A survey of zoonotic diseases in trade cattle slaughtered at Tanga city abattoir: a cause of public health concern

Objective

To estimate the prevalence of hydatidosis, cysticercosis, tuberculosis, leptospirosis, brucellosis and toxoplasmosis in slaughtered bovine stock (aged ±3 years) at Tanga city abattoir, Tanzania.

Methods

Prevalence estimation of the five zoonotic diseases was undertaken through an active abattoir and sero-survey was carried out in Tanga city, during the period of January 2002 and March 2004. Serum samples collected from a sub-sample (n=51) of the slaughter stock were serologically screened for antibodies against brucellosis, leptospirosis and toxoplasmosis using Rose Bengal plate test, microscopic agglutination test (for 5 serovars of Leptospira interrogans) and Eiken latex agglutination test, respectively. The same animals were tested for tuberculosis using the single intradermal tuberculin test.

Results

Post mortem examination of 12 444 slaughter cattle (10 790 short horn zebu and 1 654 graded) over a period of twenty two months, showed a prevalence of 1.56% (194) for hydatidosis, 1.49% (185) for cysticercosis and 0.32% (40) for tuberculosis. In all three zoonoses, a statistically significant difference in infection rates was noted between the short horn zebu and graded breeds (P<0.05). The overall seroprevalences of animals with brucellosis, toxoplasmosis and leptospirosis antibodies were found to be 12%, 12% and 51%, respectively. The most common leptospiral antibodies detected were those against antigens of serovars Leptospira hardjo (29%), Leptospira tarassovi (18%), Leptospira bataviae (4%) and Leptospira pomona (0%). With regard to tuberculosis, 10% (n=5) of the animals tested were classified as non-specific reactors or inconclusive.

Conclusions

The study findings suggest that brucellosis, toxoplasmosis and leptospirosis are prevalent in Tanga and provide definitive evidence of slaughtered stock exposure to these zoonotic agents with concurrent public health consequences.     

Assessment of microalbuminuria and glycated hemoglobin in type 2 diabetes mellitus complications

ObjectiveTo relate microalbuminuria with the degree of glycaemic control in type 2 diabetic patients and determine the prevalence of poor glycemic control amongst the normotensive diabetes mellitus (NDM) and hypertensive diabetes mellitus (HDM) with or without microalbuminuria.MethodsA total of 95 type 2 diabetes mellitus patients and 30 healthy controls were randomly selected and studied. 17 of the 95 patients were normotensive diabetic with microalbuminuria, 40 of them were HDM presenting with microalbuminuria and 38 were NDM without microalbuminuria. Their blood was obtained for fasting plasma glucose and glycated haemoglobin while their urine was obtained for albumin and creatinine estimation and the ratio was calculated.ResultsOut of the 95 diabetic patients studied, 57 (60%) of them had microalbuminuria while 38 (40%) had normoalbuminuria. The mean ages in the diabetics with microalbuminuria were higher than those without microalbuminuria (P=0.054 6). The mean glycated haemoglobin was the highest (5.95±2.06)% in NDM with microalbuminuria when compared with HDM with microalbuminuria (5.83±1.62)% and that in (5.66±2.49)% in NDM without microalbuminuria (P=0.000 9). Similarly, fasting plasma glucose was the highest (9.09±4.31) mmol/L in NDM with microalbuminuria than those without microalbuminuria (7.70±3.33) mmol/L (P=0.000 1). The prevalence of poor glycaemic control was the highest (29%) in NDM with microalbuminuria while the least (21%) in NDM without microalbuminuria.ConclusionsThe risk of microalbuminuria increases with poor glycemic control. Persistent increase in glycated haemoglobin may be an indicator of worsening albumin creatinine ratio and diabetic nephropathy. Therefore, regular screening for microalbuminuria in addition to continuous (3-monthly) glycated HbA1c estimation is advised.     

Prevalence of alveolar bone loss in healthy children treated at private pediatric dentistry clinics

Objectives

The purpose of this study was to evaluate the prevalence of alveolar bone loss (BL) in healthy children treated at private pediatric dentistry clinics in Brasília, Brazil.

Material and Methods

The research included 7,436 sites present in 885 radiographs from 450 children. The BL prevalence was estimated by measuring the distance from the cementoenamel junction (CEJ) to alveolar bone crest (ABC). Data were divided in groups: (I) No BL: distance from CEJ to ABC is ≤2 mm; (II) questionable BL (QBL): distance from CEJ to ABC is >2 and <3 mm; (III) definite BL (DBL): distance from CEJ to ABC ≥3 mm. Data were treated by the chi-square nonparametric test and Fisher''s exact test (p<0.05).

Results

Among males, 89.31% were classified in group I, 9.82% were classified in group II and 0.85% in group III. Among females, 93.05%, 6.48% and 0.46% patients were classified in Group I, II and III, respectively. The differences between genders were not statistically significant (Chi-square test, p = 0.375). Group composition according to patients’ age showed that 91.11% of individuals were classified as group I, 8.22% in group II and 0.67% in group III. The differences among the age ranges were not statistically significant (Chi-square test, p = 0.418). The mesial and distal sites showed a higher prevalence of BL in the jaw, QBL (89.80%) and DBL (79.40%), and no significant difference was observed in the distribution of QBL (Fisher’s exact test p = 0.311) and DBL (Fisher’s exact test p = 0.672) in the dental arches. The distal sites exhibited higher prevalence of both QBL (77.56%) and DBL (58.82%).

Conclusions

The periodontal status of children should never be underestimated because BL occurs even in healthy populations, although in a lower frequency.     

IL-10/TGF-β–Modified Macrophages Induce Regulatory T Cells and Protect against Adriamycin Nephrosis

IL-10/TGF-β–modified macrophages, a subset of activated macrophages, produce anti-inflammatory cytokines, suggesting that they may protect against inflammation-mediated injury. Here, macrophages modified ex vivo by IL-10/TGF-β (IL-10/TGF-β Μ2) significantly attenuated renal inflammation, structural injury, and functional decline in murine adriamycin nephrosis (AN). These cells deactivated effector macrophages and inhibited CD4⁺ T cell proliferation. IL-10/TGF-β Μ2 expressed high levels of the regulatory co-stimulatory molecule B7-H4, induced regulatory T cells from CD4⁺CD25⁻ T cells in vitro, and increased the number of regulatory T cells in lymph nodes draining the kidneys in AN. The phenotype of IL-10/TGF-β Μ2 did not switch to that of effector macrophages in the inflamed kidney, and these cells did not promote fibrosis. Taken together, these data demonstrate that IL-10/TGF-β–modified macrophages effectively protect against renal injury in AN and may become part of a therapeutic strategy for chronic inflammatory disease.Macrophages are a diverse and dynamic population of cells that have the capacity to perform a wide range of critical functions.^1,2 They can be classified into two major functional subsets: Classically activated macrophages (M1), which after stimulation by LPS or IFN-γ are defined by antimicrobial and cytotoxic properties, and alternatively activated macrophages (M2), which after incubation with Th2 cytokines such as IL-4 and IL-10 are characterized by anti-inflammatory and regulatory properties. M2 have been further subdivided into three groups: M2a, induced by IL-4 or IL-13; M2b, induced by immune complexes with IL-1 or LPS; and M2c, induced by IL-10, TGF-β, or glucocorticoids.^3,4 In most types of human kidney disease, macrophage accumulation correlates closely with the degree of renal structural injury and renal dysfunction.⁵ Thus, macrophages have been considered to be important mediators of injury in both immune and nonimmune renal disease.⁶ Depletion of macrophages has been shown to reduce renal injury,⁷ and adoptive transfer of macrophages has been shown to worsen inflammation in animal models of renal injury.⁸ Recently, we demonstrated in macrophage transfer studies that marked renal injury can be caused by transfusion of small numbers of M1 macrophages.⁹ In contrast to M1, the role of M2 in chronic kidney disease is poorly defined. Although M2 macrophages have been studied extensively in regard to their membrane molecules, cytokine secretion, suppressive activity, and ability to modulate wound healing and angiogenesis, the role of M2 in vivo and their therapeutic potential have received little attention to date. Previously, we reported¹⁰ the polarization of macrophages to an IL-4/13 macrophage phenotype and their administration as an effective treatment for adriamycin-induced nephropathy in SCID mice, an inflammatory renal disease analogous to human FSGS. That study provided direct proof that IL-4/13 macrophages are able to protect against renal injury, suggesting ex vivo modulation of macrophages into M2 as a potential strategy for treating chronic inflammatory renal disease; however, the effects of macrophages modified by IL-10/TGF-β, another subset of M2, are unknown.The aim of this study was to examine the effects of IL-10/TGF-β–modified macrophages in immunocompetent mice with adriamycin nephrosis (AN). The potential mechanisms underlying their protective role against renal injury were explored. The phenotypic stability of transfused IL-10/TGF-β macrophages was also examined.     

P16 protein expression in primary cutaneous melanoma with positive and negative lymph node biopsies: Particular aspects of a study performed at the Hospital de Clinicas de Porto Alegre, Brazil

BACKGROUND:

Cutaneous melanoma dermal invasion, identified through measurement of maximum tumour thickness and sentinel lymph node (SLN) biopsy, is important to establish melanoma prognosis and progression. P16 protein expression has been shown to be a predictive factor for melanoma evolution and prognosis.

OBJECTIVE:

To investigate p16 protein expression in cutaneous melanomas with and without SLN metastasis.

PATIENTS AND METHODS:

Sixty-seven paraffin-embedded cutaneous melanoma specimens of patients who had undergone SLN investigation were evaluated from 1995 to 2007. SLN biopsy was negative for metastasis in 34 of these patients (controls); in the remaining 33 patients, SLN biopsy was positive (cases). The expression of p16 protein in the primary tumour was measured using an immunohistochemical assay. The samples were classified according to their nuclear expression.

RESULTS:

P16 nuclear expression was absent in 14 cases and in 15 controls; P=0.812. There was no statistically significant difference in p16 nuclear expression between cases and controls.

CONCLUSIONS:

The present study does not support the findings of other studies that suggest p16 protein expression is important in the prognosis of cutaneous melanoma.