Effects of glutamine alone or in combination with zinc and vitamin A on growth, intestinal barrier function, stress and satiety-related hormones in Brazilian shantytown children

OBJECTIVE: To determine the impact of supplemental zinc, vitamin A, and glutamine alone or in combination on growth, intestinal barrier function, stress and satiety-related hormones among Brazilian shantytown children with low median height-for-age z-scores. METHODS: A randomized, double-blind, placebo-controlled trial was conducted in children aged two months to nine years from the urban shanty compound community of Fortaleza, Brazil. Demographic and anthropometric information was assessed. The random treatment groups available for testing (a total of 120 children) were as follows: (1) glutamine alone, n = 38; (2) glutamine plus vitamin A plus zinc, n = 37; and a placebo (zinc plus vitamin A vehicle) plus glycine (isonitrogenous to glutamine) control treatment, n = 38. Leptin, adiponectin, insulin-like growth factor (IGF-1), and plasma levels of cortisol were measured with immune-enzymatic assays; urinary lactulose/mannitol and serum amino acids were measured with high-performance liquid chromatography. ClinicalTrials.gov: NCT00133406. RESULTS: Glutamine treatment significantly improved weight-for-height z-scores compared to the placebo-glycine control treatment. Either glutamine alone or all nutrients combined prevented disruption of the intestinal barrier function, as measured by the percentage of lactulose urinary excretion and the lactulose:mannitol absorption ratio. Plasma leptin was negatively correlated with plasma glutamine (p = 0.002) and arginine (p = 0.001) levels at baseline. After glutamine treatment, leptin was correlated with weight-for-age (WAZ) and weight-for-height z-scores (WHZ) (p≤0.002) at a 4-month follow-up. In addition, glutamine and all combined nutrients (glutamine, vitamin A, and zinc) improved the intestinal barrier function in these children. CONCLUSION: Taken together, these findings reveal the benefits of glutamine alone or in combination with other gut-trophic nutrients in growing children via interactions with leptin

History, Rats, Fleas, and Opossums. II. The Decline and Resurgence of Flea-Borne Typhus in the United States, 1945–2019

Flea-borne typhus, due to Rickettsia typhi and R. felis, is an infection causing fever, headache, rash, and diverse organ manifestations that can result in critical illness or death. This is the second part of a two-part series describing the rise, decline, and resurgence of flea-borne typhus (FBT) in the United States over the last century. These studies illustrate the influence of historical events, social conditions, technology, and public health interventions on the prevalence of a vector-borne disease. Flea-borne typhus was an emerging disease, primarily in the Southern USA and California, from 1910 to 1945. The primary reservoirs in this period were the rats Rattus norvegicus and Ra. rattus and the main vector was the Oriental rat flea (Xenopsylla cheopis). The period 1930 to 1945 saw a dramatic rise in the number of reported cases. This was due to conditions favorable to the proliferation of rodents and their fleas during the Depression and World War II years, including: dilapidated, overcrowded housing; poor environmental sanitation; and the difficulty of importing insecticides and rodenticides during wartime. About 42,000 cases were reported between 1931–1946, and the actual number of cases may have been three-fold higher. The number of annual cases of FBT peaked in 1944 at 5401 cases. American involvement in World War II, in the short term, further perpetuated the epidemic of FBT by the increased production of food crops in the American South and by promoting crowded and unsanitary conditions in the Southern cities. However, ultimately, World War II proved to be a powerful catalyst in the control of FBT by improving standards of living and providing the tools for typhus control, such as synthetic insecticides and novel rodenticides. A vigorous program for the control of FBT was conducted by the US Public Health Service from 1945 to 1952, using insecticides, rodenticides, and environmental sanitation and remediation. Government programs and relative economic prosperity in the South also resulted in slum clearance and improved housing, which reduced rodent harborage. By 1956, the number of cases of FBT in the United States had dropped dramatically to only 98. Federally funded projects for rat control continued until the mid-1980s. Effective antibiotics for FBT, such as the tetracyclines, came into clinical practice in the late 1940s. The first diagnostic test for FBT, the Weil-Felix test, was found to have inadequate sensitivity and specificity and was replaced by complement fixation in the 1940s and the indirect fluorescent antibody test in the 1980s. A second organism causing FBT, R. felis, was discovered in 1990. Flea-borne typhus persists in the United States, primarily in South and Central Texas, the Los Angeles area, and Hawaii. In the former two areas, the opossum (Didelphis virginiana) and cats have replaced rats as the primary reservoirs, with the cat flea (Ctenocephalides felis) now as the most important vector. In Hawaii, 73% of cases occur in Maui County because it has lower rainfall than other areas. Despite great successes against FBT in the post-World War II era, it has proved difficult to eliminate because it is now associated with our companion animals, stray pets, opossums, and the cat flea, an abundant and non-selective vector. In the new millennium, cases of FBT are increasing in Texas and California. In 2018–2019, Los Angeles County experienced a resurgence of FBT, with rats as the reservoir

Primary esophageal lymphoma: a diagnostic challenge in acquired immunodeficiency syndrome--two case reports and review

Although extranodal presentation occurs in the majority of cases of acquired immunodeficiency syndrome-associated non-Hodgkin lymphoma, the esophagus is only rarely affected. We discuss two patients with acquired immunodeficiency syndrome who presented with dysphagia and weight loss, who were found to have human immunodeficiency virus-associated primary esophageal lymphoma. Both patients died within a few weeks of diagnosis, reflecting the poor prognosis associated with this malignancy. Primary esophageal lymphoma should be considered in the differential diagnosis in a human immunodeficiency virus-seropositive patient presenting with dysphagia

Flea-Borne Typhus Causing Hemophagocytic Lymphohistiocytosis: An Autopsy Case

Infection with members of the order Rickettsiales (the genera Rickettsia, Anaplasma, Orientia, and Ehrlichia) is known to cause hemophagocytic lymphohistiocytosis (HLH). The literature is scant on flea-borne typhus (FBT) being implicated in this process. We present a case of autopsy-proven HLH caused by FBT in a 71-year-old diabetic female who was initially suspected of having diabetic ketoacidosis who rapidly suffered decompensated multi-organ failure. Although she was suspected of having FBT and HLH pre-mortem, due to her rapid progression to multi-organ failure, she was transitioned to comfort care by her family five days after admission. A literature search yielded five other cases of HLH secondary to FBT, which are analyzed in this review. The literature on HLH occurring with infection due to other members of the order Rickettsiales is also surveyed

Hemoptysis in the Immunocompromised Patient: Do Not Forget Strongyloidiasis

Strongyloidiasis, due to infection with the nematode Strongyloides stercoralis, affects millions of people in the tropics and subtropics. Strongyloides has a unique auto-infective lifecycle such that it can persist in the human host for decades. In immunosuppressed patients, especially those on corticosteroids, potentially fatal disseminated strongyloidiasis can occur, often with concurrent secondary infections. Herein, we present two immunocompromised patients with severe strongyloidiasis who presented with pneumonia, hemoptysis, and sepsis. Both patients were immigrants from developing countries and had received prolonged courses of corticosteroids prior to admission. Patient 1 also presented with a diffuse abdominal rash; a skin biopsy showed multiple intradermal Strongyloides larvae. Patient 1 had concurrent pneumonic nocardiosis and bacteremia with Klebsiella pneumoniae and Enterococcus faecalis. Patient 2 had concurrent Aspergillus and Candida pneumonia and developed an Aerococcus meningitis. Both patients had negative serologic tests for Strongyloides; patient 2 manifested intermittent eosinophilia. In both patients, the diagnosis was afforded by bronchoscopy with lavage. The patients were successfully treated with broad-spectrum antibiotics and ivermectin. Patient 1 also received albendazole. Strongyloidiasis should be considered in the differential diagnosis of hemoptysis in immunocompromised patients with possible prior exposure to S. stercoralis