Among 1141 inpatients from Arizona with community-acquired pneumonia, 865 (75.8%) were tested for Coccidioides infection and 85 (9.8%) had positive results. Patients more commonly underwent testing if they had concerning radiographs, fever, dyspnea, or fatigue. Patients with night sweats, rash, headache, or eosinophilia more commonly had positive results.

A 69-year-old female was admitted with a four-day history of unexplained fever. Lung examination revealed coarse breath sounds, and laboratory tests showed elevated inflammatory markers. She had no identifiable environmental or occupational exposure, and initial screening for common respiratory pathogens was negative. Chest computed tomography (CT) scan demonstrated patchy ground-glass opacities and reticular shadows distributed along the bronchovascular bundles in the right upper lobe and dorsal segments of both lower lobes, with lesions showing the reversed halo sign (RHS). Initial empirical antibiotic therapy was ineffective. Subsequent bronchoalveolar lavage (BAL) culture yielded heavy growth of Pseudomonas putida, with negative fungal and tuberculosis nucleic acid testing. Based on antimicrobial susceptibility testing, the treatment regimen was adjusted to a combination of ceftazidime and amikacin. Following this targeted therapy, the patient's symptomatic improvement occurred while imaging abnormalities persisted, indicating a clinical-radiological dissociation. The patient was discharged after a 15-day hospital stay. This case highlights the following: (1) In community-acquired pneumonia with atypical imaging features (such as the RHS) that is refractory to conventional therapy, the differential diagnosis should be expanded to include environmental opportunistic pathogens like P. putida; (2) The RHS is a non-specific imaging finding, and its diagnostic significance must be interpreted in conjunction with lesion distribution, dynamic changes, and the complete clinical context; (3) Obtaining microbiological evidence through minimally invasive techniques such as BAL is crucial for shifting from empirical to precise targeted therapy, thereby improving patient prognosis.

After severe depletion of CD4 T cells in AIDS patients, they are not only prone to a first-time Nocardia infection, but also, even if cured, unable to form protective immune memory, leaving them susceptible to reinfection with the same pathogen. More seriously, in the absence of immune surveillance, irregular drug use can accelerate the selection of drug-resistant strains. A 32-year-old man with AIDS and persistent CD4+ count below 100 cells/μL for over three years (nadir 2 cells/μL) developed right lower lobe pneumonia caused by Nocardia farcinica four years before the current admission, which was cured with a TMP-SMX-containing regimen. The isolate was sensitive to trimethoprim-sulfamethoxazole (TMP-SMX), and the lesion nearly resolved after treatment. He was prescribed long-term TMP-SMX prophylaxis at discharge but stopped taking it on his own. One year before the current admission, he received sulfadiazine plus pyrimethamine for clinically diagnosed cerebral toxoplasmosis, but his adherence was poor and irregular. On current admission (day 1), he was readmitted with high fever and sepsis. Chest CT showed multiple cavities in the left lower lobe. Blood cultures flagged positive at 25 hours and were identified as Nocardia farcinica. The microbiologist reviewed his old records, found the previous nocardial history, and recommended bronchoalveolar lavage (BAL). BAL metagenomic next-generation sequencing again identified Nocardia farcinica, but susceptibility testing now showed resistance to TMP-SMX (MIC ≥8/152). He improved after switching to imipenem plus amikacin. He received intravenous imipenem plus amikacin for 14 days, followed by oral linezolid for 6 weeks. At the last follow-up (approximately one year after discharge), his CD4[+] had risen to only 11 cells/μL, and he had no further nocardial infection. This case shows that when CD4[+] stays below 100 for a long time, even a first nocardial infection can be cured but may leave insufficient immune memory, rendering the patient susceptible to subsequent infection. The distinction between true reinfection and late relapse could not be definitively established in the absence of strain-level homology data. Irregular, sub-therapeutic sulfonamide exposure, combined with a non-functional immune system, can select for resistant strains.

Kawasaki disease (KD) is a systemic inflammatory illness characterized by medium blood vessel vasculitis and is considered to be the leading cause of acquired heart disease in children less than 5 years old in developed countries. KD can present as either a classical or atypical/incomplete presentation based on distinct laboratory parameters seen in Table 1. The exact cause of KD remains unknown; however, specific purported infectious agents have been theorized to be linked to it. It classically presents with fever and four of the following: conjunctival injection, oral mucosal changes, cervical lymphadenopathy, changes in the extremities and polymorphous rash. Rarely, KD can present with hepatobiliary syndrome such as hepatic congestion, obstructive jaundice, acalculous cholecystitis and gallbladder hydrops. We present a case of a 12-year-old, otherwise healthy male who presented with an 8-day history of upper respiratory infection symptoms and fevers up to 102 F along with significant jaundice, dilated common bile duct and transaminitis initially thought to be ascending cholangitis. His clinical course evolved to also show rash, abdominal pain, vomiting, diarrhea, cervical lymphadenopathy and non-exudative, bilateral conjunctival injection with limbic sparing. Absence of improvement to antibiotic and distinct clinical evolution prompted the diagnosis of atypical KD. He received high dose IVIG and high dose aspirin with apparent clinical improvement. His surveillance echocardiography studies and subsequent physical exam findings have all been reassuring. This case underscores how KD can initially present as cholangitis and how it can manifest as a concomitant process during a viral infection.

VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a newly described inflammatory disease characterized by recurrent autoimmune manifestations, such as chondritis and uveitis, in the setting of classic laboratory abnormalities, including elevated inflammatory markers and macrocytic anemia. It is caused by an acquired mutation in the UBA1 gene within the myeloid lineage, ultimately resulting in cell death and systemic inflammation. Timely diagnosis can help expedite treatment and encourage monitoring for complications of the disease, most notably a predilection to infections. A 77-year-old male presented to the emergency room due to new-onset fevers and shortness of breath. His history was notable for six months of non-specific symptoms such as fatigue and weight loss, as well as recurrent inflammatory syndromes, including uveitis and joint swelling. At one point, he was treated empirically with steroids due to concern for giant cell arteritis; however, biopsy did not confirm this diagnosis. Labs were notable for significantly elevated inflammatory markers and a macrocytic anemia. His hospitalization was notable for acute hypoxemic respiratory failure requiring high-flow nasal cannula oxygen. His condition improved with broad-spectrum antibiotics, and he was ultimately diagnosed with Legionella pneumonia when Legionella PCR from pleural fluid returned positive. Prior to discharge, genetic testing for the UBA1 gene mutation and bone marrow biopsy demonstrating vacuolization of myeloid precursors confirmed the diagnosis of VEXAS syndrome. He was started on prednisone and azacitidine in the outpatient setting, which led to significant improvement in symptoms, inflammatory markers, and cell counts.

Kawasaki disease (KD) is an acute vasculitis and the leading cause of acquired heart disease in children. Coronary artery aneurysms (CAAs) arise from vascular inflammation during the acute phase; however, in some patients, inflammation may persist despite treatment, and reliable clinical indicators of ongoing disease activity remain limited. Acute scrotal involvement is a rare manifestation of KD, and its clinical significance has not been well established. Here, we report a case of a previously healthy 49-month-old boy who presented with 4 days of fever and the five principal features of KD. He was initially treated with intravenous immunoglobulin, aspirin, and prednisolone, resulting in transient improvement. On Day 7 of illness, he developed recurrent fever and right inguinal pain. Fever persisted on Day 8, accompanied by recurrent lip erythema and worsening inflammation, prompting a second dose of intravenous immunoglobulin. His fever improved on Day 9, when right-sided scrotal erythema and swelling became evident. Ultrasonography revealed a right hydrocele with preserved blood flow and no epididymal torsion. Echocardiography on Day 11 demonstrated medium-sized bilateral CAAs, which were subsequently confirmed by coronary computed tomography. The scrotal findings resolved completely within 1 month. This clinical course suggests that acute scrotal involvement may represent a potential clinical clue to persistent disease activity in KD, warranting careful reassessment for evolving coronary artery involvement.