica, E. nana is not considered an invasive or disease-producing organism.

Epidemiology

E. nana occurs worldwide.

It may be detected incidentally during stool examination, including in individuals who have no gastrointestinal symptoms.

Clinical Significance

Endolimax nana is generally considered nonpathogenic.

Therefore, detection of the organism does not usually explain symptoms such as diarrhea or abdominal pain.

If a symptomatic patient is found to have E. nana, other infectious or noninfectious causes of the symptoms should be considered.

Commensal Nature

The organism behaves primarily as a commensal intestinal protozoan.

This means it may live in the gastrointestinal tract without causing tissue invasion or clinically important disease.

Diagnosis

Diagnosis is based on parasitologic examination of concentrated stool specimens.

Characteristic protozoal forms may be identified microscopically.

Treatment

No treatment is required.

Because E. nana is considered nonpathogenic, antimicrobial or antiparasitic therapy is generally unnecessary.

High-Yield Clinical Pattern

Protozoan detected on stool examination

• ●

Patient has no symptoms or symptoms are better explained by another cause

• ●

Organism identified as Endolimax nana

→ Think nonpathogenic intestinal commensal

Exam Essentials

Organism: Endolimax nana

Type: Protozoan

Distribution: Worldwide

Pathogenicity: Nonpathogenic

Clinical role: Intestinal commensal

Diagnosis: Concentrated stool examination

Treatment: None required

Key clinical pearl: Finding Endolimax nana in stool usually represents nonpathogenic intestinal colonization, so treatment is not indicated and another cause should be sought if gastrointestinal symptoms are present.

Infectious Disease and Microbiology – Encephalitis Viruses of the Flaviviridae Family

Overview

Several members of the Flaviviridae family, particularly the genus Flavivirus, are arthropod-borne viruses (arboviruses) capable of causing encephalitis. These viruses are transmitted mainly by mosquitoes, although the broader group of arboviral encephalitides also includes tick-borne infections.

Important mosquito-borne flaviviral encephalitis viruses include Japanese encephalitis virus, Kunjin virus, Murray Valley encephalitis virus, St. Louis encephalitis virus, and Rocio virus.

Classification of Arboviral Encephalitis

Arthropod-borne viral encephalitides can broadly be considered according to their vectors, including:

• Mosquito-borne arboviral encephalitis

• Tick-borne arboviral encephalitis

Mosquito-borne encephalitis viruses belong to several different viral families or groups.

Major Groups of Mosquito-Borne Encephalitis Viruses

Important mosquito-borne encephalitis viruses include:

Alphaviruses

• Eastern equine encephalitis virus

• Western equine encephalitis virus

Bunyavirus-related viruses

• La Crosse virus

• California encephalitis virus

• Jamestown Canyon virus

• Snowshoe hare virus

Flaviviruses

• Japanese encephalitis virus

• Kunjin virus

• Murray Valley encephalitis virus

• St. Louis encephalitis virus

• Rocio virus

Microbiologic Characteristics

Flaviviruses associated with encephalitis are:

• Single-stranded RNA viruses

• Positive-sense RNA viruses

• Approximately spherical

• Enveloped

The presence of a lipid envelope distinguishes them from naked RNA viruses such as enteroviruses.

Incubation Period

The incubation period is generally approximately:

5–15 days

The exact interval varies according to the particular virus and host factors.

Epidemiology

Flaviviral encephalitis is relatively uncommon, although outbreaks can occur in endemic regions.

Transmission patterns depend heavily on:

• Geographic location

• Mosquito-vector distribution

• Climate and season

• Animal reservoirs

• Human exposure to mosquito habitats

Transmission

These encephalitis viruses are generally transmitted through the bite of an infected mosquito.

The virus is maintained in nature through transmission cycles involving mosquitoes and animal reservoirs.

Humans are often incidental hosts rather than essential components of the natural transmission cycle.

Clinical Infection

Flaviviruses can cause epidemic outbreaks of encephalitis.

Many infections may be asymptomatic or produce only a nonspecific febrile illness, while a smaller proportion progress to neurologic disease.

Encephalitis

When the central nervous system becomes involved, patients may develop:

• Fever

• Severe headache

• Altered mental status

• Confusion

• Behavioral changes

• Seizures

• Reduced level of consciousness

Severe disease may progress to coma or death.

Neurologic Manifestations

Depending on the specific flavivirus and severity of infection, neurologic manifestations may include:

• Encephalitis

• Meningoencephalitis

• Tremor

• Abnormal movements

• Weakness

• Seizures

• Altered consciousness

Survivors of severe encephalitis may occasionally have persistent neurologic deficits.

Japanese Encephalitis Virus

Japanese encephalitis virus (JEV) is one of the most important mosquito-borne causes of viral encephalitis in endemic areas of Asia.

Most infections are asymptomatic, but symptomatic neuroinvasive disease can be severe.

A major distinguishing feature is the availability of an effective vaccine.

St. Louis Encephalitis Virus

St. Louis encephalitis virus is another mosquito-borne flavivirus capable of causing outbreaks of encephalitis.

Neurologic disease tends to be more clinically significant in older adults.

Kunjin Virus

Kunjin virus is a flavivirus associated particularly with Australia.

It can produce febrile illness and, less commonly, encephalitis.

It is now generally regarded as a subtype/variant within the West Nile virus group.

Murray Valley Encephalitis Virus

Murray Valley encephalitis virus is a mosquito-borne flavivirus associated predominantly with Australia and surrounding regions.

Although infection is uncommon, neurologic disease can be severe.

Rocio Virus

Rocio virus is a mosquito-borne flavivirus historically associated with outbreaks of encephalitis in Brazil.

Human infection is uncommon but can result in significant neurologic disease.

Diagnosis

Traditional diagnostic methods include:

• Cell culture

• Serologic testing

Serology is particularly useful for demonstrating virus-specific antibodies.

Molecular Diagnosis

PCR can be used to detect viral genetic material in appropriate clinical specimens.

The choice of PCR, serology, and specimen type depends on the particular virus and the timing of specimen collection.

Treatment

Treatment is primarily supportive and symptomatic.

Management of severe encephalitis may include:

• Maintenance of airway and ventilation

• Fluid and electrolyte management

• Treatment of seizures

• Management of increased intracranial pressure when present

• Intensive supportive care for severe neurologic disease

Antiviral Therapy

For the flaviviral encephalitides described here, the source notes:

No specific antiviral treatment is available.

Management therefore focuses on supportive care and prevention of complications.

Prevention

The major preventive strategy is to avoid mosquito bites.

Measures include:

• Appropriate insect repellents

• Protective clothing

• Mosquito nets when appropriate

• Window and door screens

• Reduction of mosquito breeding sites

• Following local vector-control recommendations

Japanese Encephalitis Vaccination

Unlike most other mosquito-borne encephalitis viruses in this group, Japanese encephalitis can be prevented by vaccination.

Vaccination may be recommended for travelers whose itinerary, duration of travel, season, and activities create a meaningful risk of exposure in endemic areas.

The source particularly emphasizes vaccination for long-term travelers staying in rural endemic areas.

High-Yield Clinical Pattern

Recent mosquito exposure in an endemic region

• ●

Acute fever

• ●

Altered mental status ± seizures or other neurologic abnormalities

• ●

Serologic or molecular evidence of flavivirus infection

→ Consider flaviviral encephalitis

Japanese Encephalitis High-Yield Pattern

Travel or residence in endemic Asia

• ●

Mosquito exposure, particularly in rural areas

• ●

Acute encephalitis

→ Think Japanese encephalitis virus

Major prevention clue → Vaccine available

Exam Essentials

Group: Flavivirus

Family: Flaviviridae

Genome: Positive-sense single-stranded RNA

Envelope: Present

Shape: Approximately spherical

Vector: Primarily mosquitoes for the viruses discussed here

Incubation: Approximately 5–15 days

Major manifestation: Encephalitis/meningoencephalitis

Epidemiology: Usually uncommon, but outbreaks occur

Important viruses: Japanese encephalitis, Kunjin, Murray Valley encephalitis, St. Louis encephalitis, and Rocio viruses

Diagnosis: Serology, PCR, and historically viral culture

Treatment: Supportive

Routine specific antiviral therapy: None

General prevention: Avoid mosquito bites

Vaccine-preventable member: Japanese encephalitis virus

Key clinical pearl: Mosquito-borne flaviviruses are enveloped, positive-sense single-stranded RNA viruses that can cause epidemic encephalitis; Japanese encephalitis is especially important because an effective vaccine is available for people with appropriate exposure risk.

Infectious Disease and Microbiology – Emmonsia parva

Overview

Emmonsia parva is a filamentous fungus (mold) that is a rare cause of human infection. Although infection is uncommon worldwide, the organism has been associated with several forms of localized and invasive fungal disease, particularly in immunocompromised patients.

Reported manifestations include osteomyelitis, prosthetic valve endocarditis, respiratory and sinonasal infections, central nervous system extension, pneumonia, and disseminated disease.

Microbiologic Characteristics

Emmonsia parva is a:

• Filamentous fungus

• Mold

• Rare human fungal pathogen

Human disease caused by this organism is uncommon.

Epidemiology

E. parva has a worldwide distribution, but clinically significant human infection is rare.

Severe or disseminated disease is more likely to occur in individuals with impaired immune defenses.

Clinical Infections

A variety of uncommon infections have been attributed to E. parva, including:

• Osteomyelitis

• Prosthetic valve endocarditis

• Rhinitis

• Sinusitis

• CNS extension from sinus disease

• Pneumonia

• Disseminated infection

Osteomyelitis

Rare cases of E. parva osteomyelitis have been reported.

Fungal involvement of bone may produce a chronic infection requiring both prolonged antifungal therapy and, in selected cases, surgical management.

Prosthetic Valve Endocarditis

E. parva has rarely been associated with prosthetic valve endocarditis.

Fungal prosthetic valve infections are potentially serious because eradication can be difficult with antifungal therapy alone.

Rhinitis and Sinusitis

The organism may produce rhinitis or sinusitis.

Although these infections are rare, invasive sinus disease can potentially spread beyond the sinonasal structures.

CNS Extension

A particularly serious complication is extension of sinus infection into the central nervous system.

This represents an invasive form of disease requiring aggressive management.

Pneumonia

E. parva may occasionally cause pulmonary infection or pneumonia.

Pulmonary disease is especially concerning in patients with significant immunosuppression.

Disseminated Infection

In immunocompromised patients, infection may spread beyond its original site and produce disseminated fungal disease.

Multiple organs may potentially become involved in severe invasive infection.

Diagnosis

Diagnosis is established through:

• Fungal culture

• Identification of the fungus in tissue biopsy specimens

Because infection is rare, demonstrating fungal elements within affected tissue can be particularly important in establishing the organism’s clinical significance.

Tissue Biopsy

Histopathologic examination of a tissue biopsy can demonstrate fungal structures within the lesion.

Culture of biopsy material can then assist with definitive identification of the pathogen.

Thus, diagnosis often depends on a combination of:

Compatible lesion + tissue evidence of fungus + positive culture

Treatment

The treatment described in the source is:

Intravenous amphotericin B

This is used particularly for serious or invasive infection.

Surgical Management

Surgical intervention can be an important component of management.

Removal or debridement of infected lesions may help control localized disease and reduce the fungal burden.

Surgery may be particularly relevant when infection involves:

• Bone

• Localized masses or lesions

• Invasive sinus disease

• Prosthetic material

High-Yield Clinical Pattern

Immunocompromised patient

• ●

Unusual invasive fungal infection

• ●

Pneumonia, sinusitis with CNS extension, osteomyelitis, or dissemination

• ●

Filamentous fungus identified in culture or tissue

→ Consider Emmonsia parva

Exam Essentials

Organism: Emmonsia parva

Type: Filamentous fungus (mold)

Distribution: Worldwide

Frequency: Rare human pathogen

Important risk group: Immunocompromised patients

Possible infections: Osteomyelitis, prosthetic valve endocarditis, rhinitis, sinusitis, CNS extension, pneumonia, and disseminated infection

Diagnosis: Culture + identification in tissue biopsy

Treatment described in source: IV amphotericin B

Additional management: Surgical removal/debridement of lesions

Key clinical pearl: Emmonsia parva is a rare filamentous fungal pathogen that can cause serious localized or disseminated disease, especially in immunocompromised patients; diagnosis relies on culture and tissue identification, while treatment traditionally involves amphotericin B plus surgical management when appropriate.

Infectious Disease and Microbiology – Eikenella corrodens

Overview

Eikenella corrodens is a microaerophilic Gram-negative bacillus that belongs to the HACEK group. It is part of the normal human oral flora but can become pathogenic when introduced into normally sterile tissues.

It is particularly associated with human bite wounds, infections in intravenous drug users, endocarditis, and polymicrobial pulmonary infections.

Microbiologic Characteristics

Eikenella corrodens is characterized as:

• Gram-negative bacillus

• Microaerophilic

• Member of the HACEK group

• Normal inhabitant of the human oral cavity

The HACEK organisms are notable for their association with infective endocarditis.

HACEK Group

The traditional HACEK group consists of:

H – Haemophilus species

A – Aggregatibacter species

C – Cardiobacterium hominis

E – Eikenella corrodens

K – Kingella species

These are Gram-negative organisms associated particularly with infections originating from the oral or upper respiratory flora and with endocarditis.

Epidemiology

E. corrodens occurs worldwide, although clinically significant infection is relatively uncommon.

Because it normally colonizes the mouth, many infections result from introduction of oral flora into deeper tissues.

Normal Oral Flora

An important concept is that E. corrodens is part of the normal oral microbiota.

This explains its strong association with:

• Human bite wounds

• Oral contamination of traumatic wounds

• Head and neck infections

• Some pulmonary infections

• Infective endocarditis

Human Bite-Wound Infection

E. corrodens is a classic pathogen associated with human bites.

Human bite wounds are typically polymicrobial, and E. corrodens may be introduced into the wound together with other organisms from the oral cavity.

Clenched-Fist Injury

A particularly high-yield presentation is the clenched-fist injury, sometimes called a “fight bite.”

This occurs when a person’s fist strikes another person’s teeth, producing a small wound over a metacarpophalangeal joint.

Oral organisms such as E. corrodens may then be inoculated into deeper tissues, potentially resulting in:

• Cellulitis

• Abscess

• Septic arthritis

• Tenosynovitis

• Osteomyelitis

Infection in Intravenous Drug Users

E. corrodens can cause skin and soft-tissue infections in intravenous drug users.

These infections may be polymicrobial, particularly when oral flora contaminate injection equipment or the injection site.

Internal Jugular Vein Thrombophlebitis

E. corrodens has also been associated with internal jugular vein thrombophlebitis.

This represents a potentially serious invasive infection involving thrombosis and inflammation of the internal jugular vein.

Endocarditis

Because E. corrodens belongs to the HACEK group, it is an important though uncommon cause of infective endocarditis.

Clinical manifestations may include:

• Persistent fever

• Constitutional symptoms

• New or changing cardiac murmur

• Embolic phenomena

• Other manifestations of valvular infection

Pulmonary Infection

E. corrodens may cause several pulmonary and pleural infections, including:

• Pneumonia

• Lung abscess

• Empyema

These infections are commonly polymicrobial, reflecting the organism’s origin in the oral flora.

Diagnosis

Diagnosis is established by culture of appropriate clinical specimens.

Depending on the syndrome, specimens may include:

• Blood cultures

• Wound cultures

• Abscess material

• Pleural fluid

• Other infected tissue or fluids

Treatment

The source lists the principal treatments as:

Penicillin G

or

Amoxicillin–clavulanate

For human bite wounds, amoxicillin–clavulanate provides useful broad coverage because these infections are frequently polymicrobial.

Additional Treatment Options

Other agents described as potential alternatives include:

• Doxycycline

• Second-generation cephalosporins

• Third-generation cephalosporins

The source also lists aminoglycosides among possible agents.

Treatment of serious infection should ultimately be guided by culture and antimicrobial susceptibility results.

Beta-Lactamase Production

Some strains of E. corrodens produce beta-lactamases.

This possibility should be considered when selecting antimicrobial therapy, particularly if susceptibility results are not yet available.

Important Antibiotic Resistance

A particularly important feature of E. corrodens is its resistance to several antibiotics that might otherwise be considered for skin, oral, or anaerobic infections.

It is characteristically resistant to:

• Metronidazole

• Clindamycin

• Oxacillin

• First-generation cephalosporins

Human Bite Wound – Antibiotic Warning

Because E. corrodens may be present in human bite wounds:

Clindamycin alone should not be relied upon for empiric treatment.

Similarly, first-generation cephalosporins such as cephalexin or cefazolin do not provide reliable Eikenella coverage.

This resistance pattern is a major exam point.

High-Yield Clinical Pattern

Human bite or clenched-fist injury

• ●

Polymicrobial wound infection

• ●

Gram-negative bacillus from normal oral flora

• ●

Resistance to clindamycin and first-generation cephalosporins

→ Think Eikenella corrodens

Another High-Yield Association

HACEK organism

• ●

Subacute infective endocarditis

• ●

Oral flora

→ Consider Eikenella corrodens

Exam Essentials

Organism: Eikenella corrodens

Type: Microaerophilic Gram-negative bacillus

Group: HACEK

Normal habitat: Human oral flora

Classic infection: Human bite wound / clenched-fist injury

Other infections: Skin infection in IV drug users, internal jugular thrombophlebitis, endocarditis, pneumonia, lung abscess, and empyema

Pulmonary infections: Often polymicrobial

Diagnosis: Culture

Treatment: Penicillin G or amoxicillin–clavulanate

Possible alternatives: Doxycycline or second-/third-generation cephalosporins

Beta-lactamase: Some strains produce it

Important resistance: Metronidazole, clindamycin, oxacillin, and first-generation cephalosporins

Key clinical pearl: The classic association is human bite or fight-bite wound + normal oral flora + HACEK Gram-negative bacillus resistant to clindamycin and first-generation cephalosporins = Eikenella corrodens.

Microbiologic Characteristics Eikenella corrodens is characterized as: • Gram-negative bacillus

• Microaerophilic

• Member of the HACEK group

• Normal inhabitant of the human oral cavity The HACEK organisms are notable for their association with infective endocarditis.

HACEK Group The traditional HACEK group consists of: H – Haemophilus species

A – Aggregatibacter species

C – Cardiobacterium hominis

E – Eikenella corrodens

K – Kingella species These are Gram-negative organisms associated particularly with infections originating from the oral or upper respiratory flora and with endocarditis.

Epidemiology E. corrodens occurs worldwide, although clinically significant infection is relatively uncommon. Because it normally colonizes the mouth, many infections result from introduction of oral flora into deeper tissues.

Normal Oral Flora An important concept is that E. corrodens is part of the normal oral microbiota. This explains its strong association with: • Human bite wounds

• Oral contamination of traumatic wounds

• Head and neck infections

• Some pulmonary infections

• Infective endocarditis

Human Bite-Wound Infection E. corrodens is a classic pathogen associated with human bites. Human bite wounds are typically polymicrobial, and E. corrodens may be introduced into the wound together with other organisms from the oral cavity.

Clenched-Fist Injury A particularly high-yield presentation is the clenched-fist injury, sometimes called a “fight bite.” This occurs when a person’s fist strikes another person’s teeth, producing a small wound over a metacarpophalangeal joint. Oral organisms such as E. corrodens may then be inoculated into deeper tissues, potentially resulting in: • Cellulitis

• Abscess

• Septic arthritis

• Tenosynovitis

• Osteomyelitis

Infection in Intravenous Drug Users E. corrodens can cause skin and soft-tissue infections in intravenous drug users. These infections may be polymicrobial, particularly when oral flora contaminate injection equipment or the injection site.

Internal Jugular Vein Thrombophlebitis E. corrodens has also been associated with internal jugular vein thrombophlebitis. This represents a potentially serious invasive infection involving thrombosis and inflammation of the internal jugular vein.

Endocarditis Because E. corrodens belongs to the HACEK group, it is an important though uncommon cause of infective endocarditis. Clinical manifestations may include: • Persistent fever

• Constitutional symptoms

• New or changing cardiac murmur

• Embolic phenomena

• Other manifestations of valvular infection

Pulmonary Infection E. corrodens may cause several pulmonary and pleural infections, including: • Pneumonia

• Lung abscess

• Empyema These infections are commonly polymicrobial, reflecting the organism’s origin in the oral flora.

Diagnosis Diagnosis is established by culture of appropriate clinical specimens. Depending on the syndrome, specimens may include: • Blood cultures

• Wound cultures

• Abscess material

• Pleural fluid

• Other infected tissue or fluids

Treatment The source lists the principal treatments as: Penicillin G or Amoxicillin–clavulanate For human bite wounds, amoxicillin–clavulanate provides useful broad coverage because these infections are frequently polymicrobial.

Additional Treatment Options Other agents described as potential alternatives include: • Doxycycline

• Second-generation cephalosporins

• Third-generation cephalosporins The source also lists aminoglycosides among possible agents. Treatment of serious infection should ultimately be guided by culture and antimicrobial susceptibility results.

Beta-Lactamase Production Some strains of E. corrodens produce beta-lactamases. This possibility should be considered when selecting antimicrobial therapy, particularly if susceptibility results are not yet available.

Important Antibiotic Resistance A particularly important feature of E. corrodens is its resistance to several antibiotics that might otherwise be considered for skin, oral, or anaerobic infections. It is characteristically resistant to: • Metronidazole

• Clindamycin

• Oxacillin

• First-generation cephalosporins

Human Bite Wound – Antibiotic Warning Because E. corrodens may be present in human bite wounds: Clindamycin alone should not be relied upon for empiric treatment. Similarly, first-generation cephalosporins such as cephalexin or cefazolin do not provide reliable Eikenella coverage. This resistance pattern is a major exam point.

High-Yield Clinical Pattern Human bite or clenched-fist injury  ●  Polymicrobial wound infection  ●  Gram-negative bacillus from normal oral flora  ●  Resistance to clindamycin and first-generation cephalosporins → Think Eikenella corrodens

Another High-Yield Association HACEK organism  ●  Subacute infective endocarditis  ●  Oral flora → Consider Eikenella corrodens

Exam Essentials Organism: Eikenella corrodens

Type: Microaerophilic Gram-negative bacillus

Group: HACEK

Normal habitat: Human oral flora

Classic infection: Human bite wound / clenched-fist injury

Other infections: Skin infection in IV drug users, internal jugular thrombophlebitis, endocarditis, pneumonia, lung abscess, and empyema

Pulmonary infections: Often polymicrobial

Diagnosis: Culture

Treatment: Penicillin G or amoxicillin–clavulanate

Possible alternatives: Doxycycline or second-/third-generation cephalosporins

Beta-lactamase: Some strains produce it

Important resistance: Metronidazole, clindamycin, oxacillin, and first-generation cephalosporins

Key clinical pearl: The classic association is human bite or fight-bite wound + normal oral flora + HACEK Gram-negative bacillus resistant to clindamycin and first-generation cephalosporins = Eikenella corrodens.

Infectious Disease and Microbiology – Edwardsiella tarda

Overview

Edwardsiella tarda is an aerobic, Gram-negative bacillus that is an uncommon cause of human infection. It is found worldwide and is associated with the intestinal flora of various animals, including snakes.

The major human infections are gastroenteritis and bacteremia.

Microbiologic Characteristics

Edwardsiella tarda is an:

• Aerobic Gram-negative bacillus

• Enteric bacterium

• Organism associated with the gastrointestinal tracts of various animals

It can be isolated using standard bacterial culture techniques.

Epidemiology

Human E. tarda infection is rare but occurs worldwide.

The organism may be part of the normal intestinal flora of various animals, particularly:

• Reptiles, including snakes

• Fish and other aquatic animals

• Other animal species

Human infection may therefore have an environmental or animal-associated source.

Transmission and Exposure

Exposure may occur through contact with colonized animals or contaminated aquatic environments and through consumption of contaminated food.

Because of its association with aquatic animals and reptiles, a history of fish, water, or reptile exposure may provide an important epidemiologic clue.

Clinical Infections

The two principal clinical manifestations described for E. tarda are:

1. Gastroenteritis

2. Bacteremia

Most infections remain gastrointestinal, but invasive bloodstream infection can occur and requires more aggressive management.

Gastroenteritis

E. tarda can cause an acute gastrointestinal illness characterized primarily by diarrhea and abdominal symptoms.

Possible manifestations include:

• Diarrhea

• Abdominal pain or cramping

• Nausea and vomiting

• Fever

The clinical presentation may resemble gastroenteritis caused by other enteric Gram-negative organisms.

Bacteremia

E. tarda can occasionally invade the bloodstream and produce bacteremia.

This represents a more serious form of infection and may be associated with systemic manifestations such as:

• Fever

• Chills

• Hypotension in severe disease

• Sepsis

Recognition of bloodstream infection is important because intravenous antimicrobial treatment is required.

Diagnosis

Diagnosis is established by bacterial culture.

Depending on the clinical syndrome, appropriate specimens include:

• Stool culture for gastroenteritis

• Blood cultures for suspected bacteremia

• Cultures from other infected sites when appropriate

Identification of the organism should be accompanied by antimicrobial susceptibility testing in serious infections.

Treatment

The primary antimicrobial treatment described in the source is a:

Fluoroquinolone

For patients with E. tarda bacteremia, the source specifically recommends intravenous treatment with a quinolone.

Additional Treatment Options

Other antimicrobial agents with potential activity include:

• Ampicillin

• Aminoglycosides

• Cephalosporins

For invasive infection, antimicrobial selection should be guided by the isolate’s susceptibility pattern and the clinical severity of disease.

High-Yield Clinical Pattern

Animal, reptile, fish, or aquatic exposure

• ●

Gastroenteritis

or

Bacteremia/sepsis

• ●

Aerobic Gram-negative bacillus isolated by culture

→ Consider Edwardsiella tarda

Exam Essentials

Organism: Edwardsiella tarda

Type: Aerobic Gram-negative bacillus

Distribution: Worldwide

Frequency: Rare human pathogen

Reservoir: Intestinal flora of animals, including snakes

Important exposures: Reptiles and aquatic environments/animals

Major infections: Gastroenteritis and bacteremia

Diagnosis: Culture

Primary treatment: Fluoroquinolone

Bacteremia: Intravenous antimicrobial therapy is required

Additional options: Ampicillin, aminoglycosides, or cephalosporins

Key clinical pearl: Think of Edwardsiella tarda when gastroenteritis or bacteremia occurs after aquatic-animal or reptile exposure; invasive bloodstream infection is the major serious manifestation and requires systemic antimicrobial therapy.

Infectious Disease and Microbiology – Echovirus

Overview

Echoviruses are members of the enterovirus group and are common causes of human infection. They can produce a wide spectrum of clinical syndromes ranging from mild respiratory or mucocutaneous illness to aseptic meningitis, encephalitis, myopericarditis, and severe disseminated neonatal infection.

Like other enteroviruses, echoviruses are small, nonenveloped, single-stranded RNA viruses.

Microbiologic Characteristics

Echoviruses have the following major characteristics:

• Single-stranded RNA genome

• Icosahedral symmetry

• Naked (nonenveloped) virus

• Member of the enterovirus group

The absence of a lipid envelope contributes to the environmental stability characteristic of enteroviruses.

Incubation Period

The incubation period is generally:

A few days

However, the exact duration varies according to the clinical syndrome produced by the virus.

Epidemiology

Echoviruses have a worldwide distribution and are common human pathogens.

In patients with gastrointestinal infection, the virus may be isolated from stool for approximately 1 week, reflecting viral replication and shedding through the gastrointestinal tract.

Transmission

Transmission occurs predominantly through the fecal–oral route, although respiratory transmission may also contribute to the spread of some enteroviruses.

Viral shedding in stool facilitates transmission between individuals, particularly when hygiene and sanitation are inadequate.

Clinical Infections

Echoviruses can produce several different clinical syndromes.

Important manifestations include:

• Exanthems and enanthems

• Upper respiratory tract infection

• Herpangina

• Pleurodynia

• Myopericarditis

• Neonatal disseminated infection

• Meningitis

• Encephalitis

• Chronic meningoencephalitis in immunocompromised patients

• Rarely, paralysis

Exanthems and Enanthems

Echovirus infection may cause exanthems, characterized by cutaneous eruptions, and enanthems, involving mucosal surfaces.

These manifestations commonly occur as part of an acute febrile viral illness.

Upper Respiratory Infection

Some echovirus infections present as a nonspecific upper respiratory tract illness.

Manifestations may include fever, sore throat, and other symptoms resembling those caused by many common respiratory viruses.

Herpangina

Echoviruses may occasionally produce a herpangina-like syndrome involving painful vesicular or ulcerative lesions of the posterior oropharynx.

Herpangina is more classically associated with other enteroviruses, particularly group A coxsackieviruses.

Pleurodynia

Pleurodynia is characterized by acute, sometimes severe pain involving the chest or upper abdominal muscles.

Although classically associated with group B coxsackieviruses, it may also occur with other enteroviruses, including echoviruses.

Myopericarditis

Echoviruses can cause inflammation involving the myocardium and/or pericardium, producing myopericarditis.

Possible manifestations include:

• Chest pain

• Dyspnea

• Arrhythmias

• Cardiac dysfunction in severe cases

Meningitis

Aseptic meningitis is an important manifestation of enterovirus infection, including echovirus infection.

Patients may present with:

• Fever

• Severe headache

• Neck stiffness

• Photophobia

• Nausea and vomiting

Enteroviruses are important causes of viral meningitis.

Encephalitis

Echoviruses may also cause encephalitis, although this is less common than uncomplicated aseptic meningitis.

Neurologic manifestations may include altered mental status, seizures, or other signs of cerebral involvement.

Paralysis

Paralytic disease is rare with echovirus infection.

Nevertheless, some non-polio enteroviruses can occasionally produce neurologic syndromes involving motor weakness or paralysis.

Disseminated Neonatal Infection

Echovirus infection can be particularly severe in newborn infants.

Disseminated neonatal disease may involve multiple organs and can become life-threatening.

Potential manifestations include:

• Sepsis-like illness

• Hepatitis

• Myocarditis

• Encephalitis

• Coagulopathy

• Multiorgan dysfunction

Chronic Meningoencephalitis

An especially important association is chronic enteroviral meningoencephalitis in patients with impaired humoral immunity.

Patients with agammaglobulinemia are particularly susceptible because antibodies are important for controlling enterovirus infections.

Diagnosis

Traditional diagnostic techniques include:

• Cell culture

• Serologic testing

• Immunohistochemistry on biopsy material

These methods can provide evidence of enterovirus infection depending on the clinical syndrome and specimen obtained.

Molecular Diagnosis

Reverse-transcription polymerase chain reaction (RT-PCR) can detect viral RNA and is an important method for diagnosing enterovirus infections.

Depending on the clinical syndrome, appropriate specimens may include stool, respiratory samples, blood, or cerebrospinal fluid.

For suspected meningitis or encephalitis, detection of enteroviral RNA in CSF can be particularly useful.

Treatment

Treatment is primarily supportive and symptomatic.

Management depends on the clinical syndrome and may include:

• Hydration

• Fever and pain control

• Management of neurologic complications

• Cardiac support for severe myopericarditis

• Intensive supportive care for severe neonatal disease

Antiviral Therapy

The source describes:

No specific antiviral treatment

Therefore, routine management primarily focuses on supportive care and treatment of complications.

Prevention

Good hygiene and infection-control practices help reduce enterovirus transmission.

The source recommends enteric isolation for approximately 7 days to decrease transmission.

Additional preventive measures include:

• Careful hand hygiene

• Appropriate handling of fecally contaminated materials

• Environmental cleaning

• Avoiding sharing contaminated objects

High-Yield Clinical Pattern

Acute febrile illness

• ●

Aseptic meningitis, rash, respiratory illness, or myopericarditis

• ●

Enterovirus detected by RT-PCR

→ Consider echovirus

Important Immunodeficiency Association

Agammaglobulinemia

• ●

Persistent or recurrent neurologic symptoms

• ●

Chronic enterovirus infection

→ Think chronic enteroviral meningoencephalitis

Exam Essentials

Virus: Echovirus

Group: Enterovirus

Genome: Single-stranded RNA

Capsid: Icosahedral

Envelope: Absent (naked)

Incubation: Usually a few days

Major transmission route: Fecal–oral

Common syndromes: Exanthems, enanthems, respiratory infection, meningitis

Other manifestations: Herpangina, pleurodynia, myopericarditis, encephalitis

Severe population: Newborns

Important immunodeficiency association: Agammaglobulinemia → chronic meningoencephalitis

Paralysis: Rare

Modern diagnostic method: RT-PCR for viral RNA

Treatment: Supportive

Specific routine antiviral therapy: None described

Prevention: Hygiene and appropriate enteric precautions

Key clinical pearl: Echoviruses are naked, single-stranded RNA enteroviruses with a broad clinical spectrum; particularly high-yield associations are aseptic meningitis, severe disseminated neonatal disease, and chronic meningoencephalitis in patients with agammaglobulinemia.

Infectious Disease and Microbiology – Echinostoma ilocanum

Overview

Echinostoma ilocanum is a trematode helminth (intestinal fluke) that can infect the human gastrointestinal tract. Human infection is uncommon and primarily occurs in parts of Southeast and East Asia.

The parasite is a rare cause of small-bowel infection.

Microbiologic Characteristics

Echinostoma ilocanum is a trematode helminth belonging to the group of intestinal flukes.

The adult parasite resides within the small intestine, where it can produce eggs that are subsequently passed in the stool.

Epidemiology

Human E. ilocanum infection has been reported particularly in:

• Philippines

• Indonesia

• Malaysia

• China

The infection is relatively rare even within endemic regions.

Transmission

Human echinostomiasis is a foodborne trematode infection.

Infection is generally acquired by consuming raw or inadequately cooked intermediate hosts containing infective metacercariae, such as certain freshwater snails or other aquatic organisms.

Clinical Infection

E. ilocanum is a rare cause of small-bowel infection.

Many infections may produce few or nonspecific manifestations.

When symptomatic, intestinal irritation may result in gastrointestinal complaints, particularly with a greater parasite burden.

Gastrointestinal Manifestations

Possible manifestations of intestinal echinostomiasis include:

• Abdominal discomfort or pain

• Diarrhea

• Other nonspecific gastrointestinal symptoms

The severity of illness generally depends on the intensity of infection.

Diagnosis

Diagnosis is based primarily on parasitologic examination of stool specimens.

The recommended approach in the source is:

Examination of concentrated stool specimens for parasite eggs

Microscopic identification of characteristic trematode eggs supports the diagnosis.

Treatment

The treatment described in the source is:

Praziquantel 25 mg/kg orally every 8 hours for 2 days

Praziquantel is used to eliminate the intestinal trematode infection.

High-Yield Clinical Pattern

Exposure in Southeast or East Asia

• ●

Intestinal/small-bowel symptoms

• ●

Trematode eggs detected in concentrated stool

→ Consider Echinostoma ilocanum

Exam Essentials

Organism: Echinostoma ilocanum

Type: Trematode helminth

Location of infection: Small intestine

Geographic distribution: Philippines, Indonesia, Malaysia, and China

Frequency: Rare human infection

Major disease: Intestinal echinostomiasis

Diagnosis: Concentrated stool examination for parasite eggs

Treatment: Praziquantel 25 mg/kg PO every 8 hours for 2 days

Key clinical pearl: Echinostoma ilocanum is a rare intestinal trematode of Southeast and East Asia that causes small-bowel infection and is diagnosed by finding parasite eggs in concentrated stool specimens.

Infectious Disease and Microbiology – Ebola and Marburg Viral Diseases

Overview

Ebola virus and Marburg virus belong to the filovirus group and cause severe systemic illnesses known as viral hemorrhagic fevers. Both infections are uncommon but potentially life-threatening, with rapid onset of fever, constitutional symptoms, gastrointestinal manifestations, and, in severe cases, hemorrhage, shock, and multiorgan dysfunction.

Microbiologic Characteristics

Ebola and Marburg viruses are filoviruses characterized by:

• Single-stranded RNA genomes

• Helical nucleocapsid symmetry

• Lipid envelopes

• Characteristic filamentous viral particles

Because they are enveloped viruses, appropriate infection-control and disinfection procedures are important for preventing transmission.

Important Species

The two major viruses in this group are:

Ebola virus → causes Ebola virus disease (EVD)

Marburg virus → causes Marburg virus disease (MVD)

Both can produce severe viral hemorrhagic fever syndromes.

Incubation Period

For Ebola virus disease, the incubation period is approximately:

2–21 days

For Marburg virus disease, the source describes an incubation period of:

3–9 days

Symptoms begin after the incubation period rather than immediately following exposure.

Epidemiology

Ebola and Marburg virus infections are relatively rare.

Ebola virus outbreaks have primarily occurred in Africa.

Marburg virus disease has also been associated mainly with Africa, although historically cases have been recognized in Europe following exposure to infected animals or imported infections.

Transmission

Transmission can occur through direct contact with the blood or other body fluids of an infected person, contaminated materials, or infected animals.

Healthcare-associated transmission can occur when appropriate infection-control precautions are not followed.

Clinical Manifestations

The illness typically begins abruptly.

Early manifestations may include:

• High fever

• Severe headache

• Myalgia

• Malaise

• Pharyngitis

These symptoms may initially resemble several other acute febrile illnesses.

Gastrointestinal Manifestations

Prominent gastrointestinal manifestations may develop, including:

• Vomiting

• Diarrhea

• Abdominal symptoms

Severe vomiting and diarrhea can contribute to major fluid and electrolyte losses.

Skin Manifestations

A maculopapular rash may develop during the course of illness.

The rash can occur together with progressive systemic manifestations.

Hemorrhagic Manifestations

Despite the traditional term “hemorrhagic fever,” clinically obvious bleeding does not occur in every patient.

Severe disease may nevertheless produce:

• Mucosal bleeding

• Gastrointestinal bleeding

• Coagulopathy

• Thrombocytopenia

• Disseminated intravascular coagulation

Severe Disease

Severe Ebola or Marburg virus disease may progress to:

Profound fluid loss → hypotension → shock → multiorgan dysfunction

The illnesses have historically been associated with high case-fatality rates, although mortality varies considerably between outbreaks and according to the viral species, supportive care, and availability of specific therapies.

Diagnosis

The source describes diagnosis using:

• Cell culture

• Serologic testing

Because these are highly hazardous pathogens, viral culture requires specialized high-containment laboratory facilities.

Molecular Diagnosis

In contemporary clinical practice, RT-PCR or other nucleic-acid amplification testing is particularly important for confirming acute Ebola or Marburg virus infection.

Serologic testing may also have a role depending on the stage of infection.

Treatment

The foundation of management is intensive supportive care, including:

• Fluid and electrolyte replacement

• Hemodynamic support

• Management of shock

• Oxygen and organ support when required

• Treatment of associated complications

Early, high-quality supportive care can substantially influence outcome.

Ebola-Specific Therapy

The source states that there is no specific antiviral treatment; however, this reflects older management information.

For certain forms of Ebola virus disease, particularly disease caused by Zaire ebolavirus, specific monoclonal-antibody therapies have subsequently become available.

This is an important distinction when interpreting older infectious-disease references.

Marburg Virus Treatment

Management of Marburg virus disease remains primarily supportive, with careful management of fluid loss, shock, and organ dysfunction.

Infection Control

Patients with suspected or confirmed filovirus infection require strict infection-control precautions.

Important measures include:

• Appropriate patient isolation

• Personal protective equipment

• Careful handling of blood and body fluids

• Safe injection practices

• Appropriate environmental decontamination

• Safe handling of laboratory specimens

Healthcare workers require particularly rigorous protection because direct exposure to infected body fluids can transmit disease.

Sexual Transmission and Survivors

Filoviruses can persist in certain body fluids after recovery, including semen.

The source recommends avoiding sexual intercourse for 3 months or until semen is demonstrated to be free of virus.

Modern survivor guidance may use testing-based and public-health recommendations rather than relying exclusively on a fixed 3-month period.

High-Yield Clinical Pattern

Recent exposure in an outbreak or contact with an infected person

• ●

Abrupt high fever + severe headache + myalgia

• ●

Vomiting and profuse diarrhea

• ●

Possible rash, bleeding, shock, and multiorgan dysfunction

→ Consider Ebola or Marburg virus disease

Exam Essentials

Virus group: Filovirus

Important viruses: Ebola virus and Marburg virus

Genome: Single-stranded RNA

Envelope: Present

Symmetry: Helical

Ebola incubation: 2–21 days

Marburg incubation in source: 3–9 days

Typical onset: Abrupt febrile illness

Major symptoms: Fever, headache, myalgia, vomiting, diarrhea, pharyngitis, rash

Severe complications: Shock, coagulopathy, hemorrhage, multiorgan dysfunction

Modern acute diagnosis: RT-PCR

Core treatment: Intensive supportive care

Ebola: Specific monoclonal-antibody treatment is available for some Ebola virus infections

Marburg: Primarily supportive management

Prevention: Strict infection-control precautions and avoidance of exposure to infected blood/body fluids

Key clinical pearl: Think of filovirus disease when a patient with an appropriate epidemiologic exposure develops abrupt fever, severe constitutional symptoms, vomiting and diarrhea followed by possible rash, coagulopathy, shock, or multiorgan failure; hemorrhage is an important manifestation but is not required for the diagnosis.

Infectious Disease and Microbiology – Dracunculus medinensis 

Overview 

Dracunculus medinensis is a nematode helminth that causes dracunculiasis, also known as Guinea worm disease. 

Humans acquire the infection by drinking contaminated water. After a long incubation period of about 1 year, the adult female worm migrates to the skin, where it produces a painful blister that later ulcerates and allows the worm to emerge. 

⸻ 

Microbiologic Characteristics 

D. medinensis is a nematode helminth. 

Humans become accidental hosts after ingesting water contaminated with infected freshwater organisms that carry the larval stage of the parasite. 

⸻ 

Incubation Period 

The incubation period is typically: 

About 1 year 

Patients may remain asymptomatic for many months before the worm reaches the skin. 

⸻ 

Epidemiology 

Dracunculiasis has historically occurred in: 

• Sub-Saharan Africa • The Middle East • Parts of Asia 

Transmission is associated with drinking unsafe water from sources such as ponds and step wells. 

⸻ 

Transmission 

Humans acquire infection by drinking contaminated water. 

The infective larvae are carried by small freshwater crustaceans called copepods. 

⸻ 

Life Cycle 

The simplified life cycle is: 

Contaminated water containing infected copepods 

↓ 

Human drinks the water 

↓ 

Larvae are released in the gastrointestinal tract 

↓ 

Larvae mature and reproduce 

↓ 

Adult female worm migrates to the skin 

↓ 

Painful vesicle forms 

↓ 

Skin ulcer develops and worm emerges 

↓ 

Contact with water stimulates release of larvae 

This allows the parasite to continue its transmission cycle. 

⸻ 

Guinea Worm Disease 

The characteristic manifestation is a skin vesicle followed by ulcer formation, usually where the adult worm begins to emerge. 

Patients may develop: 

• Burning pain • Local swelling • Erythema • Painful blister • Ulcer formation • Visible protruding worm 

The lower extremities are commonly affected. 

⸻ 

Secondary Bacterial Infection 

Secondary bacterial infection of the open skin lesion is common. 

Possible complications include: 

• Cellulitis • Abscess formation • Local tissue infection • Delayed wound healing 

Appropriate wound care is therefore important. 

⸻ 

Tetanus Risk 

Open Guinea worm lesions may become contaminated and can increase the risk of tetanus. 

Maintaining appropriate tetanus immunization helps reduce this risk. 

⸻ 

Diagnosis 

Diagnosis is usually based on direct identification of the worm in the skin lesion. 

The adult worm may be visibly protruding from the ulcer. 

⸻ 

Microscopic Diagnosis 

Microscopic examination of material from the skin lesion may demonstrate larvae of the parasite. 

However, the visible emerging worm is often sufficient to strongly suggest the diagnosis. 

⸻ 

Treatment 

The principal treatment is: 

Extraction of the worm 

The worm is removed gradually and carefully from the affected tissue. 

⸻ 

Mechanical Extraction 

The emerging worm may be slowly wound around a small object and progressively removed. 

Careful extraction is important because breaking the worm within the tissue may increase inflammation and complicate removal. 

⸻ 

Additional Treatment 

The source describes the use of: 

Thiabendazole 50 mg/kg/day orally in 2 divided doses for 2 days 

or 

Metronidazole 10 mg/kg/day divided into 3 doses for 1 week 

These drugs may help reduce inflammation surrounding the lesion. 

Importantly: 

They do not kill or eliminate the worm itself. 

⸻ 

Prevention 

Prevention focuses on interrupting transmission through contaminated water. 

Important measures include: 

• Drink only safe, potable water • Avoid drinking untreated water from ponds or wells • Prevent infected individuals from entering drinking-water sources • Protect community water supplies from contamination • Maintain good wound care 

⸻ 

Preventing Water Contamination 

Patients with active skin lesions should not enter sources of drinking water. 

When the emerging worm contacts water, it can release larvae and contaminate the water source, allowing transmission to continue. 

⸻ 

Tetanus Prevention 

Patients should have appropriate tetanus vaccination. 

This does not prevent Guinea worm infection itself but helps prevent tetanus associated with secondary bacterial contamination of the skin lesion. 

⸻ 

High-Yield Clinical Pattern 

Unsafe drinking water exposure 

Incubation of about 1 year 

Painful skin blister followed by ulceration 

Long worm protruding from the lesion 

→ Think Dracunculus medinensis 

⸻ 

Exam Essentials 

Organism: Dracunculus medinensis Disease: Dracunculiasis / Guinea worm disease Type: Nematode helminth Incubation: About 1 year Transmission: Drinking contaminated water Intermediate host: Copepod Classic lesion: Skin vesicle → ulcer → emerging worm Major complication: Secondary bacterial infection Diagnosis: Identification of the adult worm or larvae Primary treatment: Mechanical extraction Additional drugs: Thiabendazole or metronidazole for inflammation Important limitation: These drugs do not kill the worm Prevention: Safe drinking water and keeping infected patients out of water sources Additional prevention: Tetanus immunization 

⸻ 

Key clinical pearl: The classic sequence is contaminated water → about 1 year of incubation → painful skin blister → ulcer with an emerging worm = Guinea worm disease due to Dracunculus medinensis.

Infectious Disease and Microbiology – Dirofilaria Species

Overview

Dirofilaria species are nematode helminths that primarily infect animals. Human infection is uncommon and usually represents an accidental zoonotic infection.

Important species include D. immitis, D. repens, D. tenuis, and D. ursi.

Microbiologic Characteristics

Dirofilaria species are filarial nematodes.

Humans are not the usual definitive hosts, which is why the parasite often fails to complete its normal life cycle in human tissues.

Epidemiology

Different species are associated with different animal reservoirs.

D. immitis is the dog heartworm and only rarely causes human disease.

D. tenuis is primarily a parasite of raccoons in the United States.

D. repens is mainly a parasite of dogs and cats in Europe.

D. ursi is associated with bears in Canada.

Human Infection

Human infection is rare.

Because humans are accidental hosts, disease usually results from localization of immature or adult worms in tissue rather than from widespread filarial infection.

Dirofilaria immitis

D. immitis may cause either pulmonary or cutaneous disease in humans.

Pulmonary infection often results from a worm lodging in a branch of the pulmonary circulation.

Pulmonary Dirofilariasis

Pulmonary infection may produce a localized pulmonary nodule.

Patients are often asymptomatic, and the lesion may be discovered incidentally on chest imaging.

The nodule can sometimes resemble:

• Primary lung cancer

• Metastatic disease

• Granulomatous infection

The diagnosis is frequently made only after surgical excision and histopathologic examination.

Cutaneous Dirofilariasis

D. immitis and several other Dirofilaria species may occasionally produce cutaneous or subcutaneous lesions.

These may appear as:

• Subcutaneous nodules

• Localized swelling

• Inflammatory masses

Some lesions may contain a recognizable worm.

Other Species

Other Dirofilaria species, particularly D. repens and D. tenuis, may also cause cutaneous manifestations in humans.

These infections remain uncommon and are usually localized.

Microfilaremia

Microfilaremia is rare in humans.

This is an important distinction from classic human filarial diseases, in which circulating microfilariae may be a major diagnostic feature.

Diagnosis

Diagnosis is usually made by detecting the worm in tissue.

This typically requires:

• Biopsy of the lesion

• Surgical excision

• Histopathologic identification of the nematode

Blood tests are generally less useful because circulating microfilariae are rarely present.

Treatment

The principal treatment is surgical removal of the affected lesion or tissue.

Once the localized worm is removed, additional antiparasitic therapy is often unnecessary.

High-Yield Clinical Pattern

Incidental pulmonary nodule

• ●

No obvious pulmonary symptoms

• ●

Histology showing a filarial nematode

→ Consider Dirofilaria immitis

Exam Essentials

Genus: Dirofilaria

Type: Nematode helminth

Human role: Accidental host

Classic species: D. immitis

Animal association: Dog heartworm

Human manifestations: Pulmonary or cutaneous disease

Other species: D. repens, D. tenuis, D. ursi

Microfilaremia: Rare in humans

Diagnosis: Worm identified in excised tissue

Treatment: Surgical removal

Key clinical pearl: Human dirofilariasis is usually a localized zoonotic infection, often presenting as a pulmonary or subcutaneous nodule, and diagnosis is typically made by histologic identification of the worm after excision.