{'fraction_non_alphanumeric': 0.023477157360406092, 'fraction_numerical': 0.006979695431472081, 'mean_word_length': 5.977876106194691, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Secondary bacterial infection in plasma endotoxin levels and the acute‐phase response of mice infected with Trypanosoma brucei brucei

Murine Trypanosoma brucei brucei infection leads to elevated plasma endotoxin‐like activity levels not related to parasitaemia levels accompanied by the development of acute‐phase response and increased plasma levels of serum amyloid P (SAP) and haptoglobin (Hp). To determine the source of the endotoxin‐like activity and role of secondary bacterial infection in the pathogenesis of trypanosomosis, infected mice were treated with the antibiotic ciprofloxacin. Plasma endotoxin‐like activity levels, irrespective of treatment, were elevated three‐ to fourfold, beginning 7 days after infection. Plasma protein concentrations increased markedly following infection from 7 days after infection (DAI). Peak Hp and SAP concentrations in ciprofloxacin‐treated and ‐untreated infected mice were attained 7 and 14 DAI, respectively. Thereafter, both protein levels gradually declined until the end of the experiment, but Hp levels for non‐treated mice declined up to 21 DAI and thereafter significantly increased on 28 and 35 DAI. Whole‐trypanosome lysate and the membrane‐enriched fraction demonstrated endotoxin‐like activity, with the former having higher levels. The results suggest that the endotoxin‐like activity in trypanosome fractions and plasma of infected mice is due to the trypanosome. Further elevation of haptoglobin during the late stages of infection in non‐treated mice suggests the involvement of secondary bacterial infection.