Background. Leprosy morbidity is increased by 2 pathologic immune reactions, reversal reaction (RR) and erythema nodosum leprosum (ENL). Methods. To discover host factors related to immune reactions, global transcriptional profiles of peripheral blood mononuclear cells were compared between 11 RR, 11 ENL, and 19 matched control patients, with confirmation by quantitative polymerase chain reaction. Encoded proteins were investigated in skin biopsy specimens by means of immunohistochemistry. Results. There were 275 genes differentially expressed in RR and 517 differentially expressed in ENL on the microarray. Pathway analysis showed immunity-related pathways represented in RR and ENL transcriptional profiles, with the “complement and coagulation” pathway common to both. Interferon γ was identified as a significant upstream regulator of the expression changes for RR and ENL. Immunohistochemical staining of skin lesions showed increased C1q in both RR and ENL. Conclusions. These data suggest a previously underrecognized role for complement in the pathogenesis of both RR and ENL, and we propose new hypotheses for reaction pathogenesis.

SUMMARY: The lack of an adequate model forLeishmania(Viannia)braziliensisinfection is a limiting factor for studying American tegumentary leishmaniasis (ATL). The golden hamster (Mesocricetus auratus) is a promising model because besides being highly susceptible to dermotropicLeishmaniainfection, the lesions are very similar to cutaneous leishmaniasis (CL) in humans. However, differentLeishmaniaisolates or species and/or protocols have resulted in different outcomes, whereas no study has evaluated the reproducibility ofL. braziliensisinfection in this model. The natural history ofL. braziliensisinfection in 34 hamsters was evaluated by using a single parasite isolate in 8 independent experiments under similar experimental conditions. Clinical, histological and immunological analyses were performed. The hamsters presented skin ulcers similar to those observed in ATL. The intra-experiment lesion increment tended to show an intermediary variance. Histological analysis of infected skins showed granulomatous reaction, scarce amastigotes, and Schaumann's bodies. Blood lymphocytes proliferated in response to leishmanial antigens. The severity of the infection was positively correlated to spleen weight, and the titres of anti-LeishmaniaIgG antibodies. Our findings indicate that the hamster is an appropriate model for immunopathogenesis studies of CL caused byL. braziliensis, supporting its use in clinical, vaccine and chemotherapy experimental protocols.

Background. Leishmania infection is a cofactor in the heightened cellular activation observed in patients with American visceral leishmaniasis and human immunodeficiency virus type 1 (HIV) infection, with or without progression to AIDS (AVL/HIV). Thus, the persistence of a high parasite load despite antileishmanial therapy could be responsible for the continued immune stimulation. Methods. CD8⁺ T cells expressing CD38, parasite load, lipopolysaccharide (LPS), soluble CD14, macrophage migration inhibitory factor (MIF), intestinal fatty acid–binding protein (IFABP), and proinflammatory cytokines (interleukin 1β, interleukin 6, interleukin 8, interleukin 17, interferon γ, and tumor necrosis factor) were measured in 17 patients with AVL/HIV, 16 with HIV, and 14 healthy subjects (HS). Results. Lower Leishmania parasitemia was observed after antileishmanial and antiretroviral therapies. However, higher levels of CD38⁺ on CD8⁺ T cells were observed in both clinical phases of leishmaniasis, compared with HIV cases. AVL/HIV and HIV patients showed higher levels of LPS and IFABP than HS. Proinflammatory cytokine levels were significantly augmented in patients with active coinfection, as well as those with remission of Leishmania infection. LPS levels and Leishmania infection were positively correlated with CD38 expression on CD8⁺ T cells and with IL-6 and IL-8 levels. Conclusions. LPS levels along with the immune consequences of Leishmania infection were associated with elevated cellular activation in coinfected patients. As a consequence, secondary chemoprophylaxis for leishmaniasis or even the use of antiinflammatory drugs or antibiotics may be considered for improving the prognosis of AVL/HIV.

The golden hamster ( Mesocricetus auratus ) is a susceptible model to Leishmania ( Viannia ) spp.; however, available studies employ different infection protocols, which account for clinical and pathological presentation differences. Herein, L . ( V .) braziliensis preparations were standardized to contain 10 ⁴ , 10 ⁵ , or 10 ⁶ parasites to determine an optimal inoculum that ensured cutaneous lesions without causing a disseminated infection in hamsters. Lesion development was followed for 105 days by size measurements, and skin, draining lymph node, spleen, and sera were investigated to check parasite load, spleen visceralization, cytokine expression, histopathological changes, and anti- Leishmania IgG levels. The lesion emergence time was inversely proportional to the parasite concentration in the inocula. Animals infected by 10 ⁴ parasites presented nodular lesions, while those infected with 10 ⁶ parasites often exhibited ulcerated lesions. The differences in the final lesion sizes were observed between 10 ⁴ and 10 ⁵ inocula or 10 ⁴ and 10 ⁶ inocula. High IFNG expression, anti- Leishmania IgG levels, and parasite load occurred independently of the inoculum used. A mild inflammatory skin involvement was observed in animals infected with 10 ⁴ parasites, while extensive tissue damage and parasite spleen visceralization occurred with 10 ⁵ and 10 ⁶ parasites. These results indicate that inocula with different concentrations of parasites generate differences in the time of lesion emergence, clinical presentation, and systemic commitment, despite high and similar IFNG expression and parasite load. This suggests that a modulation in the immune response to different parasite numbers occurs in an early phase of the infection, which could dictate the establishment and magnitude of the chronic phase of the disease.

This survey aims to estimate the prevalence of intestinal parasitic infections in Santa Isabel do Rio Negro, Amazonian Brazil, through three distinct techniques, correlating the prevalence rates with family income and age groups as well as assessing the household clustering of infections. Prevalence rates were assessed through Graham (n=113), Baermann-Moraes (n=232) and Ritchie (n=463) methods. The Graham method was adopted only for children under 5 years old, 15% of whom were positive for Enterobius vermicularis. By the Baermann-Moraes technique, 5·6% of the samples were positive for Strongyloides stercoralis larvae. The Ritchie technique disclosed the following results: Ascaris lumbricoides (26%), Trichuris trichiura (22·5%), hookworms (9·5%), Entamoeba histolytica/Entamoeba dispar (25·3%), Giardia lamblia (12·5%) and E. vermicularis (0·6%). Children aged 5-14 years presented the highest prevalence for pathogenic parasites. Giardiasis and hookworm infection rates were inversely related to family income. The presence of positive contacts in the same household substantially increased the risk of infection by enteric parasites: odds ratio (OR)=2·70, 95% confidence interval (CI)=1·69-4·29 for ascariasis; OR=2·17, 95% CI=1·34-3·51 for trichuriasis; OR=2·13, 95% CI=1·08-4·17 for hookworm disease; OR=3·42, 95% CI=1·86-6·30 for giardiasis; and OR=2·16, 95% CI=1·35-3·47 for amoebiasis, supporting infection clustering in the home. Intestinal parasitoses are extremely frequent in the studied area, and routine methods for diagnosis may underestimate the prevalence of enterobiasis and strongyloidiasis.

We report the finding of eggs of Calodium spp. (syn. Capillaria spp.; Hepaticola spp.) in a fecal sample from an old woman living in a riverine community in the Negro River Basin and describe the associated epidemiological investigation. The case probably does not represent true parasitism; the eggs, which were compatible with the species Calodium hepaticum, were most likely ingested upon consumption of infected tapir (Tapirus terrestris) liver, subsequently passing through the gut and being eliminated. The evolution of these eggs to infective stages in the environment, given the poor sanitation background, could provide the risk of occurrence of hepatic disease in humans.