Cronobacter sakazakii Infection in Early Postnatal Rats Impaired Contextual-Associated Learning: a Putative Role of C5a-Mediated NF-κß and ASK1 Pathways.

This study was designed to test whether the Cronobacter sakazakii infection-impaired contextual learning and memory are mediated by the activation of the complement system; subsequent activation of inflammatory signals leads to alternations in serotonin transporter (SERT). To test this, rat pups (postnatal day, PND 15) were treated with either C. sakazakii (107 CFU) or Escherichia coli OP50 (107 CFU) or Luria bertani broth (100 µL) through oral gavage and allowed to stay with their mothers until PND 24. Experimental groups' rats were allowed to explore (PNDs 31-35) and then trained in contextual learning task (PNDs 36-43). Five days after training, individuals were tested for memory retention (PNDs 49-56). Observed behavioural data showed that C. sakazakii infection impaired contextual-associative learning and memory. Furthermore, our analysis showed that C. sakazakii infection activates complement system complement anaphylatoxin (C5a) (a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS1)) and mitogen-activated protein kinase kinase1 (MEKK1). Subsequently, MEKK1 induces pro-inflammatory signals possibly through apoptosis signal-regulating kinase-1 (ASK-1), c-Jun N-terminal kinase (JNK1/3) and protein kinase B gamma (AKT-3). In parallel, activated nuclear factor kappa-light-chain-enhancer B cells (NF-κB) induces interleukin-6 (IL-6) and IFNα-1, which may alter the level of serotonin transporter (SERT). Observed results suggest that impaired contextual learning and memory could be correlated with C5a-mediated NF-κß and ASK1 pathways.

Neurobrucellosis associated with feral swine hunting in the southern United States.

Although uncommon, Brucella infection can occur outside the areas of high endemicity, such as the USA. In the southern USA, hunters of wild swine are at risk for brucellosis. We present a case of a patient with fever, headache and constitutional symptoms that were ongoing for 11 months. He was diagnosed with neurobrucellosis. The patient was treated successfully with intravenous ceftriaxone, oral doxycycline and oral rifampin therapy. He had persistent neurological sequelae after completing treatment. This case illustrates the high index of suspicion needed to diagnose neurobrucellosis in a non-endemic country because initial symptoms can be subtle. The disease can be treated successfully, but long-lasting neurological sequelae are common.

Gut microbiota depletion from early adolescence alters adult immunological and neurobehavioral responses in a mouse model of multiple sclerosis.

Emerging evidence indicates that gut microbiota interacts with immune and nervous systems in the host and plays a critical role in the pathogenesis of multiple sclerosis (MS) and many psychiatric disorders such as depression and anxiety. The aim of this study was to explore the influence of gut bacterial depletion from early adolescence on adult immunological and neurobehavioral responses in mice with experimental-autoimmune-encephalomyelitis (EAE). We used an animal model of gut microbiota depletion induced by antibiotics from weaning to adulthood to assess clinical signs, cognitive function and depression-and anxiety-related symptoms in non-EAE and EAE-induced mice. We measured levels of interferon (IFN)-γ, interleukin (IL)-17A and IL-10 in serum, and BDNF, IL-1ß and tumor necrosis factor (TNF)-α) in the hippocampus. Antibiotic-treated mice displayed a significant delay in the onset of clinical symptoms of EAE. However, a higher severity of EAE was found between days 19-22 post-immunization in antibiotics-treated mice, while a reduction in the clinical signs of MS was observed at days 24-25 post-immunization. Antibiotic administration decreased IFN-γ and IL-17A levels and increased IL-10 in serum of EAE-induced mice. Antibiotic treatment significantly decreased hippocampal BDNF and enhanced learning and memory impairments in EAE-induced mice. However, no significant changes were found in non-EAE mice. Non-EAE and EAE mice treated with antibiotics exhibited increased anxiety-related behaviors, whereas depression-related symptoms and increased hippocampal TNF-α and IL-1ß were only observed in EAE-induced mice treated with antibiotics. This study supports the view that depletion of gut microbiota by antibiotics from weaning profoundly impacts adult immunological and neurobehavioral responses.

Alterations to the microbiota-colon-brain axis in high-fat-diet-induced obese mice compared to diet-resistant mice.

Obesity is underpinned by both genetic and environmental factors, including a high-saturated-fat diet. Some mice develop diet-induced obesity (DIO), but others remain diet resistant (DR) despite intake of the same high-saturated-fat diet, a phenomenon that mimics characteristics of the human obese phenotype. Microbiota-colon-brain axis regulation is important for energy metabolism and cognition. Using DIO and DR mouse models, this study aimed to examine gut microbiota, colonic inflammation and cognitive function to elucidate the role of microbiota-gut-brain regulation in DIO. C57Bl6/J mice fed a chronic saturated-palmitic-acid diet for 22 weeks showed significant body weight gain differences, with the top one third gaining 48% heavier body weight than the lower one third. There was significant reduction in gut microbiota richness and diversity in DIO mice but not in DR mice. At the phylum level, DIO mice had increased abundance of Firmicutes and Antinobacteria, and decreased abundance of Bacterioides and Proteobacteria in gut microbiota. DIO mice exhibited reduced tight junction proteins, increased plasma endotoxin lipopolysaccharide (LPS) and increased inflammation in the colon and liver. Recognition memory and spatial memory were impaired in DIO mice, associated with decreased Bacteroidetes. Further examination showed that hippocampal brain-derived neurotrophic factor was significantly decreased in DIO mice (vs. DR). Conversely, DR mice showed no changes in the above parameters measured. Therefore, gut microbiota, colon inflammation and circulating LPS may play a major role in the development of the obese phenotype and cognitive decline associated with a chronic high-saturated-palmitic-acid diet.

High-fat diet causes psychiatric disorders in mice by increasing Proteobacteria population.

The excessive intake of a high-fat diet (HFD) leads to obesity, including metabolic syndromes, disturbs gut microbiota composition, causes colitis, and increases the plasma concentration of lipopolysaccharide (LPS). In the present study, we examined the role of gut microbiota in the occurrence of HFD-induced psychiatric disorders in mice. C57BL/6 J male mice fed a HFD for 9 weeks were led to obesity; their memory impairment was assessed by the Y-maze and novel object recognition test, and anxiety-like behaviors by the elevated plus maze. The intake of a HFD suppressed brain-derived neurotrophic factor (BDNF) expression in the hippocampus and increased blood TNF-α and LPS levels. HFD treatment more potently increased NF-κB activation and Iba1+ (microglial) cell populations in the hippocampus. Furthermore, HFD feeding increased TNF-α expression, myeloperoxidase activity, and CD11b+/CD11c+ cell (macrophages and dendritic cells) populations in the colon and altered gut microbiota composition including increases in the Proteobacteria population, and increases in fecal LPS levels. The stool lysates of HFD-treated mice suppressed BDNF expression and CREB phosphorylation in SH-SY5Y cells and increased NF-κB activation in BV-2 microglial cells compared to those of low-fat diet-treated mice while these effects were attenuated by treatment with anti-LPS antibody. These findings suggest that excessive intake of HFD can simultaneously cause obesity and psychiatric disorders by suppressing hippocampal BDNF expression with the disturbance of gut microbiota composition, particularly the increase in Proteobacteria population and LPS production.

Microglia and amyloid precursor protein coordinate control of transient Candida cerebritis with memory deficits.

Bloodborne infections with Candida albicans are an increasingly recognized complication of modern medicine. Here, we present a mouse model of low-grade candidemia to determine the effect of disseminated infection on cerebral function and relevant immune determinants. We show that intravenous injection of 25,000 C. albicans cells causes a highly localized cerebritis marked by the accumulation of activated microglial and astroglial cells around yeast aggregates, forming fungal-induced glial granulomas. Amyloid precursor protein accumulates within the periphery of these granulomas, while cleaved amyloid beta (Aß) peptides accumulate around the yeast cells. CNS-localized C. albicans further activate the transcription factor NF-κB and induce production of interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor (TNF), and Aß peptides enhance both phagocytic and antifungal activity from BV-2 cells. Mice infected with C. albicans display mild memory impairment that resolves with fungal clearance. Our results warrant additional studies to understand the effect of chronic cerebritis on cognitive and immune function.

Comparison of Clinical Course and Treatment Outcome for Patients With Early Disseminated or Early Localized Lyme Borreliosis.

Importance: Multiple erythema migrans (MEM) has been suggested as a risk factor for unfavorable antibiotic treatment outcome compared with solitary erythema migrans (EM). However, no direct comparison of early Lyme borreliosis manifested as MEM with solitary EM has been undertaken. Objective: To investigate the potential differences in clinical course and treatment outcome between MEM and solitary EM. Design, Setting, and Participants: This prospective cohort study was conducted from June 1, 2010, to October 31, 2015, at the University Medical Center Ljubljana, Slovenia. Data were analyzed from June 1, 2017, to January 3, 2018. Of the 778 consecutive adult patients with early Lyme borreliosis evaluated, 200 patients with MEM and 403 patients with solitary EM were enrolled. Patients were asked to refer a family member or a friend of similar age (±5 years) without a history of Lyme borreliosis to serve as a control participant. Clinical course and posttreatment outcome of MEM were compared with those of solitary EM. Outcome was assessed at 14 days and at 2, 6, and 12 months after enrollment. At each visit, patients completed a written questionnaire about their symptoms; controls completed the same questionnaire. Nonspecific symptoms reported by patients and controls without a history of Lyme borreliosis were compared. Main Outcomes and Measures: The proportion of patients with incomplete response at 12 months after enrollment and the associated 2-sided 95% CI for the difference between MEM and solitary EM were estimated using the normal approximation with continuity correction. Results: A total of 200 patients with MEM and 403 patients with solitary EM were included. Among the 200 patients with MEM, 94 (47.0%) were males and 106 (53.0%) were females, with a median (interquartile range [IQR]) age of 47 (35-58) years. Among the 403 patients with solitary EM, 182 (45.2%) were males and 221 (54.8%) were females, with a median (IQR) age of 55 (42-62) years. Patients with MEM reported Lyme borreliosis-associated constitutional symptoms at enrollment more often than those with solitary EM (93 [46.5%]; 95% CI, 39.4-53.7 vs 96 [23.8%]; 95% CI, 19.7-28.3; P < .001). During the initial 6 months after treatment, the proportion of patients with incomplete response was higher in the MEM group than in the solitary EM group (14 days: 62 of 193 [32.1%] vs 72 of 391 [18.4%]; P < .001; 2 months: 38 of 193 [19.7%] vs 55 of 394 [14.0%]; P = .28; 6 months: 29 of 182 [15.9%] vs 31 of 359 [8.6%]; P = .02). However, at the 12-month visit, the outcome was comparable: 10 of 170 (5.9%) patients with MEM vs 20 of 308 (6.5%) patients with solitary EM showed incomplete response (-0.6; 95% CI, -5.5 to 4.3; P = .95). The frequency of nonspecific symptoms in patients was similar to that in controls. Conclusions and Relevance: The long-term outcome at 12 months after treatment was comparable, regardless of dissemination. Follow-up of at least 12 months after treatment is thus recommended for future studies that investigate post-Lyme borreliosis symptoms.

Chronic infection with Mycobacterium lepraemurium induces alterations in the hippocampus associated with memory loss.

Murine leprosy, caused by Mycobacterium lepraemurium (MLM), is a chronic disease that closely resembles human leprosy. Even though this disease does not directly involve the nervous system, we investigated a possible effect on working memory during this chronic infection in Balb/c mice. We evaluated alterations in the dorsal region of the hippocampus and measured peripheral levels of cytokines at 40, 80, and 120 days post-infection. To evaluate working memory, we used the T-maze while a morphometric analysis was conducted in the hippocampus regions CA1, CA2, CA3, and dentate gyrus (DG) to measure morphological changes. In addition, a neurochemical analysis was performed by HPLC. Our results show that, at 40 days post-infection, there was an increase in the bacillary load in the liver and spleen associated to increased levels of IL-4, working memory deterioration, and changes in hippocampal morphology, including degeneration in the four subregions analyzed. Also, we found a decrease in neurotransmitter levels at the same time of infection. Although MLM does not directly infect the nervous system, these findings suggest a possible functional link between the immune system and the central nervous system.

Cafeteria diet and probiotic therapy: cross talk among memory, neuroplasticity, serotonin receptors and gut microbiota in the rat.

The western diet is known to have detrimental effects on cognition and the gut microbiota, but few studies have investigated how these may be related. Here, we examined whether a probiotic could prevent diet-induced memory deficits. Rats were pre-exposed to vehicle, low or high doses of VSL#3 for 2 weeks before half were switched from chow to a cafeteria diet (Caf) for 25 days; VSL#3 treatment continued until death. High-dose VSL#3 prevented the diet-induced memory deficits on the hippocampal-dependent place task, but the probiotic caused deficits on the perirhinal-dependent object task, irrespective of diet or dose. No differences were observed in anxiety-like behaviour on the elevated plus maze. Gut microbial diversity was dramatically decreased by Caf diet and here, VSL#3 was able to increase the abundance of some taxa contained in the probiotic such as Streptococcus and Lactobacillus and also other taxa including Butyrivibrio, which were decreased by the Caf diet. This affected the predicted profile of microbial metabolic pathways related to antioxidant and bile biosynthesis, and fat and carbohydrate metabolism. In the hippocampus, the Caf diet increased the expression of many genes related to neuroplasticity and serotonin receptor (5HT) 1A, which was normalised in Caf-High rats. Distance-based linear modelling showed that these genes were the best predictors of place memory, and related to microbiota principal component (PC) 1. Neuroplasticity genes in the perirhinal cortex were also affected and related to PC1 but object memory performance was correlated with perirhinal 5HT2C expression and microbiota PC3. These results show that probiotics can be beneficial in situations of gut dysbiosis where memory deficits are evident but may be detrimental in healthy subjects.

Gastrointestinal inflammation by gut microbiota disturbance induces memory impairment in mice.

In this study, we tested our hypothesis regarding mechanistic cross-talk between gastrointestinal inflammation and memory loss in a mouse model. Intrarectal injection of the colitis inducer 2,4,6-trinitrobenzenesulfonic acid (TNBS) in mice caused colitis via activation of nuclear factor (NF)-κB and increase in membrane permeability. TNBS treatment increased fecal and blood levels of lipopolysaccharide (LPS) and the number of Enterobacteriaceae, particularly Escherichia coli (EC), in the gut microbiota composition, but significantly reduced the number of Lactobacillus johnsonii (LJ). Indeed, we observed that the mice treated with TNBS displayed impaired memory, as assessed using the Y-maze and passive avoidance tasks. Furthermore, treatment with EC, which was isolated from the feces of mice with TNBS-induced colitis, caused memory impairment and colitis, and increased the absorption of orally administered LPS into the blood. Treatment with TNBS or EC induced NF-κB activation and tumor necrosis factor-α expression in the hippocampus of mice, as well as suppressed brain-derived neurotrophic factor expression. However, treatment with LJ restored the disturbed gut microbiota composition, lowered gut microbiota, and blood LPS levels, and attenuated both TNBS- and EC-induced memory impairment and colitis. These results suggest that the gut microbiota disturbance by extrinsic stresses can cause gastrointestinal inflammation, resulting in memory impairment.

The study of memory and executive dysfunction in patients infected with Helicobacter pylori.

Background Infectious agents are considered as potential causes of Alzheimer's disease. Recently, evidence of a high prevalence of Helicobacter pylori (H. pylori) infection in patients with Alzheimer's disease has been observed. The aim of this study was to investigate memory and executive function in H. pylori positive persons not suffering from Alzheimer's or other marked cognitive disorders. Methods This is a cross-sectional study. A total 140 participants were selected using purposive sampling from the patients within the age group of 18-60 years old at Fayyaz Bakhsh Hospital, Tehran in spring 2016. The participants were divided into two groups of H. pylori positive and negative according to results of the serologic tests to measure the levels of specific antibodies of IgA and IgG against H. pylori using ELISA method. They were subsequently assessed using two tests of Trail Making (TMT) part A and B and Wechsler Memory Scale - Third Edition. Data were analyzed using independent t-test and chi-square. The level of significance was considered P-value ≤ 0.05. Results Out of 140 participants, there were 41 male (29.3%) and 99 female (70.7%) among which 84 patients (60%) suffered from H. pylori infection (seropositive) and 56 patients (40%) were not infected. Comparison of the results using independent t-test showed a significant difference (P = 0.006) between the memory scores of patients (M: 106, SD: 8.12) and healthy ones (M: 112, SD: 1.12). In addition, the executive function showed there is a significant difference in the executive ability of seropositive individuals in the two age groups of 20-50 years old (Part A: M: 1.36, SD: 7.11, and Part B: M: 8.8, SD: 8.25 p = 0.01) and over 50 years old (Part A: M: 55, SD: 8.20, and Part B: M: 106, SD: 7.22, p = 0.009). Conclusion The results of this study showed that the infected patients have a lower cognitive performance in comparison to healthy individuals. In other words, H. pylori infection increases the prevalence of memory and executive dysfunction.

Behavioural and neurochemical consequences of chronic gut microbiota depletion during adulthood in the rat.

Gut microbiota colonization is a key event for host physiology that occurs early in life. Disruption of this process leads to altered brain development which ultimately manifests as changes in brain function and behaviour in adulthood. Studies using germ-free (GF) mice highlight the extreme impact on brain health that results from life without commensal microbes. However, the impact of microbiota disturbances occurring in adulthood is less studied. To this end, we depleted the gut microbiota of 10-week-old male SpragueDawley rats via chronic antibiotic treatment. Following this marked, sustained depletion of the gut bacteria, we investigated behavioural and molecular hallmarks of gut-brain communication. Our results reveal that depletion of the gut microbiota during adulthood results in deficits in spatial memory as tested by Morris water maze, decreased visceral sensitivity and a greater display of depressive-like behaviours in the forced swim test. In tandem with these clear behavioural alterations we found changes in altered CNS serotonin concentration along with changes in the mRNA levels of corticotrophin releasing hormone receptor 1 and glucocorticoid receptor. Additionally, we found changes in the expression of brain derived neurotrophic factor (BDNF), a hallmark of altered microbiota-gut-brain axis signalling. In summary, this model of antibiotic-induced depletion of the gut microbiota can be used for future studies interested in the impact of the gut microbiota on host health without the confounding developmental influence of early-life microbial alterations.

Sulfate-reducing bacteria impairs working memory in mice.

The ability of gut microbes to bi-directionally communicate with the brain and vice versa form the basis of the gut microbiome-central nervous system axis. It has been shown that inoculation with pathogenic gut bacteria alters the behavior of mice; however, it is not known whether or not non-pathogenic resident microbes have similar effects. In this study, we tested the hypothesis that the administration of sulfate-reducing bacteria (SRB), a specific group of resident gut bacteria that generate hydrogen sulfide (H2S), impair learning and memory performance in mice tested in an 8-arm radial maze and Morris water maze. We found that mice spent more time in the center of the maze when they were gavaged with live SRB as compared to mice given saline (control), lactulose+mannitol (L/M), or killed SRB. SRB-gavaged mice were also tested using the Morris water maze and were found to take longer to complete the test, spend more time further from the platform, and have a longer path length to reach the platform. This effect of SRB on maze performance was associated with a higher concentration of H2S in the small intestine and cecum. We conclude that SRB, a specific resident gut bacterial species, could impair cognitive function in mice.

Nervous system Lyme disease.

Lymphocytic meningitis, cranial neuritis or radiculoneuritis occur in up to 15% of patients with untreated Borrelia burgdorferi infection. Presentations of multifocal PNS involvement can range from painful monoradiculitis to confluent mononeuropathy multiplex. Serologic testing is highly accurate after 4 to 6 weeks of infection. In CNS infection, production of anti-Bburgdorferi antibody is often demonstrable in CSF. Oral antimicrobials are microbiologically curative in virtually all patients, including acute European neuroborreliosis. Severe cases may require parenteral treatment. The fatigue and cognitive symptoms seen in some patients with extra-neurological disease are neither evidence of CNS infection nor specific to Lyme disease.

The role of hepatic and splenic macrophages in E. coli-induced memory impairments in aged rats.

Bi-directional communication between the peripheral and central nervous systems has been extensively demonstrated. Aged rats exhibit a prolonged proinflammatory response in the hippocampus region of the brain following a peripheral bacterial infection, and this response in turn causes robust memory declines. Here we aimed to determine whether hepatic or splenic macrophages play a role in the maintenance of this central response. Proinflammatory cytokines measured in liver and spleen four days following an Escherichia coli infection revealed a potentiated proinflammatory response in liver, and to a lesser extent in spleen, in aged relative to young rats. To determine whether this potentiated response was caused by impaired bacterial clearance in these organs, E. coli colony forming units in liver and spleen were measured 4 days after infection, and there were no difference between young and aged rats in either organ. No E. coli was detected in the hippocampus, eliminating the possibility that the aged blood brain barrier allowed E. coli to enter the brain. Depletion of hepatic and splenic macrophages with clodronate-encapsulated liposomes effectively eliminated the proinflammatory response to E. coli at four days in both organs. However, this treatment failed to reduce the proinflammatory response in the hippocampus. Moreover, depletion of peripheral macrophages from liver and spleen did not prevent E. coli-induced memory impairment. These data strongly suggest that hepatic and splenic macrophages do not play a major role in the long-lasting maintenance of the proinflammatory response in the hippocampus of aged rats following a bacterial infection, or the memory declines that this response produces.

Cognitive impairment and memory loss associated with histoplasmosis: a case study.

Histoplasmosis is a rare disease caused by inhalation of the fungus Histoplasma capsulatum. It can spread via cerebral circulation to the central nervous system as a manifestation of a disseminated infection; particularly in patients with immune suppression, which can result in isolated ring-enhancing lesions and inflammation in the brain. Of the reported disseminated histoplasmosis cases (approximately 1 in 2000 per year), only 5-20% have evidence of central nervous system involvement. This paper reviews a single case study of a 57-year-old female diagnosed with disseminated CNS histoplasmosis. Patient's complaints included reduced short-term memory, word-finding problems, and difficulty organizing, making decisions, getting lost while driving, recalling names, retaining information while reading, and slowed processing speed. There was also a history of mild depression and anxiety. Direct testing revealed deficits in multiple cognitive domains including complex attention, processing speed, semantic fluency, visual scanning, motor speed, set-shifting, naming, nonverbal memory, and verbal memory. Neuropsychological deficits suggest cortical and subcortical brain dysfunction, including anterior, temporal, and mesial-temporal regions. This case illustrates the need for neuropsychologists to understand histoplasmosis, the related pathophysiology, and the neuropsychological impact; particularly with the potential for delayed progression.

Evaluation of the brain-derived neurotrophic factor, nerve growth factor and memory in adult rats survivors of the neonatal meningitis by Streptococcus agalactiae.

Streptococcus agalactiae (GBS) is a major cause of severe morbidity and mortality in neonates and young infants, causing sepsis, pneumonia and meningitis. The survivors from this meningitis can suffer serious long-term neurological consequences, such as, seizures, hearing loss, learning and memory impairments. Neurotrophins, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) control the neuronal cell death during the brain development and play an important role in neuronal differentiation, survival and growth of neurons. Neonate Wistar rats, received either 10µL of sterile saline as a placebo or an equivalent volume of GBS suspension at a concentration of 1×10(6)cfu/mL. Sixty days after induction of meningitis, the animals underwent behavioral tests, after were killed and the hippocampus and cortex were retired for analyze of the BDNF and NGF levels. In the open-field demonstrated no difference in motor, exploratory activity and habituation memory between the groups. The step-down inhibitory avoidance, when we evaluated the long-term memory at 24h after training session, we found that the meningitis group had a decrease in aversive memory when compared with the long-term memory test of the sham group. BDNF levels decreased in hippocampus and cortex; however the NGF levels decreased only in hippocampus. These findings suggest that the meningitis model could be a good research tool for the study of the biological mechanisms involved in the behavioral alterations secondary to GBS meningitis.

Central nervous system tuberculosis masquerading as primary dementia: a case report.

Primary dementias are the most common cause of memory impairment in patients above the age of 60. Hypothyroidism, depression, vitamin B12 deficiency and infectious diseases such as syphilis at times may present with memory impairment mimicking primary dementias in their clinical presentation. We present here a 64-year-old female who presented with complaints of forgetfulness, confusion, memory loss and impaired concentration for the past 3 months. Neuroimaging and computed tomography of the chest were suggestive of active tuberculosis. Anti-tubercular therapy led to resolution of enhancing lesions in the brain and abatement of memory deficits.

Convalecencia de mujeres que sufrieron dengue serotipo 3 durante el embarazo / Convalescence of pregnant women who suffered from dengue serotype 3

Introducción: el dengue es una enfermedad infecciosa producida por un virus de genoma ARN, al cual se le reconocen 4 serotipos (DEN-1, DEN-2, DEN-3 y DEN-4) transmitidos por el Aedes aegypti como principal vector. En el embarazo se manifiesta clínicamente de forma similar a la población general, pero con la diferencia de estar en presencia de un ecosistema constituido por la madre y el feto, donde se introduce el virus con sus características genéticas con condiciones especiales para su desarrollo y evolución. Objetivo: investigar la evolución de los síntomas del dengue en mujeres que enfermaron durante el embarazo por 1 año de seguimiento. Métodos: se realizó una investigación observacional y descriptiva con el fin de conocer la presencia de secuelas con posterioridad a la infección por dengue 3 en mujeres que enfermaron durante su embarazo. Se estudió una cohorte de 28 embarazadas que ingresaron en el Hospital General Dr Juan Bruno Zayas Alfonso durante el brote de dengue de abril a noviembre de 2006. El diagnóstico se confirmó por métodos serológicos. Resultados: se observó hasta el año de seguimiento, pérdida de memoria (25 por ciento) y trastornos menstruales (14,3 por ciento). La pérdida de memoria resultó significativa cuando la infección se produjo en el tercer trimestre del embarazo, p= 0,0377. Conclusión: la infección por el virus dengue 3 es capaz de dejar secuela de pérdida de memoria en mujeres que sufrieron dengue durante el embarazo, preferentemente en el tercer trimestre de gravidez(AU)

Introduction: dengue is an infectious disease caused by ARN genome virus and has 4 recognized serotypes (DEN-1, DEN-2, DEN-3 and DEN-4) that are transmitted by Aedes aegypti as the main vector. The clinical manifestations of dengue in pregnancy are similar to those of the general population, except that the ecosystem is made up by the mother and the fetus where the virus with its genetic characteristics is introduced and finds special conditions for development and evolution. Objective: to study the progression of the dengue symptoms in women who got sick during their pregnancy for one year of follow-up. Methods: an observational descriptive research was conducted to find out the existence of sequelae in women who were infected with dengue 3 during their pregnancy. A cohort of 28 pregnant women, who had been admitted to Juan Bruno Zayas Alfonso General Hospital at the time of the dengue outbreak from April to November 2006, was studied. The diagnosis was serologically confirmed. Results: after one-year of follow-up, it was observed that amnesia (25 percent) and menstrual disorders (14.3 percent) affected these women. Amnesia was significant when the infection occurred in the third trimester of pregnancy, p= 0.0377. Conclusions: dengue 3 infection may cause amnesia in pregnant women who suffered this disease, particularly in their third trimester of pregnancy(AU)