Vol. 21, No. 5
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Tuesday, February 12, 2002
A. Provided by Karen Fujii, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene.
10 outbreaks were reported to DHMH during MMWR Week 6 (February 3-February
1 outbreak of influenza (3 positive rapid antigen tests) at a nursing home (Frederick Co.)Case presentation:
2 outbreaks of influenza-like illness at nursing homes (Montgomery Co. and Washington Co.)
1 outbreak of influenza-like illness/pneumonia (1 diagnosis of pneumonia) at a nursing home (Baltimore City)
2 outbreaks of pneumonia at nursing homes (Anne Arundel Co. and Baltimore City)
1 outbreak of gastroenteritis at an adult day program (Baltimore City)
1 outbreak of foodborne gastroenteritis associated with a youth conference (Montgomery Co.; cases from multiple states)
1 outbreak of pertussis at a private home (Baltimore City)
1 outbreak of Fifth Disease (Talbot Co.)B. The Johns Hopkins Hospital, Department of Pathology, Information provided by M. Ali Ansari-Lari, MD, Ph. D.
The patient is a 40 year-old Caucasian male with a past medical history significant for human immunodeficiency virus infection first diagnosed in 1990, community acquired pneumonia x 3, oral candidiasis, weight loss, and appendectomy who presented to The Johns Hopkins Hospital with complaints of abdominal pain involving his left lower quadrant, and intermittent diarrhea. On admission, his medications included Amprenavir, Trizivir, and bactrim. His physical examination was notable for temperature of 101ºF, diffusely tender abdomen with normal bowel sounds, hepatosplenomegaly, and left groin lymphadenopathy. His laboratory data was significant for CD4 count 28, viral load of >500,000, hemoglobin 10, platelet 95,000, and white cell count of 8,700 with 50% bands, 42% neutrophils, 4% lymphocytes, and 4% monocytes and normal liver function tests. The CT of pelvis and abdomen revealed moderate retroperitoneal and celiac axis lymphadenopathy. He underwent a bone marrow biopsy, which was negative for lymphoma or leukemia but grew Histoplasma capsulatum after 18 days. His urine was positive for Histoplasma antigen. Amphotericin B therapy was initiated.
Histoplasma capsulatum
Identification and diagnosis:
H. capsulatum is a dimorphic fungus, growing as a mycelial and a yeast form. H. capsulatum grows as a silky, hair-like, white to gray-tan mold on enriched fungal media after 10 to 30 days of incubation at 25 to 30 C. Microscopically, the hyphae are delicate, averaging 1 to 2 ?m in diameter. In addition to microconidia which appear early in growth phase, rough, spiked-walled macroconidia ranging in size from 5 to 15 ?m develop after prolonged incubation. In culture, the conversion from mold form to yeast form is often difficult. On 5% sheep blood agar plate at 37 C, yeast form grows as small, yellowish colonies. Microscopically, the yeast forms are spherical to oval shape, 2-3 ?m in diameter, occasionally with single buds attached with narrow necks. On methenamine silver or PAS stains of tissue sections, the organism is typically found inside histiocytes and appears to have a pseudo-capsule due to a shrinking fixation artifact (hence the name Histoplasma capsulatum). Immunocompetent hosts typically develop caseating granulomas with few organisms, while immunosuppressed hosts have many macrophages filled with organisms. Old lesions in immunocompetent hosts may become fibrotic and calcifed (histoplasmoma).
Usually medium that is used to recover H. capsulatum includes brain-heart infusion agar containing blood plus antibiotics and cyclohexamide to inhibit growth of saprophytic fungi and bacteria. Typically, cultures are incubated at 30 C for up to 6 weeks, and growth is often noted between 7 to 21 days. The success rate for recovering the organism depends on the number of specimen collected, source of the specimen, and the burden of infection. Use of the isolator system, which results in lysis of the infected cells and release of the microorganism improves the yields and speed of recovery from blood. DNA probe can be used for identification of H. capsulatum from the mold form without a prolonged and often difficult conversion to the yeast form. The nucleic acid probe is a chemiluminescent, acridinium ester-labeled single-stranded DNA complementary to the rRNA of H. capsulatum mold form, with very high sensitivity and specificity.
By radioimmunoassay or enzyme-linked immunosorbent assay techniques H. capsulatum polysaccharide antigen can be detected in urine, serum, bronchoalveolar fluid, and cerebrospinal fluid with 95%, 80%, 70%, and 50% sensitivity, respectively. These assays can be used to monitor antifungal therapy and relapse of the disease. Serologic assays can be used for the diagnosis of the infection. However, the major limitation of the serologic tests is that in up to 50% of actively infected immunocompromised patients, especially those with AIDS, the results are negative.
Epidemiology:
In the Western Hemisphere, infection is concentrated in the eastern United States, but is also found in the Caribbean, and Central and South America. The infection rate in Europe is low. The major endemic areas of histoplasmosis in the United States include the Ohio, Mississippi, and Missouri River valleys. The organism is found in organic-rich, warm (22 C – 29 C), moist soil, especially if it contains bird or bat excreta. Birds are not infected with fungus, but bats carry the organism in their gastrointestinal tracts.
Individuals involved in agriculture, construction, excavation or recreational activities that expose them to soil are at the highest risk of infection. The disease appears to infect more males than females (4:1), although the skin test reactivity to the H. capsulatum antigen is similar among men and women.
Clinical presentations:
Most cases of histoplasmosis present as an acute pulmonary illness of varying degrees of severity, characterized by fever, cough, chills, headache, chest pain, and often mediastinal lymphadenopathy. Other pulmonary presentations include chronic infection or cavitary lesions. Some of the Complications of histoplasmosis include postobstructive pneumonia, superior vena cava obstruction, fibrosing mediastinitis, and pericardial fibrosis. Approximately 50% to 75% of AIDS patients with histoplasmosis present with a progressive disseminated disease, an AIDS-defining illness. Clinical manifestations include fever, fatigue, weight loss, splenomegaly, and pancytopenia. AIDS patients may develop disseminated disease years after exposure in an endemic area. CXR may show discrete nodules or a milliary pattern. In AIDS patients, other organ system that may become involved include central nervous system (meningitis, cerebral or spinal cord mass lesions), gastrointestinal tract (ulcer, mass, or constricting lesions), oropharynx, eyes (endophthalmitis), and skin (pustules, folliculitis, eczematous changes, erythema multiforme). In AIDS patients with histoplasmosis, initial therapy with Amphotericin B followed by a lifelong therapy with Itraconazole may be required.
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