A Diagnostic Dilemma: Clindamycin-Resistant Group A Streptococcal Toxic Shock Syndrome Leading to Acute Respiratory Distress Syndrome (ARDS) With Multiple Possible Sources.

Group A Streptococcal (GAS) infections can potentially progress into streptococcal toxic shock syndrome (STSS) with multiorgan failure. Even with a benign presentation, GAS can rapidly lead to fatal necrotizing infections. While myositis and cutaneous infections are the typical initial presentation of STSS, genitourinary infections are a less common source. This report presents a case of a previously healthy woman with the chief complaint of ankle pain who subsequently developed streptococcal toxic shock syndrome and multiorgan failure from a Group A streptococcus infection of the genitourinary tract. She was treated with antibiotics and medical management for her septic shock and required prone ventilation for her acute respiratory distress syndrome (ARDS) but eventually recovered without surgery. This case highlights the importance of recognizing unusual presentations of Group A Strep infections, which have the potential to lead to rapid deterioration in patients. Also described are antibiotic and ventilator strategies that can be used to treat these severe systemic infections.

A water-damaged home and health of occupants: a case study.

A family of five and pet dog who rented a water-damaged home and developed multiple health problems. The home was analyzed for species of mold and bacteria. The diagnostics included MRI for chronic sinusitis with ENT and sinus surgery, and neurological testing for neurocognitive deficits. Bulk samples from the home, tissue from the sinuses, urine, nasal secretions, placenta, umbilical cord, and breast milk were tested for the presence of trichothecenes, aflatoxins, and Ochratoxin A. The family had the following diagnosed conditions: chronic sinusitis, neurological deficits, coughing with wheeze, nose bleeds, and fatigue among other symptoms. An infant was born with a total body flare, developed multiple Cafe-au-Lait pigmented skin spots and diagnoses with NF1 at age 2. The mycotoxins were detected in bulk samples, urine and nasal secretions, breast milk, placenta, and umbilical cord. Pseudomonas aueroginosa, Acinetobacter, Penicillium, and Aspergillus fumigatus were cultured from nasal secretions (father and daughter). RT-PCR revealed A. fumigatus DNA in sinus tissues of the daughter. The dog had 72 skin lesions (sebaceous glands and lipomas) from which trichothecenes and ochratoxin A. were detected. The health of the family is discussed in relation to the most recent published literature regarding microbial contamination and toxic by-products present in water-damaged buildings.

Fungal exposure endocrinopathy in sinusitis with growth hormone deficiency: Dennis-Robertson syndrome.

A retrospective study was carried out on 79 patients with a history of mold exposure, fatigue, and chronic rhinosinusitis (CRS) to determine whether there is a causal relationship between fungal exposure and chronic sinusitis, fatigue, and anterior hypopituitarism, especially growth hormone deficiency (GHD). Of the patients, 94% had a history of CRS, endoscopically and/or computed tomography (CT) confirmed; 100% had chronic fatigue and 100% had either significant history of indoor mold exposure and/or positive mold plate testing as measured by settle plates, with an average colony count of 21 (0-4 normal). A total of 62 had positive mold plate testing and 17 had positive history of mold exposure. Of 75, 73 (97.3%) had positive serum immunoglobulin G (IgG)-specific antibodies to fungal antigens. Out of 8, 7 were positive for urinary trichothecenes. Resting levels of insulin-like growth factor 1 (IGF-1) averaged 123 ng/mL (range 43-285, normal 88-249 ng/mL). Despite normal resting levels of IGF-1, significant deficiency of serum human growth hormone (GH) was confirmed by insulin tolerance test (ITT) in 40 of 50 tested. In all, 51% (40/79) were GH deficient. Primary or secondary hypothyroidism in T3 and/or T4 was seen in 81% (64/79) patients; 75% (59/79) had adrenocorticotrophic hormone (ACTH) deficiency. Fungal exposure endocrinopathy likely represents the major cause of GHD, affecting approximately 4.8 million people compared to approximately known 60,000 cases from all other causes. A literature review indicates a possible mechanism of GHD in fungal exposure is that the fungal glucan receptors in the lenticulostellate cells of the anterior pituitary bind to fungal cells wall glucans and activate the innate immune system, which activates macrophages that destroy the fungus and lenticulostellate tissue. Treatment of patients included normal saline nasal irrigations, antifungal and antibiotic nasal sprays, appropriate use of oral antibiotics and antifungals, facial steamer with CitriDrops. Thymate and/or Intramax vitamin supplements, hormone replacement, and reduction of indoor mold levels. Resolution of rhinosinusitis was seen in 93% (41 of 45) of the patients who achieved a mold count by settling plates of 0-4 colonies. Thirty patients were unable to lower their mold counts below four colonies and had various degrees of mucosal disease and fatigue remaining. Fatigue was improved in all 37 patients who received GH and cortisol and/or thyroid hormone, which were deficient. Fatigue was partially relieved in 7 of the 37 who did not achieve mold counts of fewer than four colonies.

Chronic sinusitis: defective T-cells responding to superantigens, treated by reduction of fungi in the nose and air.

In this study, the author used endoscopic sinus photography to study the effects of reduction of fungi in the nose, and in environmental air, on the sinus mucosa of 639 patients diagnosed with chronic rhinosinusitis. Sinus mucosal photographs were taken before and after reduction of fungal load in the nose and air, to determine if there was an optimum environmental air fungal load associated with sinus mucosal recovery to normal appearance. Systemic symptoms associated with fungal exposure, which resolved when fungus was removed from the patient and the environmental air and reappeared with recurrent environmental fungal exposure, are also discussed and are termed systemic fungal symptoms. Interventions consisted of nasal fungal load reduction with normal saline nasal irrigations and antimicrobial nasal sprays, and environmental air fungal load reduction with high-efficiency particulate air (HEPA) filtration in combination with ionizers or evaporation of a solution of botanical extract. Main outcome measures were obtained with environmental air 1-hr gravity-plate fungal colony counts, laser air particle counts, and endoscopic sinus photography. Blood levels of immunoglobulins IgG and IgE for 7 common molds were also determined. After intervention, 94% of patients who used antimicrobial nasal sprays and who reduced their environmental fungal air count to 0-4 colonies per 1-hr agar gravity-plate exposure (n = 365) exhibited normal sinus mucosa by endoscopic exam. Environmental air fungal counts that exceeded 4 colonies resulted in sinus mucosal abnormalities ranging from edema, to pus and/or nasal polyps at higher counts. Neutralization of allergy, and/or surgery, were used as appropriate following implementation of environmental measures. On the basis of these observations, as well as detailed clinical experience and a review of the current literature, the author hypothesizes that the pathogenesis of chronic rhinosinusitis, allergic fungal sinusitis, and systemic fungal symptoms is a genetic defect at the variable beta chain helper T-cell receptor (TCR Vbeta) site which requires the presence of an antigen (fungus). Chronic sinusitis patients who have recurring exposure to environmental air that contains fungal concentrations in excess of 4 colonies per 1-hr agar plate exposure appear to have an increased risk of persistent chronic sinusitis and/or systemic symptoms, regardless of the medical treatment provided.