Polyphasic Rhabdomyositis in California Sea Lions (Zalophus Californianus): Pathology and Potential Causes.

A myositis syndrome has been recognized for more than a decade in California sea lions (CSLs; Zalophus californianus) but a detailed description of the lesions and potential causes of this condition is lacking. The tissues of 136 stranded CSLs with rhabdomyositis were examined. Rhabdomyositis was considered incidental in 67% (91/136) of the CSLs, and a factor contributing to the animal stranding (significant rhabdomyositis) in 33% (45/136). Of the 91 cases with incidental rhabdomyositis, lesions consisted of a few small foci of lymphohistiocytic inflammation. Of the 45 cases with significant rhabdomyositis, 28 (62%) also presented with major comorbidities such as leptospirosis (2 animals) and domoic acid toxicosis (6 animals), whereas 17 (38%) had severe polyphasic rhabdomyositis as the only major disease process associated with mortality. In these animals, most striated muscles had multiple white streaks and diffuse atrophy. Microscopically, there was myofiber necrosis surrounded by lymphocytes and histiocytes admixed with areas of myofiber regeneration, and/or moderate to severe rhabdomyocyte atrophy usually adjacent to intact Sarcocystis neurona cysts. At the interface of affected and normal muscle, occasional T lymphocytes infiltrated the sarcoplasm of intact myocytes, and occasional myofibers expressed MHCII proteins in the sarcoplasm. S. neurona antibody titers and cyst burden were higher in animals with significant polymyositis antibody titers of (26125 ± 2164, 4.5 ± 1.2 cysts per section) and active myonecrosis than animals with incidental rhabdomyositis antibody titers of (7612 ± 1042, 1.7 ± 0.82 cysts per section). The presented findings suggest that S. neurona infection and immune-mediated mechanisms could be associated with significant polyphasic rhabdomyositis in CSLs.

The Association Between Neurocysticercosis and Hippocampal Atrophy is Related to Age.

Neurocysticercosis (NCC) has been associated with hippocampal atrophy, but the prevalence and pathogenic mechanisms implicated in this relationship are unknown. Using a population-based, case-control study design, residents in a rural village (Atahualpa) aged ≥ 40 years with calcified NCC were identified as cases and paired to NCC-free individuals (control subjects) matched by age, sex, and level of education. Cases and control subjects underwent magnetic resonance imaging for hippocampal rating according to the Scheltens' scale for medial temporal atrophy and were interviewed to identify those with a clinical seizure disorder. The prevalence of hippocampal atrophy was compared between cases and control subjects by the use of the McNemar's test for correlated proportions. Seventy-five individuals with calcified NCC and their matched control subjects were included in the analysis. Hippocampal atrophy was noted in 26 (34.7%) cases and nine (12%) control subjects (odds ratio: 4.4; 95% confidence interval: 1.6-14.9, P < 0.0021). Stratification of pairs according to tertiles of age revealed an age-related trend in this association, which became significant only in those aged ≥ 68 years (P = 0.027). Only five cases and one control had recurrent seizures (P = 0.221); three of these five cases had hippocampal atrophy, and the single control subject had normal hippocampi. This study confirms an association between NCC and hippocampal atrophy, and shows that this association is stronger in older age groups. This suggests that NCC-related hippocampal atrophy takes a long time to develop.

Invasion of Flukes of the Echinostomatidae Family in Racing Pigeon ( Columba livia var. domestica) Lofts.

Over 4 years, only two known cases of fluke invasions were diagnosed in racing pigeons ( Columba livia ) originating from different regions of Poland. In both cases, the invasion was characterized by a very high mortality (approximately 70%), and the source of the infestation was snails of the Lymnaeidae family eaten by pigeons. Fluke invasions in pigeons are extremely rare and to date have not been described in Poland. Therefore, the occurrence of the symptoms of hemorrhagic diarrhea and sudden deaths of either adult pigeons or nestlings were suspected to be associated with poisoning. Autopsy revealed an invasion of flukes causing hemorrhagic enteritis. Renal failure and spleen atrophy were also found in the birds. Using molecular biology techniques, infestation with the fluke Echinostoma revolutum was determined in the second case.

Successful treatment of atrophic facial leishmaniasis scars by co2 fractional laser.

BACKGROUND: A permanent, unpleasant atrophic leishmaniasis scar is a potentially disfiguring condition that causes social stigma with limited treatment choices. Fractionated carbon dioxide (CO2) laser resurfacing is expected to be a safe and effective treatment for leishmaniasis scars. OBJECTIVE: To assess the safety and efficacy of ablative fractional resurfacing (AFR) with a CO2 laser for facial leishmaniasis atrophic scars. METHODS: Eleven patients (five males, age 18-47 years) underwent the fractional CO2 laser procedure. The mean duration for scars was 18.3 years. Three to five treatment sessions with the fractional laser eCO2 (10,600 nm, Lutronic Corporation, Gyeonggi-do, Korea ) were performed for each patient, at 2-month intervals, under topical anesthesia. Two passes (with tip type 120, density 150 spots/cm2 in static mode, and peak power of 30 watts) were performed on each leishmaniasis scar. Pulse energies ranged between 100 and 140 mJ. Posttreatment improvements in texture, atrophy, and overall satisfaction with appearance were graded on a quartile scale 1 month after the second session and 3 months after the final session. Scar improvement was graded using a 4-point score with a maximum score of 20. RESULTS: At the 3-month posttreatment follow-up, all subjects were rated as having at least 50% improvement in texture, atrophy, borders, and overall appearance of scars. The median score of improvement was 18 of 20 (range 11-19). Mild postinflammatory hyperpigmentation was the only adverse effect, observed in 18% (2 of 11) of subjects. After the procedure, moderate to severe erythema and edema typically resolved within 24 to 48 hours. No additional adverse effects were observed. CONCLUSION: Fractional CO2 resurfacing represents a safe, effective, and well-tolerated potential treatment for atrophic facial leishmaniasis scars in ethnic skin.

Molecular genotyping of anisakis larvae in Middle Eastern Japan and endoscopic evidence for preferential penetration of normal over atrophic mucosa.

BACKGROUND: Anisakiasis is a parasitic disease caused primarily by Anisakis spp. larvae in Asia and in Western countries. The aim of this study was to investigate the genotype of Anisakis larvae endoscopically removed from Middle Eastern Japanese patients and to determine whether mucosal atrophy affects the risk of penetration in gastric anisakiasis. METHODS: In this study, 57 larvae collected from 44 patients with anisakiasis (42 gastric and 2 colonic anisakiasis) were analyzed retrospectively. Genotyping was confirmed by restriction fragment length polymorphism (RFLP) analysis of ITS regions and by sequencing the mitochondrial small subunit (SSU) region. In the cases of gastric anisakiasis, correlation analyses were conducted between the frequency of larval penetration in normal/atrophic area and the manifestation of clinical symptoms. RESULTS: Nearly all larvae were A. simplex seusu stricto (s.s.) (99%), and one larva displayed a hybrid genotype. The A. simplex larvae penetrated normal mucosa more frequently than atrophic area (p = 0.005). Finally, patients with normal mucosa infection were more likely to exhibit clinical symptoms than those with atrophic mucosa infection (odds ratio, 6.96; 95% confidence interval, 1.52-31.8). CONCLUSIONS: In Japan, A. simplex s.s. is the main etiological agent of human anisakiasis and tends to penetrate normal gastric mucosa. Careful endoscopic examination of normal gastric mucosa, particularly in the greater curvature of the stomach will improve the detection of Anisakis larvae.

Chagas disease is independently associated with brain atrophy.

Chagas disease (CD) remains a major cause of cardiomyopathy and stroke in developing countries. Brain involvement in CD has been attributed to left ventricular dysfunction, resulting in chronic brain ischemia due to hypoperfusion and/or embolic infarcts. However, cognitive impairment in CD may occur independently of cardiac disease. Therefore, we aimed to investigate head computed tomography (CT) findings in patients with Chagas disease cardiomyopathy (CDC) in comparison with other cardiomyopathies (OC). We studied 73 patients with CDC (n = 41) or OC (n = 32) matched for age and gender. These patients underwent head CT, rated by an investigator blinded to all clinical information. Head CT was rated for the presence of lacunar or territorial infarcts, as well as for measuring the total volumes of the brain, cerebellum and ventricles. Total brain volume was smaller in CDC as compared to OC patients (1,135 +/- 150 vs. 1,332 +/- 198 cm(3), P < 0.001). Cerebellar and ventricular volumes did not differ between the groups. The prevalence of brain infarcts did not differ significantly between the groups. Chagas disease was the only independent predictor of brain atrophy in the multivariable analysis (OR = 1.38; 95% CI = 1.06-1.79, P = 0.017). Chagas disease is associated with brain atrophy independent of structural cardiac disease related to cardiomyopathy. Brain atrophy, rather than multiple infarcts, may represent the main anatomical substrate of cognitive impairment in Chagas disease.

Dyke-Davidoff-Masson syndrome in postcerebral malaria.

Dyke-Davidoff-Masson syndrome is a disorder involving hemiatrophy or hypoplasia of 1 cerebral hemisphere secondary to an insult in the developing brain. Often this will manifest with seizures, hemiparesis, mental retardation, and facial changes. Associated with this pathology are the radiologically evident changes, such as thickening of the calvarium, hyperpneumatization of the sinuses, and dilation of the ipsilateral lateral ventricle among others. The following is a case presentation of an 18-year-old female emigrating from Ghana who presented to the emergency department with complaints of seizures diagnosed as being caused by cerebral malaria at 13 years of age. We hypothesize that the cerebral malaria and related vascular occlusion are the causes of her acquired cerebral changes. Included are computed tomography images.

Neurological and behavioral abnormalities, ventricular dilatation, altered cellular functions, inflammation, and neuronal injury in brains of mice due to common, persistent, parasitic infection.

BACKGROUND: Worldwide, approximately two billion people are chronically infected with Toxoplasma gondii with largely unknown consequences. METHODS: To better understand long-term effects and pathogenesis of this common, persistent brain infection, mice were infected at a time in human years equivalent to early to mid adulthood and studied 5-12 months later. Appearance, behavior, neurologic function and brain MRIs were studied. Additional analyses of pathogenesis included: correlation of brain weight and neurologic findings; histopathology focusing on brain regions; full genome microarrays; immunohistochemistry characterizing inflammatory cells; determination of presence of tachyzoites and bradyzoites; electron microscopy; and study of markers of inflammation in serum. Histopathology in genetically resistant mice and cytokine and NRAMP knockout mice, effects of inoculation of isolated parasites, and treatment with sulfadiazine or alphaPD1 ligand were studied. RESULTS: Twelve months after infection, a time equivalent to middle to early elderly ages, mice had behavioral and neurological deficits, and brain MRIs showed mild to moderate ventricular dilatation. Lower brain weight correlated with greater magnitude of neurologic abnormalities and inflammation. Full genome microarrays of brains reflected inflammation causing neuronal damage (Gfap), effects on host cell protein processing (ubiquitin ligase), synapse remodeling (Complement 1q), and also increased expression of PD-1L (a ligand that allows persistent LCMV brain infection) and CD 36 (a fatty acid translocase and oxidized LDL receptor that mediates innate immune response to beta amyloid which is associated with pro-inflammation in Alzheimer's disease). Immunostaining detected no inflammation around intra-neuronal cysts, practically no free tachyzoites, and only rare bradyzoites. Nonetheless, there were perivascular, leptomeningeal inflammatory cells, particularly contiguous to the aqueduct of Sylvius and hippocampus, CD4+ and CD8+ T cells, and activated microglia in perivascular areas and brain parenchyma. Genetically resistant, chronically infected mice had substantially less inflammation. CONCLUSION: In outbred mice, chronic, adult acquired T. gondii infection causes neurologic and behavioral abnormalities secondary to inflammation and loss of brain parenchyma. Perivascular inflammation is prominent particularly contiguous to the aqueduct of Sylvius and hippocampus. Even resistant mice have perivascular inflammation. This mouse model of chronic T. gondii infection raises questions of whether persistence of this parasite in brain can cause inflammation or neurodegeneration in genetically susceptible hosts.

Hepatic atrophy-hypertrophy complex due to Echinococcus granulosus.

Obstruction of a major hepatic vein, or major portal vein, or biliary tree branch causes atrophy of the related hepatic region, and frequently, hypertrophy in the remaining liver-the atrophy-hypertrophy complex (AHC). Whether hydatid cysts can cause AHC is controversial. The records of 370 patients who underwent surgery for hepatic hydatid disease between August 1993 and July 2002 were evaluated retrospectively. Excluding six patients with previous interventions on the liver, AHC had been recorded in the operative notes of 16 patients (4.4%); for all patients, a cyst located in the right hemiliver had caused atrophy of the right hemiliver and compensatory hypertrophy of the left hemiliver. The computed tomography images of seven patients were suitable for volumetric analysis. The median (range) right and left hemiliver volumes were 334 (0-686) ml and 1084 (663-1339) ml, respectively. The median (range) cyst volume was 392 (70-1363) ml. AHC due to Echinococcus granulosus was confirmed by objective volumetric analysis. The presence of AHC should alert the surgeon to two implications. First, pericystectomy may be hazardous due to association with major vascular and biliary structures. Second, in patients with AHC, the hepatoduodenal ligament rotates around its axis; this should be considered to avoid vascular injury if a common bile duct exploration is to be performed.

A clinical classification and grading system of the cutaneous changes in onchocerciasis.

Although onchocerciasis is one of the most important diseases of the skin and eye in the tropical world, to date there has been no formal consensus regarding the description and terminology of skin lesions. Furthermore, the contribution of cutaneous pathology to the morbidity and socio-economic effects of the disease has been largely neglected. We present a clinical classification and grading system for recording the cutaneous changes of onchocerciasis, and propose that this system be used as a standard method of description to convey clinical information between workers in all endemic areas to assist local and comparative research.

Mini-review: the ultrasonographical and serological changes and their improvement after praziquantel treatment in Schistosoma japonicum infected patients in Leyte, Philippines.

We have identified the specific ultrasonographical (US) changes in Schistosoma japonicum infected patients with the serological changes in general liver function markers. The US examination with the following haematological and biochemical serum analysis was performed on 102 patients in Schistosomiasis Hospital, Leyte, Philippines. The US liver images were classified into 4 patterns according to the development of periportal fibrosis and the patterns of echogenic bands. Among various haematological and biochemical serum parameters of liver damage. The serum levels of total bile acid (TBA) and procollagen-III-peptide (P-III-P) correlated well with the development of hepatic fibrosis and the portal hypertension. These patients were subsequently treated with praziquantel (3 x 20 mg/kg), and the improvement of the thickening of the portal vein wall and the intensity of the echogenic band formation was detected 6 months after treatment. The significant US changes could not be detected in the patients with severe hepatic fibrosis caused in the long term infection. The results revealed that the US examination with the serum TBa level would provider a sensitive tool to monitor the severity of the infection and also the improvement occurred shortly after praziquantel treatment.

Villous atrophy, crypt hyperplasia, cellular infiltration, and impaired glucose-Na absorption in enteric cryptosporidiosis of pigs.

Intestinal morphology and fluid and electrolyte transport were examined in a neonatal porcine model of cryptosporidiosis. Sections of jejunum, ileum, and colon were obtained for morphometric analysis on days 3, 6, 9, and 12 postinfection, and in vivo perfusion studies of jejunum and ileum were conducted on days 3 and 4 postinfection. The most severe morphologic lesion was seen in the ileum on day 3, and consisted of villous atrophy, crypt hyperplasia, and cellular infiltration. Villous surface area was reduced from 2.1 +/- 0.4 x 10(5) microns2 in control ileum to 0.8 +/- 0.1 x 10(5) microns2 in infected ileum, a result associated with enterocytes that were fewer in number and reduced in cross-sectional area. Conversely, the number of inflammatory cells in the lamina propria of the villus increased from 456 +/- 116 in control to 1014 +/- 187 in infected villus without a significant change in the volume of the lamina propria. At the height of infection, there was an approximate 1:2 ratio of both organisms and inflammatory cells to villous enterocytes. In contrast, organisms were not observed in the crypts, and the concentration of inflammatory cells in crypt lamina propria was unaltered. Disappearance of organisms and polymorphonuclear cells from the ileum was associated with restoration of normal structure and was complete by day 12. Although organisms were seen in the colon, the general architecture was not severely affected. On days 3 and 4 postinfection, there was a complete impairment of the glucose-stimulated Na and water absorption in both jejunum and ileum of infected pigs; however, absorption of electrolytes and water from a basic Ringer's solution, in the absence of glucose, was not significantly affected. These results are consistent with a malabsorptive diarrheal disease associated with the morphological damage and are very similar to those seen in enteric viral disease in pigs, except that the upper intestine is more severely affected in the latter.

Development of morphological changes in the small intestine of lambs continuously infected with Trichostrongylus vitrinus.

Groups of three-month-old worm-free Suffolk cross lambs were given 2500 Trichostrongylus vitrinus larvae on five days each week for four, six, eight and 13 weeks and killed one week later. Severe villous atrophy, epithelial erosion and cellular infiltration were common features in the duodenum and the following 2 to 3 m of intestine of lambs killed at weeks 5 and 7. There was evidence of intestinal recovery in the lambs killed at weeks 9 and 14; five of the seven lambs had large areas of intestine which appeared relatively normal and worm activity appeared to be confined largely within focal areas ("fingerprint lesions'). There was no change in the linear distribution of the worms in the intestine over the course of the experiment. The highest percentage of the larval challenge was recovered from lambs killed at week 5 and worm burdens were not cumulative. Lambs killed at week 14 were resistant to larval reinfection.