Mortality, crime and access to basic needs before and after the Haiti earthquake: a random survey of Port-au-Prince households.

On 12 January 2010 an earthquake measuring 7.0 on the Richter Scale struck Haiti, causing unprecedented death, injury and destruction for an event of this magnitude. Our aim was to generate a rapid assessment of the primary consequences for the population of the metropolitan area of Port-au-Prince, the national capital. During the summer of 2009 we conducted a survey of 1,800 households in metropolitan Port-au-Prince. Six weeks after the earthquake, we attempted to trace these households in order to re-interview them. The questionnaire examined mortality and injuries generated by the natural disaster, as well as the character of victimization, food security and living arrangements following the quake. Data analysis incorporated sampling weights and adjusted for clustering within households. The original 2009 survey featured a 90 per cent response rate; in 2010 we re-interviewed 93 per cent of these households. We estimate that 158,679 people in Port-au-Prince (95 per cent CI 136,813-180,545) died during the quake or in the six-week period afterwards owing to injuries or illness. Children were at particular risk for death. In the six weeks after the earthquake, 10,813 people (95 per cent CI 6,726-14,900) were sexually assaulted, the vast majority of whom were female. In the same period 4,645 individuals (95 per cent CI 1,943-7,347) were physically assaulted. Of all households, 18.6 per cent (95 per cent CI 16.6-20.8) were experiencing severe food insecurity six weeks after the earthquake. 24.4 per cent (95 per cent CI 22.1-26.9) of respondents' homes were completely destroyed. Many residents of Port-au-Prince died during or as a result of the earthquake, albeit fewer than were widely reported. More than half of the capital's population experienced moderate to severe food insecurity, though remittances are a major protective factor in promoting food security. Survivors continue to experience high levels of sexual assault and limited access to durable shelter.

[Effects of acute and chronic Trypanosoma cruzi infection in pregnant mice]. / Efectos de la infección aguda y crónica por Trypanosoma cruzi en la gestación de los ratones.

Pathogens may impair reproduction in association or not with congenital infections. We have investigated the effect of acute infection with Trypanosoma cruzi, the protozoan agent of Chagas disease, on reproduction of female mice. In the acute, parasitemic, phase of the infection, female mice were totally unable to reproduce. Most of them (80%) were infertiles and did not develop any gestation. In the few gravid infected mice, implantation numbers were as in uninfected control mice. However, their fetuses presented a weight meanly reduced by 40% as compared to those of uninfected females, and all of them died during the gestation or whithin 48 h after birth. Such massive mortality did not result from congenital infection, which did not occur. The infertility and the fetal mortality occuring early in gestation (resorptions) were significantly correlated with a high maternal parasitemia, whereas later fetal mortality was associated with the presence of intracellular parasites in the utero-placental unit. The decidua was particularly receptive to T. cruzi multiplication, since this tissue harboured 125 fold more amastigotes than the maternal heart or other placental tissues. In addition, placentas of dead fetuses presented histopathological lesions (inflammatory infiltrates, fibrine deposits and ischemic necrosis). Such harmfull effects of acute infection were not observed when female mice were in the chronic phase of the infection, since these reproduce normally. Their fetuses only suffered from moderate and reversible growth retardation. These results indicate that, following the maternal parasite burden, T. cruzi infection may induce very deleterious effects on gestation.

[Placental lesions in human Trypanosoma cruzi infection]. / Las lesiones placentarias en la infección humana por Trypanosoma cruzi.

This histopathological study analyzes placentas of babies congenitally infected with T. cruzi (M+B+), or babies not infected but born from infected- (M+B-), or non infected-mothers (M-B-). Placentas M+B+ showed lesions of chorionitis, chorioamnionitis and cord edema with lymphocyte infiltration, whereas such lesions were infiltrated only with polymorphonuclear cells in M+B- and M-B- placentas. Parasites were found in M+B+ placentas, in fibroblasts and macrophages of chorion, membranes, chorionic plate, mainly in the area of membrane insertion, as well as in cells of Wharton jelly and myocytes of umbilical cord vessels. These results suggest that the materno-fetal transmission of parasites occurs mainly through the marginal sinus, spreading into the chorionic plate infecting fibroblasts and macrophages so far as to found a fetal vessel, inducing a fetal infection by hematogenous route.

Parasitic load and histopathology of cutaneous lesions, lymph node, spleen, and liver from BALB/c and C57BL/6 mice infected with Leishmania mexicana.

The course of infection, parasitic loads, and histopathology of cutaneous lesions, draining lymph node, spleen, and liver were compared in BALB/c and C57BL/6 mice over a period of 34 weeks after inoculation in footpad with promastigotes of a Leishmania mexicana reference strain. The results show that the primary footpad lesions first present a 12-week phase that develops similarly in both strains of mice. Thereafter, a cutaneous and visceral dissemination of L. mexicana parasites occurs in BALB/c mice; the latter experience an extensive breakdown of the lymphoid organ microarchitecture, whereas C57BL/6 mice succeed in eliminating the parasite infection from the lymph nodes but not from the primary cutaneous lesion, which does not heal. These results highlight marked differences between responses of key anatomical compartments controlling L. mexicana infection in BALB/c and C57BL/6 mice.