Coccidioidomycosis: Is the “Zone” Growing?

SOURCE: Coccidioidomycosis — USA (Nevada), Pro-MED-mail post, August 12, 2015; www.promedmail.org.

Reports of valley fever (coccidioidomycosis) appear to be steadily on the rise in California and the Southwest during the past few years. Increasing numbers of cases are being documented throughout California and the Southwest. For example, from 1998 to 2011, cases in humans in California increased from 719 to 5366 with a big jump in 2010-2011.1 While we generally see a case or two of cocci per year in our clinic, I had three cases back to back within a three-week period in July two of whom drove down Highway 5 through the Central Valley a few weeks earlier.

This new report describes a cluster of five cases of valley fever in Washoe County, NV; two of these individuals never left the area. Washoe County is just east of the Sierra Nevada mountain range, and runs northward from Reno to the Oregon border. While cocci is endemic to southern Nevada, it is unusual in this part of northern Nevada. Officials in Washoe County say that whenever a case is identified in their county, the patient has invariably traveled to an area endemic for cocci.

Little is known about the soil conditions that promote the growth of the fungi which generally grows within the top 2 to 8 inches of soil. It is thought that heavier rains in the winter to spring nourish the growth of the organism, and then spring and summer winds kick up the topsoil, carrying the infectious arthroconidia for miles. As little as 15 arthroconidia may be infectious to humans.

The fungus is endemic to the San Joaquin Valley of California, that swath of agricultural land that runs roughly south of Stockton and Fresno to the Grapevine Mountain Range north of Los Angeles. Then its range roughly follows the lower Sonoran life zone, that arid stretch of low desert land extending from Joshua Tree to southern Nevada, and parts of Arizona, New Mexico, and northern Mexico. It was, however, recently found in soil samples from southwestern Washington outside of its recognized range.2 One wonders whether these newer cases in northern Nevada are a clue that global warming or the current drought are creating conditions more favorable to the fungus and perhaps extending its range farther north and east of the Sierras and Cascades.

REFERENCES

  1. CDPH. Increase in Valley Fever in CA. California Medical Board Newsletter, Spring 2013. https://www.cdph.ca.gov/healthinfo/discond/Pages/Coccidioidomycosis.aspx.
  2. MMWR. Notes from the field: Coccidioides immitis identified in soil outside of its known range — Washington, 2013. 2014;63:450.

Cocci as a Cause of Marine Mammal Mortality

SOURCE: Huckabone SE, et al. Coccidioidomycosis and other systemic mycoses of marine mammals stranding along the central California, USA coast: 1998-2012. J Wildlife 2015;51:295-308.

This interesting article reveals some of the fascinating details of a longitudinal study of > 7000 necropsies performed on stranded marine mammals along the central California coast from 1998 to 2012. Full necropsies are routinely performed on all stranded animals at three facilities. Nineteen different kinds of mycosis have been found in 24 species of marine mammals, either captive or free-living; most commonly, these pathogens include Coccioides, Blastomyces spp, and Cryptococcus gattii.

Of these, cocci is the most common pathogen causing mycosis in marine mammals on the California coast. Thirty-six animals had either culture or histological confirmation of cocci infection, including 15 sea lions, 20 sea otters, and one wild harbor seal. Real-time quantitative PCRs and sequencing performed at University of California Davis confirmed all infections to be due to C. immitis. For both sea lions and otters, there appears to be an increasing number of fatal cases of cocci eight sea otters and one pinniped were found with cocci infection from 1998 to 2005, compared with 12 sea otters and 15 sea lions from 2006 to 2012. Similar numbers of pinnipeds have been found all along the central California coast, extending from San Luis Obispo County to Marin — but, interestingly, dead sea otters with cocci are now being found along the northern California coast for the first time in more than 45 years of monitoring.

Coccidioidomycosis appeared to be the primary cause of death for 90% of the sea otters; the remainder died from domoic acid poisoning. Dissemination of infection was the norm (92%), and pathologic findings identified pulmonary nodules (94%), pleural effusion (92%), pneumothorax (25%), peritoneal effusions (55%) and peritonitis (29%), and infected hilar, mediastinal, or other lymph nodes (100%). Many of the otters exhibited numerous tan, raised, subcutaneous plaques which turned out to be a clue to disseminated infection which demonstrated pyogranulomatous inflammation with rare spherules on sectioning. Interestingly, cardiac involvement was not uncommon: 55% of the animals had pericarditis, and 43% had fungal myocarditis. The brain was involved in eight of nine animals (89%), and coccidioidal ophthalmitis was found in one-third of animals with microscopic examinations of the eye.

Similar to the sea otters, cocci was the primary cause of death for 87% of the pinnipeds and the rest primarily died from domoic acid poisoning. Dissemination was also common to pinnipeds (91%), with a wide range of organ involvement. Coccioides-peritonitis or peritoneal effusion was found with possible greater frequency (92%) in sea lions compared with otters.

Importantly, fresh fungal growth with the development of hyphae and arthroconidia was observed in the decomposing tissues of one animal, which could be a source of infection for others. Monitoring endemic mycosis in marine mammals is not only important for marine health surveillance, but one more clue as to what might be happening to the human population in these areas. Furthermore, the finding of large numbers of cases of coccidioidomycosis along the California coast, particularly in the area of San Luis Obispo, suggests the presence of this organism in previously unrecognized habitats.

Initial and Much Too Subtle Ebola Virus Infection

SOURCE: Liddell AM, et al. Characteristics and clinical management of a cluster of 3 patients with Ebola Virus Disease, including the first domestically acquired cases in the United States. Ann Intern Med 2015;163:81-90.

These authors present a blow-by-blow picture of the presentation and clinical course of three patients cared for with Ebola Virus Disease at three different hospitals in the United States, including the index case from Liberia cared for at Texas Health Presbyterian Hospital in Dallas, and the two nurses with secondary infection who provided his care.

There are many fascinating features to this article, but one of the most striking features was the all-too-subtle and nonspecific nature of the presenting signs and symptoms for all three patients. The first nurse to be hospitalized last took care of the index case on October 7, 2014. By October 9, she thought she had an exacerbation of allergic rhinitis with nasal congestion and rhinorrhea. The following night, she had an oral temperature of 100.1 F, with mild headache, mild nasal congestion, throat discomfort, and insomnia. At that point, she presented to the emergency department (ED) for care. In the ED, her temperature was 38.1, her heart rate was 117 beats/minute, and her blood pressure was normal. Her labs were unremarkable, including a WBC 4.1, normal platelets, and normal transaminases. A plasma specimen taken at the time of presentation later proved positive for moderate amounts of EBOV RNA. Even during the first 4 days of her hospitalization, she remained stable, with fever, headache, nausea, and vomiting, but no diarrhea. It was not until day 5 of hospitalization that she developed pulmonary edema, abnormal transaminases, diarrhea, and a morbilliform rash a week into her illness.

The second nurse also last cared for the index patient on October 7, and was monitoring her symptoms and temperature. Beginning on October 10, her only complaints were fatigue and anorexia. It was not until October 14 when she developed a macular rash and two non-bloody diarrheal stools and presented to the ED, where she was found to have a temperature of 37.9 to 38.1, heart rate of 138 beats/minute, and normal blood pressure. Her WBC was 2.67 cells/mm3, platelets 120,000, and abnormal transaminases. Her plasma specimen on the day of presentation was positive for moderate amounts of EBOV RNA.

In going back over the index patient’s initial presentation to the hospital, his primary complaints were one day of headache and abdominal pain, with rhinorrhea and nasal congestion and chills. His initial temperature was only 37.8, with a heart rate of 90, and mild leukopenia (3.0 cells/mm3). He did not provide a travel history, and it’s not clear that one was requested. An abdominal CT was unremarkable. The diagnosis of Ebola was not even considered at that time.

And why would it have been, based on these signs and symptoms? I had previously thought rhinorrhea, nasal congestion, and sore throat steered the diagnosis into safer waters, and yet two of these patients had upper respiratory infection-like symptoms. The key to the diagnosis must be a detailed history of exposures and travel not the presentation which, for at least several days, may look like many other types of illness. Despite the subtlety of the presentation, and the fairly unremarkable laboratory findings for at least the first 1-7 days of illness, all three patients were actively viremic.