ABSTRACT:In response to questions about the effects of military use of fog oil (FO) obscurant smoke, the sensitivity of cell-mediated constituents of the immune system to FO smoke was tested using an avianpox challenge in red-winged blackbirds. Although immunosuppression has been observed in seabirds that have ingested petrochemicals, the immune response in blackbirds exposed to airborne FO was not compromised. The incidence and severity of disease was somewhat less and recovery more advanced in the FO-exposed blackbirds than in controls. Circulating antibody titers to sheep red blood cells were measured in house sparrows by hemagglutination titration. No differences in total, 2-mercaptoethanol-sensitive, or 2-mercaptoethanol-resistant antibody titers were observed, suggesting that humoral immunity is also unaffected by high field-typical FO exposure. Total and differential white blood cell counts were not depressed and spleen mass and structure were not affected in any of the birds exposed to the airborne FO, further indicating that the smoke did not compromise the nonspecific immune function of the birds. No FO-induced mortality, organ pathology, or end point metabolites were observed in either passerine species. These data indicate that the use of FO at normal field concentrations is unlikely to result in decreased immunological fitness of exposed birds. DISCLAIMER:The contents of this report are not to be used for advertising, publication, or promotional purposes. Citation of trade names does not constitute an official endorsement or approval of the use of such commercial products. All product names and trademarks cited are the property of their respective owners. The findings of this report are not to be construed as an official Department of the Army position unless so designated by other authorized documents.

A thrombotic microangiopathy (TMA) occurs when a patient presents with microangiopathic hemolytic anemia, thrombocytopenia and organ damage. There are many causes of TMAs, but thrombotic thrombocytopenic purpura (TTP) must always be considered because of its high mortality rate. Treatment with therapeutic plasma exchange and transfusions can reduce the mortality rate but those treatments carry their own morbidity. Severe cobalamin deficiency can cause a clinical picture similar to TTP. Understanding the pathologic changes of this pseudo-TTP can allow physicians to suspect this difference early in the clinical course. In the following case, elevations in homocysteine and methylmalonic acid, as well as changes in the CBC, allowed this distinction to be identified early, minimizing potentially dangerous treatments.

Background Patients with deficiencies of terminal components of complement are at hundreds to thousands fold increased risk of severe and fatal Neisseria spp. infections compared with the general population. Eculizumab is a newly approved monoclonal antibody C5 complement inhibitor. It is indicated for the treatment of atypical hemolytic uremic syndrome (atypical HUS), myasthenia gravis, and paroxysmal nocturnal hemoglobinuria. Because of the complement-depleting effect of Eculizumab dosing (Soliris®, Alexion Pharmaceuticals, Munich, Germany), patients are immunosuppressed for specific infectious pathogens (including Neisseria species) against which protection partially relies on normal complement activity. Because Eculizumab treatment is associated with a dramatically increased risk of Neisseria species. infections, recommendations for Neisseria meningitidis vaccination and antibiotic prophylaxis are contained in Eculizumab prescribing information. However, the most appropriate prevention of infections after Eculizumab has yet to be determined. Methods Case report and literature review. Results A previously healthy 7-year-old male was diagnosed with atypical HUS which included renal failure progressing to dialysis, persistent thrombocytopenia, hemolytic anemia, and hemoglobinuria. Stool cultures and a stool multiplex PCR panel did not detect Shiga-like producing E. coli nor E. coli O157/H7. Eculizumab dosing was therefore planned and Infectious Diseases consultation was obtained for appropriate preventions. The FDA Prescribing Information recommends Neisseria meningitidis vaccination before starting Eculizumab or, if immediate Eculizumab is necessary, to use antibiotic prophylaxis until 2 weeks after vaccination. The accepted protective titer after meningococcal vaccination is population based and uses the serum bactericidal assay (SBA). An antibody titer of >1:4 (human compliment) or 1:8 (rabbit complement) is considered protective. However, this “gold standard” assay incorporates the use of exogenous human or rabbit complement. The protective SBA titers in subjects with terminal complement component deficiencies may not be properly assessed using these same SBA titer protective thresholds. Furthermore, serious meningococcal infections have occurred after appropriate vaccination in patients receiving chronic Eculizumab treatments (ie for paroxysmal nocturnal hemoglobinuria). Finally, SBA protective levels after single Neisseria meningitidis vaccination have not been achieved in majorities of patients with renal failure receiving dialysis and or transplant immunosuppression. Conclusions The current Eculizumab prescribing information recommendations for vaccination and antimicrobial prophylaxis may be inadequate to prevent serious Neisseria infections. Repeated Neisseria meningitidis vaccination and extended antibiotic prophylaxis may afford better protection in patients chronically dosed with Eculizumab.