JOURNAL ARTICLE

A 46-Year-Old With Persistent Altered Mental Status and Respiratory Failure

Ann F Yang, Aesha Jobanputra, Thomas J Kirn, et al 

Clinical Infectious Diseases, Volume 82, Issue 1, 15 January 2026, Pages 159–161, https://doi.org/10.1093/cid/ciaf439

Question:

A 46-year-old undomiciled man with a past medical history of alcohol use disorder was found unresponsive and admitted for evaluation of altered mental status. He immigrated from Mexico in 1991 and lived in Florida for several years as a gardener.

On presentation, he exhibited emesis, agitation, tachycardia, hypertension, and a fever of 102.9 F. Tremors and tongue fasciculations were noted on physical exam. Bilateral lower lobe consolidations consistent with aspiration were noted on CT chest with negative SARS-CoV-2 PCR results. The patient was briefly intubated for airway protection and treated with empiric piperacillin/tazobactam for aspiration pneumonia and benzodiazepines for alcohol withdrawal, with improvement in mental status and pulmonary infiltrates.

On hospital day 6, a repeat SARS-CoV-2 test was done due to persistent fevers and returned positive. On hospital day 7, the patient was found to have unequal pupillary response. Repeat CT head imaging showed a new left superior cerebellar artery (SCA) infarct, along with subarachnoid and intraventricular hemorrhages. The neurosurgical team was consulted and recommended no surgical interventions. On hospital day 8, the patient required supplemental oxygen with nasal cannula and was started on dexamethasone 6 mg/day and remdesivir. On hospital day 10, digital subtraction angiography of the brain demonstrated findings consistent with vasospasms, and nimodipine therapy was initiated. The patient remained hospitalized for waxing/waning mental status.

On hospital day 15, the patient was re-intubated due to progressively worsening acute hypoxemic respiratory failure and was found to have new nodular opacity in the right upper lobe and new bilateral tree-in-bud opacities involving all lobes. Subsequently, the patient underwent bedside bronchoscopy, which demonstrated these findings on the cell culture dish (Figure 1) and gram stain (Figure 2) of the bronchoalveolar lavage (BAL). The patient remained persistently comatose with a Glasgow Coma Score of 2T despite being off sedation and a relatively benign MRI of the brain and EEG. Of note, the patient's absolute eosinophil count increased from 20 cells/µL on admission, with a peak eosinophil count at 920 cells/µL on hospital day 40. Lumbar puncture revealed cerebrospinal fluid (CSF) with a total white blood cell count of 237 cells/µL, predominantly neutrophils (192 cells/µL), and a lymphocyte count of 28 cells/µL. The red blood cell count was elevated at 2915 cells/µL. Cerebrospinal fluid glucose was decreased at 38 mg/dL (reference range: 40–80 mg/dL), and protein was markedly elevated at > 600 mg/dL (reference range: 15–45 mg/dL). A gram stain of the CSF specimen reveals these organisms with no bacterial growth on culture (Figure 3).

What is your diagnosis?

Answer:

Diagnosis: Disseminated strongyloidiasis with central nervous system involvement, reactivated following corticosteroid therapy for COVID-19 infection.

The worsening oxygenation on hospital day 15 necessitating re-intubation, following eight days of dexamethasone use for COVID-19 infection, along with new bilateral tree-in-bud opacities, and the confirmed presence of Strongyloides larvae on both BAL and CSF samples is most consistent with disseminated Strongyloides. After identification of Strongyloides stercoralis filariform larvae in the BAL, ivermectin 200 µg/kg/day and meropenem 2 g every 8 h were started. Following the identification of Strongyloides larvae in the CSF on hospital day 24, albendazole 400 mg BID was added to the regimen due to concern for disseminated strongyloidiasis. Serum enzyme-linked immunosorbent assay (ELISA) testing was positive for Strongyloides stercoralis IgG. HIV and human T-lymphotrophic virus-1 (HTLV-1) serology were negative. The patient remained persistently comatose after several weeks of treatment. In accordance with the family's wishes, the patient was transitioned to comfort measures and subsequently passed away.

While the patient was initially admitted for altered mental status attributed to alcohol withdrawal and toxic metabolic encephalopathy and then later attributed to a new SCA infarct and multi-territorial intracranial hemorrhage with vasospasms, he demonstrated interval improvement prior to re-intubation on hospital day 15. The comatose state that developed after re-intubation was a new and acute change, likely secondary to the development of Strongyloides meningitis. In this case, it is unclear if the SCA infarct and intracranial hemorrhage were an unrelated idiopathic event, an event related to COVID-19 infection, or an event that may have predisposed the patient to Strongyloides meningitis.

Asymptomatic chronic strongyloidiasis is due to Strongyloides stercoralis [1]. It is endemic to tropical and subtropical countries, with an estimated worldwide prevalence of 8.1% [2]. There are few epidemiological data regarding its prevalence in Mexico; it is currently estimated to be as high as 68% [3]. Since infection is caused by direct penetration of infectious filariform larvae present in the soil, walking barefoot and agricultural work are major risk factors for Strongyloides infection [1]. While most individuals remain asymptomatic, severe complications such as hyperinfection or disseminated disease can occur [4]. Strongyloides hyperinfection occurs due to an accelerated autoinfection from increased larval migration within organs that are normally involved in the autoinfection cycle, including the gastrointestinal tract, the pulmonary system, and the skin. The disseminated form of the infection, which the patient in our case had, occurs due to the migration of larvae to organs outside those involved in the autoinfection cycle [4, 5]

Central nervous system involvement in strongyloidiasis is an uncommon complication of the disseminated form, with brain and meningeal involvement often described post-mortem [6]. Risk factors include corticosteroid use and other immunosuppression, HTLV-1 infection, alcohol use disorder, and hematological malignancies. Most cases of strongyloidiasis after corticosteroid use occur following a cumulative prednisone-equivalent dose exceeding 1000 mg over >2 weeks. However, severe strongyloidiasis has also been reported with cumulative doses as low as 200 mg [7]. The patient in our case received a total cumulative dose of 60 mg of dexamethasone, which is equivalent to ∼400 mg of prednisone.

There is no gold standard for the diagnosis of strongyloidiasis; current methods include microscopy, serologic testing, and nucleic-acid based techniques. In this patient, the surface of the agar-plate inoculated with the BAL sample demonstrated furrows or tracks of moving larvae (Figure 1). Closer inspection of filariform larvae of Strongyloides reveals an elongated esophagus useful for sucking fluids after penetrating host tissue, identified by the esophagus–intestine junction halfway down the larval body. The tripartite pointed tail is also particularly diagnostic for infective filariform Strongyloideslarvae [8].

A few guidelines have been proposed for managing risk of Strongyloides hyperinfection in the setting of dexamethasone treatment for COVID-19, with suggestions including sending Strongyloides serology prior to initiation of dexamethasone or consideration of prophylactic anti-parasitic agents for patients identified as high risk for chronic strongyloidiasis who are about to undergo corticosteroid treatments, including COVID-19-associated regimens [9]. This case highlights that corticosteroid regimens for the treatment of COVID-19 are potent enough to cause the fatal disseminated form of strongyloidiasis, even in otherwise immunocompetent patients. This case also emphasizes the importance of maintaining clinical suspicion for patients with epidemiologic risk factors for Strongyloides reactivation prior to initiation of corticosteroid therapy.