HISTOPLASMOSIS

A Case Study

In Partial Accomplishment

of the Requirements in

Microbiology and Parasitology

Danish Stephanie C. Parales

Bachelor of Science in Nursing

Is presented to Sherleen Jane Fernandez

March 2019
Case Study: 33-Year-Old Female Presents with Chronic SOB and Cough

PATIENT PRESENTATION

History of Present Illness: A 33-year-old Caucasian female presents after admission to the general

medical/surgical hospital ward with a chief complaint of shortness of breath on exertion. She reports

that she was seen for similar symptoms previously at her primary care physician’s office six months

ago. At that time, she was diagnosed with acute bronchitis and treated with bronchodilators, empiric

antibiotics, and a short course oral steroid taper. This management did not improve her symptoms,

and she has gradually worsened over six months. She reports a 20-pound intentional weight loss

over the past year. She denies camping, spelunking, or hunting activities. She denies any sick

contacts. A brief review of systems is negative for fever, night sweats, palpitations, chest pain,

nausea, vomiting, diarrhea, constipation, abdominal pain, neural sensation changes, muscular

changes, and increased bruising or bleeding. She admits a cough, shortness of breath, and shortness

of breath on exertion.

Social History: Her tobacco use is 33 pack-years; however, she quit smoking shortly prior

to the onset of symptoms, six months ago. She denies alcohol and illicit drug use. She is married, in a

monogamous relationship, and has three children aged 15 months to 5 years. She is employed in a

cookie bakery. She has two pet doves. She traveled to Mexico for a one-week vacation, one year

ago.

Past Medical History: Hypertension

Past Surgical History: Cholecystectomy

Medications: Lisinopril 10mg by mouth every day

Allergies: No known medicine, food, or environmental allergies.

Differential Diagnosis

 Aspiration pneumonitis and pneumonia

 Bacterial pneumonia
 Immunodeficiency state and Pneumocystis jiroveci pneumonia
 Carcinoid lung tumors
 Tuberculosis
 Viral pneumonia
 Chlamydial pneumonia
 Coccidioidomycosis and valley fever
 Recurrent Legionella pneumonia
 Mediastinal cysts
 Mediastinal lymphoma
 Recurrent mycoplasma infection
 Pancoast syndrome
 Pneumococcal infection
 Sarcoidosis
 Small cell lung cancer
 Aspergillosis
 Blastomycosis
 Histoplasmosis
 Actinomycosis

EXAMINATION

Vitals: Temperature, 97.8 F

  Heart Rate 88

Respiratory Rate, 22

Blood Pressure 130/86

Body Mass Index, 28

General: She is well appearing but anxious, a pleasant female lying on a hospital stretcher. She is

conversing freely, with respiratory distress causing her to stop mid-sentence.

Respiratory: She has diffuse rales and mild wheezing; tachypneic.

Cardiovascular: She has a regular rate and rhythm with no murmurs, rubs, or gallops.

Gastrointestinal: Bowel sounds X4. No bruits or pulsatile mass.

Initial Evaluation

Laboratory Studies: Initial work-up from the emergency department revealed pancytopenia with a

platelet count of 74,000 per mm3; hemoglobin, 8.3 g per and mild transaminase elevation, AST 90

and ALT 112. Blood cultures were drawn and currently negative for bacterial growth or Gram staining.

Chest X-ray

Impression: Mild interstitial pneumonitis

Confirmatory Evaluation

CT Chest was performed to further the pulmonary diagnosis; it showed a diffuse centrilobular

micronodular pattern without focal consolidation.

On finding pulmonary consolidation on the CT of the chest, a pulmonary consultation was

obtained. Further history was taken which revealed that she has two pet doves. As this was her third

day of broad-spectrum antibiotics for a bacterial infection and she was not getting better, it was

decided to perform diagnostic bronchoscopy of the lungs with bronchoalveolar lavage to look for any

atypical or rare infections and to rule out malignancy.

Bronchoalveolar lavage returned with a fluid that was cloudy and muddy in appearance. There

was no bleeding. Cytology showed Histoplasma capsulatum.

Diagnosis

Based on the bronchoscopic findings, a diagnosis of acute pulmonary histoplasmosis in an

immunocompetent patient was made.

Discussion

Histoplasmosis, also known as Darling disease, Ohio valley disease, reticuloendotheliosis,

caver's disease, and spelunker's lung, is a disease caused by the dimorphic fungi Histoplasma

capsulatum native to the Ohio, Missouri, and Mississippi River valleys of the United States. The two

phases of Histoplasma are the mycelial phase and the yeast phase.

Etiology/Pathophysiology 

Histoplasmosis is caused by inhaling the microconidia of Histoplasma spp. fungus into the

lungs. The mycelial phase is present at ambient temperature in the environment, and upon exposure

to 37 C, such as in a host’s lungs, it changes into budding yeast cells. This transition is an important

determinant in the establishment of infection. Inhalation from soil is a major route of transmission

leading to infection. Human-to-human transmission has not been reported. Infected individuals may

harbor many yeast-forming colonies chronically which remain viable for years after initial inoculation.

The finding that individuals who have moved or traveled from endemic to non-endemic areas may

exhibit a reactivated infection after many months to years supports this long-term viability. However,

the precise mechanism of reactivation in chronic carriers remains unknown.

Infection ranges from an asymptomatic illness to a life-threatening disease, depending on the

host’s immunological status, fungal inoculum size, and other factors. Histoplasma spp. have grown

particularly well in organic matter enriched with bird or bat excrement, leading to the association that

spelunking in bat-feces-rich caves increases the risk of infection. Likewise, ownership of pet birds

increases the rate of inoculation. In our case, the patient did travel outside of Nebraska within the in

last year and owned two birds; these are her primary increased risk factors.
 Non-immunocompromised patients present with a self-limited respiratory infection. However,

the infection in immunocompromised hosts disseminated histoplasmosis progresses very

aggressively. Within a few days, histoplasmosis can reach a fatality rate of 100% if not treated

aggressively and appropriately. Pulmonary histoplasmosis may progress to a systemic infection. Like

its pulmonary counterpart, the disseminated infection is related to an exposure to soil containing

infectious yeast. The disseminated disease progresses more slowly in immunocompetent hosts

compared to immunocompromised hosts. However, if the infection is not treated, fatality rates are

similar. The pathophysiology for a disseminated disease is that, once inhaled, Histoplasma yeast are

ingested by macrophages. The macrophages travel into the lymphatic system where the disease, if

not contained, spreads to different organs in a linear fashion following the lymphatic system and

ultimately into systemic circulation. Once this occurs, a full spectrum of disease is possible. Inside the

macrophage, this fungus is contained in a phagosome. It requires thiamine for continued

development and growth and will consume systemic thiamine. In immunocompetent hosts, strong

cellular immunity including macrophages, epithelial, and lymphocytes surround the yeast buds to

keep infection localized. Eventually, it will become calcified as granulomatous tissue. In

immunocompromised hosts, the organisms disseminate to reticuloendothelial system, leading to

progressive disseminated histoplasmosis.

Symptoms of infection typically begin to show within three to17 days. Immunocompetent

individuals often have clinically silent manifestations with no apparent ill effects. The acute phase of

infection presents as nonspecific respiratory symptoms including a cough and flu. A chest x-ray is

read as normal in 40% to 70% cases. Chronic infection can resemble tuberculosis with

granulomatous changes or cavitation. The disseminated illness can lead

to hepatosplenomegaly, adrenal enlargement, and lymphadenopathy. The infected sites usually

calcify as they heal. Histoplasmosis is one of the most common causes of mediastinitis. Presentation

of the disease may vary as any other organ in the body may be affected by the disseminated

infection.
Treatment

Pulmonary histoplasmosis in asymptomatic patients is self-resolving and requires no

treatment. However, once symptoms develop such as in our above patient a decision to treat needs

to be made. In mild, tolerable cases, no treatment other than close monitoring is necessary. However,

once symptoms progress to moderate or severe or if they are prolonged for greater than four weeks,

treatment with itraconazole is indicated. The anticipated duration is 6 to 12 weeks. The patient's

response should be monitored with a chest x-ray. Furthermore, observation for recurrence is

necessary for several years following the diagnosis. If the illness is determined to be severe or does

not respond to itraconazole, amphotericin B should be initiated for a minimum of 2 weeks, but up to 1

year. Cotreatment with methylprednisolone is indicated to improve pulmonary compliance and reduce

inflammation, thus improving the work of respiration.

The disseminated disease requires similar systemic antifungal therapy to pulmonary infection.

Additionally, procedural intervention may be necessary, depending on the site of dissemination, to

include thoracentesis, pericardiocentesis, or abdominocentesis. Ocular involvement requires steroid

treatment additions and necessitates ophthalmology consultation. In pericarditis patients, antifungals

are contraindicated because the subsequent inflammatory reaction from therapy would worsen

pericarditis.

Patients may necessitate intensive care unit placement dependent on their respiratory status,

as they may pose a risk for rapid decompensation. Should this occur, respiratory support is

necessary, including non-invasive BiPAP or invasive mechanical intubation. Surgical interventions are

rarely warranted; however, bronchoscopy is useful as both a diagnostic measure to collect sputum

samples from the lung and therapeutic to clear excess secretions from the alveoli. Patients are at risk

for developing a coexistent bacterial infection, and appropriate antibiotics should be considered after

2 to 4 months of known infection if symptoms are still present.

Management

Pulmonary histoplasmosis in asymptomatic patients is self-resolving and requires no

treatment. However, once symptoms develop such as in our above patient, a decision to treat needs

to be made. In mild, tolerable cases no treatment other than close monitoring is necessary. However,

once symptoms progress to moderate or severe or if they are prolonged for greater than four weeks,

treatment with itraconazole is indicated. The anticipated duration is 6 to 12 weeks total. The response

should be monitored with a chest x-ray. Furthermore, observation for recurrence is necessary for

several years following the diagnosis. If the illness is determined to be severe or does not respond to

itraconazole, amphotericin B should be initiated for a minimum of 2 weeks, but up to 1 year.

Cotreatment with methylprednisolone is indicated to improve pulmonary compliance and reduce

inflammation, thus improving work of respiration.

References

Sandeep Sharma; Deepa Rawat. (2018)

Case Study: 33-Year-Old Female Presents with Chronic SOB and Cough

https://www.ncbi.nlm.nih.gov/books/NBK500024/