Clinical and laboratory characterizations of hepatic capillariasis.

Hepatic capillariasis is a rare and neglected parasitic disease caused by infection with Capillaria hepatica in human liver. The disease is not well described and the information for the disease's clinical manifestation, laboratory findings and disease management strategy is not well reported. The limited information for this neglected infection often results in the delay of diagnosis or misdiagnosed to other diseases, therefore the real prevalence or severity of the infection may be underestimated. More case report with systemic analysis and features summary of this disease is needed to better understand the serious zoonotic disease. This study included systemic analysis of 16 patients infected with hepatic capillariasis in China between 2011-2017, including clinical manifestations, laboratory/radiative image findings and treatment results. Clinical manifestation included sustained fever (56.25%), respiratory disorder (37.5%), abdominal pain (37.5%), diarrhea (25%), leukocytosis (93.75%) and eosinophilia (100%). No egg was detected in feces of all patients. Over 60% patients showed elevated level of hepatic enzymes and proteins related to liver fibrosis in sera. Ultrasound and MRI examinations displayed scattered parasitic granuloma leisure in affected liver. Liver biopsy revealed parasite eggs, necrotized parasitic granulomas and septal fibrosis. Treatment with albendazole combined with corticoids for several treatment courses cured all patients with capillariasis. The difficulty of diagnosis, apparent damage of liver functions and potential fibrosis make the disease's prevalence and severity underestimated.

Eosinophilic cerebrospinal fluid pleocytosis associated with neural Angiostrongylus vasorum infection in a dog.

A 1-year-old, female intact Pug dog was presented to the Small Animal Teaching Hospital of the University of Liverpool with a 4-week history of progressive multifocal intracranial signs. Magnetic resonance imaging (MRI) detected multiple hemorrhagic lesions in the brain. The Baermann and zinc sulfate flotation tests with centrifugation, performed on fecal samples, were positive for lungworm larvae and an antigenic test confirmed Angiostrongylus vasorum infection. Anthelmintic treatment was started with a consequent marked clinical improvement. Seventy days later, the dog was clinically normal, and no larvae were detected on the Baermann test. Repeat MRI of the brain revealed marked improvement of the hemorrhagic lesions. Cerebrospinal fluid analysis (CSF) showed marked eosinophilic pleocytosis, and anthelmintic treatment was restarted. A follow-up CSF analysis 4 months after the first presentation revealed resolution of the eosinophilic pleocytosis. This is the first case report of marked eosinophilic pleocytosis associated with neural A vasorum infection in a dog. The CSF eosinophilic pleocytosis persisted for several weeks after treatment, even in the absence of concurrent clinical signs and with a negative A vasorum Baermann test.

Prevalence and implications of cerebrospinal fluid leukocytosis in Papua New Guinean children hospitalized with severe malaria.

Cerebrospinal fluid (CSF) leukocytosis in severe malaria was assessed in 87 children in Papua New Guinea participating in a detailed longitudinal observational study who had undergone lumbar puncture for further investigation of altered consciousness and/or convulsions. After rigorous exclusion of non-malarial infection, 16 (20.5%) of 78 children with Plasmodium falciparum monoinfection but 0 of 9 with P. vivax/mixed-species malaria had a detectable CSF leukocytosis, which was unrelated to prior, including complex, seizures. There were eight children with a CSF leukocyte density > 10 cells/µL (9.2% of the total sample), half of whom had cerebral malaria (4 of 22, 18.1%). Cerebrospinal fluid leukocytosis is infrequent in severe pediatric malaria, especially in children with P. vivax infections, and it is generally mild. Its presence in a blood slide-positive child should prompt consideration of alternative diagnoses and empiric antibiotic therapy.

Inter-relationships of cardinal features and outcomes of symptomatic pediatric Plasmodium falciparum MALARIA in 1,933 children in Kampala, Uganda.

Malaria remains a challenging diagnosis with variable clinical presentation and a wide spectrum of disease severity. Using a structured case report form, we prospectively assessed 1,933 children at Mulago Hospital in Kampala, Uganda with acute Plasmodium falciparum malaria. Children with uncomplicated malaria significantly differed from those with severe disease for 17 features. Among 855 children with severe disease, the case-fatality rate increased as the number of severity features increased. Logistic regression identified five factors independently associated with death: cerebral malaria, hypoxia, severe thrombocytopenia, leukocytosis, and lactic acidosis. Cluster analysis identified two groups: one combining anemia, splenomegaly, and leukocytosis; and a second group centered on death, severe thrombocytopenia, and lactic acidosis, which included cerebral malaria, hypoxia, hypoglycemia, and hyper-parasitemia. Our report updates previous clinical descriptions of severe malaria, quantifies significant clinical and laboratory inter-relationships, and will assist clinicians treating malaria and those planning or assessing future research (NCT00707200) (www.clinicaltrials.gov).

Cystic echinococcosis in Arad County, Romania.

Cystic echinococcosis (CE) is a major parasitosis in Romania, a country where in the past at least one person from 45.5% of its localities underwent surgery for this disease. This survey aimed to provide new epidemiological and clinical data regarding human cases of CE in a western Romanian county. We have retrospectively investigated the medical records of the patients with CE hospitalized during the period of 2004-2010 in the surgical sections of Arad County. A total of 79 patients aged 5-88 years (mean age: 35.9±20.1 years) were diagnosed with CE during the study period. The average yearly incidence was 2.4 cases per 100,000 inhabitants, and the majority of the patients (29.1%) were aged 0-19 years. Most of the adult cases (≥18 years) were people with limited formal education (laborers) (45.6%). The analysis for trend showed an overall decrease in the affected persons over the study period (R(2)=0.66, p=0.026). Hepatic localizations of the hydatid cysts predominated within the study group (73.4%). Only 21.5% of the diseased presented complications and the mean length of hospital stay was 16.2±10.9 days. Eosinophilia of at least 10% of the leukocyte value occurred in 14% of cases and leukocytosis was noticed in 24.1% of patients. Although the rates of CE cases have decreased in Arad County (Romania), this parasitic disease continues to be a concern for public health services and requires the implementation of more stringent prophylactic measures.

Hematological parameters of Ameiva ameiva (Reptilia: Teiidae) naturally infected with hemogregarine: confirmation of monocytosis.

Little is known on how hematozoan infection changes reptile hematology. The lizard Ameiva ameiva is widely distributed in the Americas and is infected by hematozoan parasites. Previous studies on this lizard have shown that the parasite of monocytes causes a variety of ultrastructural changes in infected host cells. The present study reports that this infection does not cause any change to the erythrocytic values. However, a marked increase in the number of leukocytes (especially monocytes) was detected. This indicates that the hemogregarine not only modulates the infected monocyte, but also increases the blood pool of this leukocyte. A Plasmodium sp was also found infecting erythrocytes of one lizard.

[Retrospective clinical and laboratory study of the toxocariasis cases hospitalised between 2005 and 2008]. / Studiu clinic si de laborator, retroprospectiv, asupra cazurilor de toxocaroza la copiii spitalizati in perioada 2005-2008.

UNLABELLED: The authors present the results of retroprospective clinical and laboratory diagnosis on toxocariasis cases hospitalized in the Paediatric Diseases Clinic of Iasi, between January 2005-June 2008. MATERIAL AND METHOD: The study included a number of 228 children. RESULTS: The most frequent clinical manifestation was pulmonary symptoms 80.70%: dyspneea, wheesing, asthma, cough, interstitial pneumonitis. The most frequent digestive symptoms were abdominal pain 41.22%, hepatosplenomegaly 29.38%; cutaneous manifestations were pruritus and urticaria. The laboratory diagnosis: hypereosinophilia was present at 94.73% childrens associated with hyperleucocytosis and hyper-gammaglobulinemia. All the patients were serologic confirmed with toxocariasis. The children responded well to treatment with albendazole.

Leukocytosis caused by tropical splenomegaly during cardiopulmonary bypass.

We describe two patients undergoing cardiac surgery under cardiopulmonary bypass with concomitant enlarged tropical spleen. Volume overload and leukocytosis occurred during pump management. In the first patient this resulted in acute lung injury, but in the second case methods to reduce the impact of leukocytosis were taken, resulting in a normal postoperative course.

Vitamin E deficiency enhances pathology in acute Trypanosoma cruzi-infected rats.

Micronutrient malnutrition is usually highly prevalent in areas endemic for Chagas disease. Nevertheless, the contribution of micronutrient deficiency to the immunopathology of this infection is often overlooked. In the present work, we assessed the effects of vitamin E deficiency on acute Trypanosoma cruzi (Y strain) infection of Holtzman rats. At 20 days post infection, vitamin E deficiency induced changes in leukocyte levels and exacerbated the myocarditis and sympathetic denervation of ventricular hearts. Vitamin E-deficient infected rats displayed significant leukopenia, evidenced by the decline in the numbers of CD45RA(+)CD3(-) B-cells and CD3(+)CD4(+) T-lymphocytes in the peripheral blood compared with infected control rats. In contrast, vitamin E deficiency induced monocytosis as well as an increased differentiation rate of monocytes to macrophages, as revealed by immunohistochemical analysis.

Leukocytosis and blood eosinophilia in a polyparasitised population in north-eastern Brazil.

It has long been known that leukocytosis and blood eosinophilia are common in the tropical environment, but data derived from population-based studies are scarce. A study was undertaken in a fishing village in north-east Brazil where both intestinal helminthiases and parasitic skin diseases are common. Of 409 individuals studied, 128 (31.3%) were infected with one intestinal helminth or ectoparasite species, 93 (22.7%) with two, 61 (14.9%) with three, 25 (6.1%) with four and 11 (2.7%) with more than four species; no parasites were found in 91 (22.2%) individuals. Leukocyte counts ranged between 3,300 cells/microl and 16,100 cells/microl (median, 7,200 cells/microl) and eosinophil counts between 40 cells/microl and 5,460 cells/microl (median, 455 cells/microl). Eosinophilia (>500/microl) was detected in 44.7% of the individuals, and hypereosinophilia (>1,000/microl) in 12.9%. Thirty-six (8.8%) individuals showed leukocytosis. While 75% of individuals with normal eosinophil counts were considered parasite-free, only 14% with eosinophilia and 11% with hypereosinophilia did not have enteroparasites or ectoparasites. Multivariate regression showed that the probability of eosinophilia and hypereosinophilia, but not of leukocytosis, increased with the number of parasite species present. The data show that eosinophilia occurs in almost one-half of the individuals from a resource-poor setting and that it is significantly associated with the presence of intestinal helminths, but not with the presence of ectoparasites.

Changes in white blood cells and platelets in children with falciparum malaria: relationship to disease outcome.

Little is known about the changes in white blood cells and platelets in children with falciparum malaria in endemic areas. We measured the white cell count (WCC) and platelets of 230 healthy children from the community, 1369 children admitted to hospital with symptomatic malaria, and 1461 children with other medical conditions. Children with malaria had a higher WCC compared with community controls, and leucocytosis was strongly associated with younger age, deep breathing, severe anaemia, thrombocytopenia and death. The WCC was not associated with a positive blood culture. In children with malaria, high lymphocyte and low monocyte counts were independently associated with mortality. A platelet count of less than 150 x 109/l was found in 56.7% of children with malaria, and was associated with age, prostration and parasite density, but not with bleeding problems or mortality. The mean platelet volume was also higher in children with malaria compared with other medical conditions. This may reflect early release from the bone marrow in response to peripheral platelet destruction. Thus, leucocytosis was associated with both severity and mortality in children with falciparum malaria, irrespective of bacteraemia, whereas thrombocytopenia, although very common, was not associated with adverse outcome.

Babesia canis infection in a splenectomized dog.

The present report describes a fatal case of non-experimental babesiosis in a splenctomized 3-year-old fox terrier. A very intense parasitaemia including clusters of up to 16 Babesiae and a prominent haemophagocytic activity were the most relevant findings. A marked leukocytosis, thrombocytopenia and regenerative anaemia were observed. Despite prompt treatment with babesiacidal compounds the condition progressed to acute renal failure and resulted in the death of the animal 48 hours after the onset of symptoms.

Deficiency in the anti-apoptotic protein A1-a results in a diminished acute inflammatory response.

A1 is an anti-apoptotic member of the Bcl-2 family that is up-regulated in inflammatory myeloid cells. In the present study, we investigated the role of A1 in the maintenance of acute inflammation in mice. Mice possess three genes encoding highly related isoforms of A1. A1-a isoform mRNA was minimally expressed in resident peritoneal macrophages, but was present at a 300-fold higher level in inflammatory macrophages elicited by i.p. infection with Toxoplasma gondii. In comparison, A1-b and A1-d levels were 3- and 10-fold higher, respectively. Peritoneal leukocytosis was decreased in infected A1-a-deficient mice compared with wild-type, and this reduction was associated with a small but reproducible enhancement of survival. These effects could not be explained by an alteration in peritoneal parasite load, nor by increased apoptosis of infected inflammatory cells, which were protected from cell death by an A1-a-independent mechanism. Increased apoptosis in inflammatory neutrophils was observed sporadically in A1-a-deficient mice. Regulation of apoptosis by A1-a may be an important proinflammatory event in acute host responses.

Resistance to cerebral malaria in tumor necrosis factor-alpha/beta-deficient mice is associated with a reduction of intercellular adhesion molecule-1 up-regulation and T helper type 1 response.

Tumor necrosis factor (TNF) induced by Plasmodium berghei ANKA (PbA) infection was suggested to play an important role in the development of cerebral malaria (CM). We asked whether TNF-alpha/beta double-deficient mice, which have a complete disruption of the TNF-signaling pathways, are protected from CM and what might be the possible mechanisms of protection. PbA infection induces fatal CM in wild-type mice, which die within 5 to 8 days with severe neurological signs. In contrast, TNF-alpha/beta-deficient mice are completely resistant to PbA-induced CM. As PbA-induced up-regulation of endothelial intercellular adhesion molecule (ICAM)-1 expression as well as the systemic release of nitric oxide is found only in wild-type mice, TNF is apparently central for the recruitment of mononuclear cells and microvascular damage. Mononuclear cell adhesion to the endothelium, vascular leak and, perivascular hemorrhage are found only in the brain of wild-type mice. By contrast, the development of parasitemia and anemia is independent of TNF. Resistance to CM in TNF-alpha/beta-deficient mice is associated with reduced interferon-gamma and interleukin-12 expression in the brain, in the absence of increased T helper type 2 cytokines. In conclusion, TNF apparently is required for PbA-induced endothelial ICAM-1 up-regulation and subsequent microvascular pathology resulting in fatal CM. In the absence of TNF, ICAM-1 and nitric oxide up-regulation are reduced, and PbA infection fails to cause fatal CM.

Blastogenic responses of peripheral blood leukocytes from owl monkeys experimentally infected with Leishmania braziliensis panamensis.

The relationship of the progression and regression of cutaneous lesions of 6 owl monkeys (Aotus trivirgatus) to the responses of their peripheral blood leukocytes (PBL) in vitro to mitogens and to leishmanial antigens, as well as their delayed skin test responses (DTH) in vivo to leishmanin antigen, were studied after primary and challenge infections with Leishmania braziliensis panamensis (WR 128 or WR 539). All 6 infected monkeys developed primary and satellite cutaneous leishmanial lesions which were measured for up to 30 weeks in 3 of the monkeys and up to 52 weeks in the other 3 monkeys. Two owl monkeys which had recovered from cutaneous leishmaniasis demonstrated acquired resistance when challenged with an intradermal inoculation of L. b. panamensis (WR 128). Reactivity of PBL from infected owl monkeys to PHA, Con A, and PWM was similar during primary and challenge infections to that observed prior to infection. Reactivity to leishmanial antigens was detected at 20 to 28 weeks post-infection (PI), became statistically significant after 28 weeks and remained elevated up to 52 weeks PI and after challenge infections. During primary infections DTH responses to leishmanin antigen were detected as early as 8 weeks PI, and continued up to 27 weeks PI. After challenge infections DTH reactivity was positive at 25 and 37 weeks, the only times the response was evaluated. The immunological responses of owl monkeys to L. b. panamensis were similar in many respects to those observed in humans with localized cutaneous leishmaniasis. This nonhuman primate model should be useful for future studies involving the immunology and chemotherapy of cutaneous leishmaniasis.

The pattern of peripheral blood leucocyte changes in mice infected with Nematospiroides dubius.

Experiments were carried out to define the haematological changes taking place during the first six weeks of a primary infection with Nematospiroides dubius. The general pattern of changes was observed to comprise a rapid increase in circulating leucocytes (4 to 5-fold increase) which consisted of a neutropl a, lymphocytosis, monocytosis and an eosinophilia. However, in strong responder NIH mice leucocyte counts returned to normal more rapidly than in other strains (by day 28). In contrast, in weak responder C57BL/10 mice the leucocyte counts whilst falling significantly relative to day 7 did not return to normal within the experimental period. Mice infected with irradiated larvae did not experience as high a leucocytosis as did mice given an identical number of normal larvae. The peak lymphocytosis, neutrophilia and monocytosis were all lower. The removal of adult worms from infected animals by treatment with pyrantel on days 9, 11, 13 and 16, also significantly altered the pattern of leucocytosis. The neutrophilia which was evident on day 7 returned rapidly to normal, whereas in mice which had retained their worms a peak neutrophilia was observed on day 14. These haematological changes were discussed and related to the failure of host-protective immunity to operate effectively during the early stages of a primary infection with N. dubius.