Vários trabalhos têm mostrado que a ingestão deficiente de ferro pode causar alterações nos parâmetros morfológicos e bioquímicos do Sistema Nervoso Central (SNC) do rato assim como em seu comportamento. Também, os animais deficientes em ferro mostram redução no número de lamelas de mielina e déficits de aprendizado. Por outro lado, a estimulação tátil pode reduzir e/ou evitar os danos causados pela má nutrição sobre o SNC e comportamento. Entretanto, os danos no processo de mielinização têm também sido vistos na anemia ferro-deficiente e, uma vez que o nervo óptico é em grande parte formado pelos axônios mielinizados, o objetivo deste estudo é verificar os efeitos da anemia ferropriva e estimulação tátil sobre a morfologia do nervo óptico de ratos Wistar machos aos 18, 22 e 32 dias de idade. Os animais foram divididos em 2 grupos: Controles ( C ) (35 mg Fe / Kg de dieta), Anêmicos ( A ) (4 mg Fe / Kg de dieta). Cada grupo foi subdividido em Estimulado ( E ) e Não Estimulado ( N ). O peso corporal, hemoglobina, hematócrito, área, perímetro, diâmetro mínimo, densidade de células gliais e número de vasos no nervo óptico foram avaliados. Os animais foram anestesiados com éter sulfúrico e sacrificados por perfusão cardíaca com PBS 0,05 M em pH 7,3, seguido por paraformaldeído 2% mais glutaraldeído 1% em tampão fosfato 0,1 M (pH 7,3). O nervo óptico foi dissecado e imerso em solução de tetróxido de ósmio a 1% por duas horas a 40C, desidratado em acetona com graus de diluição crescentes e incluído em araldite. As amostras de nervo óptico foram orientadas para permitir cortes transversos de suas fibras. Secções de 0,5 m foram obtidas e coradas com azul de toluidina 1% antes de serem examinadas na microscopia de luz. Os estudos morfométricos foram feitos com um sistema analisador de imagens semi-automático (MiniMop). Os resultados mostram que a anemia levou a deficiências no peso corporal, hematócrito, hemoglobina, área, perímetro, diâmetro mínimo, número de células gliais e número de vasos do nervo óptico entre os anêmicos, e que a estimulação melhorou significativamente estes itens tanto em anêmicos quanto em controles (à exceção de hematócrito e hemoglobina) porém não recuperando totalmente os estes prejuízos provocados pela anemia. / Several works have been shown that the deficient ingestion of iron can cause alterations in the morphologic and biochemical parameters of the Central Nervous System (CNS) of the rat as well as in its behavior. Also, the iron deficient animals show reduction in the number of myelin lamellae and learning deficits. On the other hand, the tactile stimulation can reduce and/or to avoid the damages caused by the bad nutrition about CNS and behavior. However, the damages in the myelinization process have been seen also in the iron-deficient anemia and, at once that the optical nerve is formed largely by the myelinated axons, the objective of this study is to verify the effects of the anemia and tactile stimulation on the morphology of the optical nerve of Wistar males rats at the 18th, 22 nd and 32 nd days of age. The animals were divided in 2 groups: Controls © (35 mg Fe / diet Kg), Anemic (A) (4 mg Fe / diet Kg). Each group was subdivided in Stimulated (S) and No Stimulated (N). The corporal weight, haemoglobin, haematocrit, area, perimeter, minimum diameter, density of glial cells and number of vases were evaluated. The animals were anesthetized and sacrificed by heart perfusion with PBS 0,05 M in pH 7,3, following for paraformaldheyde 2% plus glutaraldheyde 1% in a phosphate buffer 0,1 M (pH 7,3). The optic nerve was dissected and submerged in solution of osmium tetroxide 1% for two hours at 40C, dehydrated in acetone with decreasing dilution degrees and included in araldite. The samples of optic nerve were guided to allow transverse cuts of their fibers. Sections sized 0,5 m were obtained and stained with toluidin blue 1% prior examinations in the light microscopy. The morphometric studies were made with a semiautomatic analyzing system of images (MiniMop). The results show that the anaemia caused differences in the corporal weight, haematocrit, haemoglobin, area, perimeter, minimum diameter, number of glial cells and vassels of the optical nerve among controls and anaemic, and that the stimulation influenced significantly on these items taking to the conclusion that it improves the damaged structures due to anaemia, but it doesn’t recover them totally.

The critical swimming speed (Ucrit) of rainbow trout parr (Oncorhynchus mykiss) and three life stages of Galaxias maculatus, larval (whitebait), postlarval inanga and adult inanga, were tested at temperatures from 5oC to 25oC. All fish were swum at their acclimation temperature under normoxic conditions to determine the optimal aerobic exercise temperature. To determine whether acclimation affected swimming ability, trout parr acclimated to either 10oC or 20oC were swum at 20oC and 10oC, respectively. The potential effect of mild hypoxia (75% saturation) on trout parr and whitebait was also examined at 10oC, 15oC and 20oC, and also tested separately and in combination were the effects of mild hypoxia and severe anaemia on the prolonged swimming ability of trout smolts at temperatures from 10oC to 20oC. For all trout experiments, blood samples were taken from non-exercised and exercised fish by acute caudal venepuncture to determine haematological responses to both acclimation and exercise. Under normoxic conditions, Ucrit max for trout parr (7.0 0.5 cm fork length) was calculated to be 5.8 body lengths per second (BL s-1) at 15.1oC, but declined at lower and higher temperatures. This result implies that swimming performance was limited by temperature below 15oC, whereas performance at higher temperatures was limited by oxygen availability. In support of this hypothesis, mild hypoxia (75% saturation) had no effect at 10oC or 15oC but caused a significant reduction in Ucrit at 20oC. However, fish acclimated at 20oC showed an adaptive elevation in oxygen carrying capacity due to an increase in mean erythrocyte volume and haemoglobin content. Furthermore, acclimation to 20oC improved warm water swimming performance. Trout parr acclimated to 10oC performed significantly worse than fish acclimated to 20oC when swum at 20oC. However, trout parr acclimated to 20oC performed as well as fish acclimated to 10oC when swum at 10oC. Following exercise, haematocrit was elevated under both normoxic and hypoxic conditions. However, the primary cause of this apparent increase in oxygen carrying capacity was splenic release of erythrocytes under normoxic conditions, whereas stress-induced erythrocytic swelling contributed to the observed increase in hypoxia. This contrasting response was most pronounced at 10oC. Larval whitebait (4.7 - 5.0 cm total length (TL)) also showed a temperature dependence of prolonged swimming ability with Ucrit max calculated to be 5.1 BL s-1 at 17.7oC. Hypoxia significantly reduced Ucrit at 15oC and 20oC, lowering the optimal aerobic temperature to 13.9oC and reducing Ucrit to 4.2 BL s-1. Mild hypoxia therefore had a more pronounced impact on inanga whitebait than trout. Postlarval inanga (3.9 - 4.0 cm TL) performed poorly at higher temperatures with Ucrit max of 5.6 BL s-1 at 9.4oC indicating an ontogenetic change in swimming ability, possibly resulting from a developmental shift in red muscle kinetics or a greater dependence on anaerobic muscle. Adult inanga (5.5 - 6.8 cm TL) prolonged swimming ability showed similar temperature dependence to that of inanga whitebait but lower relative swimming speeds due to their larger size. The dramatic decline in performance exhibited by juveniles at warmer temperatures was not apparent in adults. Ucrit max for adults was 4.0 BL s-1 at 18.3oC. The critical swimming speed of trout smolts, subjected to mild hypoxia (6.8 mg

Fanconi anaemia (FA) is an inherited disorder characterized by bone marrow failure, cancer predisposition and congenital abnormalities. The 12 known FA genes have been implicated in homologous recombination (HR), a process involved in telomere maintenance. A complex of at least 7 FA proteins promotes FANCD2 monoubiquitination and nuclear foci formation. FANCD2 colocalizes and interacts with HR proteins, however the role of FANCD2 in HR is unclear. Telomeres in dividing human somatic cells shorten until they reach a critical length, triggering most cells to undergo senescence or apoptosis. Rare immortal cells escape this crisis by expressing telomerase, or activating the Alternative Lengthening of Telomeres (ALT) pathway, which involves HR. FA core complex proteins and FANCD2 colocalize with telomeric foci in ALT, but not telomerase positive cells. Localization of FANCD2 to ALT telomeric foci requires monoubiquitination by the FA core complex, but is independent of ATM and ATR. FANCD2 primarily colocalizes with ALT telomeric DNA within ALT-associated PML bodies (APBs). Electron spectroscopic imaging and FISH experiments show that APBs contain extra-chromosomal telomeric repeat (ECTR) DNA that is non-nucleosomal. Depletion of FANCD2 causes marked increases in ECTR in ALT, but not telomerase positive cells. Overexpression of BLM, the helicase mutated in Bloom syndrome, also causes an ALT-specific increase in ECTR DNA. FANCD2 coimmunoprecipitates with BLM in ALT cells, and FANCD2 localization to ALT telomeric foci requires BLM expression. FANCD2-depleted ALT cells have reduced viability, signs of mitotic catastrophe, and multiple types of telomeric abnormalities, including increases in telomeric recombination, entanglements, colocalization with DNA repair proteins, and expression of fragile site characteristics. SiRNA depletion of FANCD2 does not cause overexpression of BLM, however codepletion of BLM with FANCD2 suppresses the telomere phenotypes caused by FANCD2 knockdown. Together this suggests that FANCD2 regulates BLM-dependent recombination and amplification of telomeric DNA within ALT cells.

Fanconi anaemia (FA) is an inherited disorder characterized by bone marrow failure, cancer predisposition and congenital abnormalities. The 12 known FA genes have been implicated in homologous recombination (HR), a process involved in telomere maintenance. A complex of at least 7 FA proteins promotes FANCD2 monoubiquitination and nuclear foci formation. FANCD2 colocalizes and interacts with HR proteins, however the role of FANCD2 in HR is unclear. Telomeres in dividing human somatic cells shorten until they reach a critical length, triggering most cells to undergo senescence or apoptosis. Rare immortal cells escape this crisis by expressing telomerase, or activating the Alternative Lengthening of Telomeres (ALT) pathway, which involves HR. FA core complex proteins and FANCD2 colocalize with telomeric foci in ALT, but not telomerase positive cells. Localization of FANCD2 to ALT telomeric foci requires monoubiquitination by the FA core complex, but is independent of ATM and ATR. FANCD2 primarily colocalizes with ALT telomeric DNA within ALT-associated PML bodies (APBs). Electron spectroscopic imaging and FISH experiments show that APBs contain extra-chromosomal telomeric repeat (ECTR) DNA that is non-nucleosomal. Depletion of FANCD2 causes marked increases in ECTR in ALT, but not telomerase positive cells. Overexpression of BLM, the helicase mutated in Bloom syndrome, also causes an ALT-specific increase in ECTR DNA. FANCD2 coimmunoprecipitates with BLM in ALT cells, and FANCD2 localization to ALT telomeric foci requires BLM expression. FANCD2-depleted ALT cells have reduced viability, signs of mitotic catastrophe, and multiple types of telomeric abnormalities, including increases in telomeric recombination, entanglements, colocalization with DNA repair proteins, and expression of fragile site characteristics. SiRNA depletion of FANCD2 does not cause overexpression of BLM, however codepletion of BLM with FANCD2 suppresses the telomere phenotypes caused by FANCD2 knockdown. Together this suggests that FANCD2 regulates BLM-dependent recombination and amplification of telomeric DNA within ALT cells.

Diss. (sammanfattning) Uppsala : Univ., 2002. / Härtill 5 uppsatser.

The goal of the thesis is to evaluate the haematologic indicators of red blood cells depending to the physiological condition and yield of cattle, sheep and dogs. The evaluation of qualitative parameters of red blood cells included 59 dairy cows, 57 meat cows, 62 sheep and 73 dogs. The evaluation of the haematologic parameters of cattle was performed based on the production (yield) type and by season; that of sheep, by season, age and sex of lambs; and that of dogs, by sex, age and size - weight. The yield types showed statistically significant difference between the number or erythrocytes, haematocrit, haemoglobin, MCV and MCH concentration. The dairy cows showed seasonal fluctuations of the number of erythrocytes, haematocrit and haemoglobin; the meat cows showed fluctuations of the haemoglobin, MCH and MCHC values. The age influenced higher values of erythrocytes in sheep and lower values of MCV and MCH in lambs. The sex of lambs did not lead to significant differences. The evaluation of dogs by age showed differences of haematocrit and haemoglobin values. The dog size (weight) and the sex did not have demonstrable influence on haematologic values. Anaemia was found in 36 % dairy cows (it did not occur in meat cattle) and in 2 sheep (3 %). By most authors, anaemia was not found in dogs.

O uso de suplemento a base de ferro é fundamental para profilaxia e tratamento da anemia ferropriva, agravo freqüente em gestantes que vivem em paises em desenvolvimento, e que se não for tratada, pode ter conseqüências tanto para mulher quanto para o feto. Entretanto, muitas mulheres não aderem a terapêutica. O objetivo deste estudo foi identificar a utilização de suplemento à base de ferro no ciclo grávido-puerperal, em um grupo de mulheres.Trata-se de um estudo descritivo com abordagem quantiqualitativa realizado em uma Unidade Básica e Distrital de Saúde (UBDS) de Ribeirão Preto, e que teve como sujeitos um grupo de mulheres, usuárias de um serviço de saúde, que compareceram a UBDS para consulta de puericultura. A coleta foi realizada através de entrevista, coleta de sangue para dosagem de hemoglobina e consulta aos prontuários. A idade das mulheres variou entre 19 a 24 anos, sendo que destas 36,3% apresentaram ensino fundamental incompleto e 75% referiu não trabalhar. Quanto a realização de pré-natal, 75% realizou em Centro ou Posto de Saúde tendo como média de consultas durante a gestação oito. Durante a gestação e o puerpério o valor médio de hemoglobina encontrado nas entrevistadas foi de 12,1 g/dl e 12 g/dl, respectivamente. Quanto ao uso de suplemento a base de ferro na gestação e puerpério, 81,8% referiu ter usado durante a gestação e 66,9% no puerpério. Assim, conseguimos identificar que a maioria das gestantes fez uso do suplemento durante a gestação e puerpério e que apresentaram hemoglobina maior que 11 g/dl, ou seja, não apresentavam anemia. Os dados qualitativos revelam que as mulheres desconhecem a importância do uso do suplemento neste período, sendo mais evidente a preocupação com a saúde do feto. / The supplement use the iron base is basic for Prophylaxis and treatment of the ferropriva anemia, I aggravate frequent in gestantes that live in paises in development, and that if it will not be treated, it can in such a way have consequences for woman how much for the embryo. However, many women do not adhere the therapeutical one. The objective of this study was to identify the use of supplement to the base of iron in the pregnant-puerperal cycle, in a group of mulheres.Trata-if of a descriptive study with carried through quantiqualitativa boarding in a Basic and District Unit of Saúde (UBDS) of Ribeirão Preto, and that a group of women had as citizens, users of a health service, who had appeared the UBDS for puericultura consultation. The collection was carried through through interview, collection of blood for dosage of hemoglobina and consults to handbooks. The age of the women varied enters the 19 24 years, being that of these 36.3% had presented incomplete basic education and 75% related not to work. How much the accomplishment of prenatal, 75% carried through in Center or Rank of Health having as average of consultations during gestation eight. During the gestation and the puerpério the average value of hemoglobina found in the interviewed ones was of 12,1 g/dl and 12 g/dl, respectively. How much to the supplement use the base of iron in the gestation and puerpério, 81.8% related to have used during gestation and 66.9% in the puerpério. Thus, we obtain to identify that the majority of the gestantes made use the supplement during the gestation and puerpério and that they had presented 11 bigger hemoglobina that g/dl, or either, they did not present anemia. The qualitative data disclose that the women are unaware of the importance of the use of the supplement in this period, being more evident the concern with the health of the embryo.

Orientador: Carmen Silvia Bertuzzo / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas / Made available in DSpace on 2018-08-07T00:23:33Z (GMT). No. of bitstreams: 1 Amstalden_LucilaGobby_M.pdf: 4346952 bytes, checksum: 99d5f1ab2aae2aeb65d633016bc318a8 (MD5) Previous issue date: 2006 / Resumo: A Anemia de Fanconi (AF) é uma doença caracterizada por múltiplas anomalias congênitas, progressiva falha da medula óssea e alto risco para desenvolvimento de câncer. E denominada também de Síndrome da Instabilidade Cromossômica devido ao fato de suas células apresentarem hipersensibilidade a agentes indutores de quebras cromossômicas. A mais importante das características clínicas é a manifestação hematológica. A incidência da anemia aplástíca, Síndrome Mieloplásica e Leucemia Mielóide Aguda é a maior resposável pela morbidade e mortalidade na AF A incidência da AF em todo o mundo é de. aproximadamente, 3 por milhão. No Brasil não há dados sobre a prevalência da doença. Foram descobertos 12 grupos de complementação e descobertos, até o momento. 11 genes relacionados ao distúrbio. São eles: FANCA. B, C, Dl, D2, E. F G, I, J, L e M. O trabalho teve como objetivo geral a análise das mutações principais (IVS8+2A>G, IVS11+lOC, IVS3+1G>C e 1794J803dellO) do gene FANCG em pacientes com quadro clínico compatível com AF. Foram analisados 38 indivíduos por meio da técnica de PCR associada à digestão e triagem por SSCP e subseqüente seqüenciamento. Nós encontramos um homozigoto para a mutação IVS8+2A>G e uma variante neutra (H482H). Concluímos com nosso estudo que, há uma heterogeneidade molecular em nosso meio; o DEB teste não é 100% eficaz na detecção de indivíduos com AF; o Teste de Complementação deve ser introduzido o quanto antes em nosso país para auxiliar no direcionamento da pesquisa para um determinado gene e minimizar os casos em que não há a confirmação de diagnóstico e, por último, há a necessidade de um Registro Brasileiro para AF com o objetivo de recolher informações clinicas e genéticas de indivíduos com o distúrbio. / Abstract: Fanconi anaemia (FA) is an autosomal recessive disease characterised by congenital abnormalities, progressive bone marrow failure and high risk of developing cancer. It's called Chromosomal Instability Syndrome due to the fact of cells presents hipersensibility to DNA cross-linking agents like mitomycin C and diepoxybutane. The most important clinical feature is hematologic. The incidence of aplastic anemia, myelodysplastic syndrome and acute myeloide leukaemia is the most important cause of morbidity and mortality in FA. The incidence of FA is approximately three per million and the heterozygote frequency is estimated at 1 in 300 in Europe and United States. In Brazil there's not data about prevalence of FA. It was discovered at least 12 complementation groups and eleven gene have been cloned: FANCA, B, C, DJ, D2, E, F, G, I, J, L eM. The study had as general objective the analysis of the main mutation (IVS8-2A>G, TVSll+lOC, IVS3+1G>C e 1794J803dell0) of FANCG gene in patients with clinical features of FA. It was analysed 38 patients through the test polymerase chain reaction (PCR) associated with digestion and mutation screening by SSCP with posterior sequencing. Molecular analysis found a homozygote to rVS8+2A>G and a neutral variant (H482H). We concluded that there's a molecular heterogeneity in our region; it's necessary to introduce the use of complementary tests in Brazil, in order to address the molecular analysis and at last, it's necessary a Brazilian Fanconi Anemia Registry (BFAR) to receive clinical and genetics information of AF patients. / Mestrado / Ciencias Biomedicas / Mestre em Ciências Médicas

Vários trabalhos têm mostrado que a ingestão deficiente de ferro pode causar alterações nos parâmetros morfológicos e bioquímicos do Sistema Nervoso Central (SNC) do rato assim como em seu comportamento. Também, os animais deficientes em ferro mostram redução no número de lamelas de mielina e déficits de aprendizado. Por outro lado, a estimulação tátil pode reduzir e/ou evitar os danos causados pela má nutrição sobre o SNC e comportamento. Entretanto, os danos no processo de mielinização têm também sido vistos na anemia ferro-deficiente e, uma vez que o nervo óptico é em grande parte formado pelos axônios mielinizados, o objetivo deste estudo é verificar os efeitos da anemia ferropriva e estimulação tátil sobre a morfologia do nervo óptico de ratos Wistar machos aos 18, 22 e 32 dias de idade. Os animais foram divididos em 2 grupos: Controles ( C ) (35 mg Fe / Kg de dieta), Anêmicos ( A ) (4 mg Fe / Kg de dieta). Cada grupo foi subdividido em Estimulado ( E ) e Não Estimulado ( N ). O peso corporal, hemoglobina, hematócrito, área, perímetro, diâmetro mínimo, densidade de células gliais e número de vasos no nervo óptico foram avaliados. Os animais foram anestesiados com éter sulfúrico e sacrificados por perfusão cardíaca com PBS 0,05 M em pH 7,3, seguido por paraformaldeído 2% mais glutaraldeído 1% em tampão fosfato 0,1 M (pH 7,3). O nervo óptico foi dissecado e imerso em solução de tetróxido de ósmio a 1% por duas horas a 40C, desidratado em acetona com graus de diluição crescentes e incluído em araldite. As amostras de nervo óptico foram orientadas para permitir cortes transversos de suas fibras. Secções de 0,5 m foram obtidas e coradas com azul de toluidina 1% antes de serem examinadas na microscopia de luz. Os estudos morfométricos foram feitos com um sistema analisador de imagens semi-automático (MiniMop). Os resultados mostram que a anemia levou a deficiências no peso corporal, hematócrito, hemoglobina, área, perímetro, diâmetro mínimo, número de células gliais e número de vasos do nervo óptico entre os anêmicos, e que a estimulação melhorou significativamente estes itens tanto em anêmicos quanto em controles (à exceção de hematócrito e hemoglobina) porém não recuperando totalmente os estes prejuízos provocados pela anemia. / Several works have been shown that the deficient ingestion of iron can cause alterations in the morphologic and biochemical parameters of the Central Nervous System (CNS) of the rat as well as in its behavior. Also, the iron deficient animals show reduction in the number of myelin lamellae and learning deficits. On the other hand, the tactile stimulation can reduce and/or to avoid the damages caused by the bad nutrition about CNS and behavior. However, the damages in the myelinization process have been seen also in the iron-deficient anemia and, at once that the optical nerve is formed largely by the myelinated axons, the objective of this study is to verify the effects of the anemia and tactile stimulation on the morphology of the optical nerve of Wistar males rats at the 18th, 22 nd and 32 nd days of age. The animals were divided in 2 groups: Controls © (35 mg Fe / diet Kg), Anemic (A) (4 mg Fe / diet Kg). Each group was subdivided in Stimulated (S) and No Stimulated (N). The corporal weight, haemoglobin, haematocrit, area, perimeter, minimum diameter, density of glial cells and number of vases were evaluated. The animals were anesthetized and sacrificed by heart perfusion with PBS 0,05 M in pH 7,3, following for paraformaldheyde 2% plus glutaraldheyde 1% in a phosphate buffer 0,1 M (pH 7,3). The optic nerve was dissected and submerged in solution of osmium tetroxide 1% for two hours at 40C, dehydrated in acetone with decreasing dilution degrees and included in araldite. The samples of optic nerve were guided to allow transverse cuts of their fibers. Sections sized 0,5 m were obtained and stained with toluidin blue 1% prior examinations in the light microscopy. The morphometric studies were made with a semiautomatic analyzing system of images (MiniMop). The results show that the anaemia caused differences in the corporal weight, haematocrit, haemoglobin, area, perimeter, minimum diameter, number of glial cells and vassels of the optical nerve among controls and anaemic, and that the stimulation influenced significantly on these items taking to the conclusion that it improves the damaged structures due to anaemia, but it doesn’t recover them totally.

The course of the haemopoietic response during canine babesiosis caused by Babesia rossi has not previously been studied. This prospective, descriptive longitudinal study on clinical cases describes the haematological kinetics during the first six days following treatment of natural babesiosis infection. Ninety client-owned dogs diagnosed with B rossi infection, based on examination of a Cam’s Quick-Stain-stained thin capillary blood smear and confirmed by polymerase chain reaction analysis, were included. At first consultation, 24 hours, three days and six days after first consultation, or until death, an EDTA sample was collected from the jugular or cephalic vein and submitted for a full automated blood count, using a CELL-DYN 3700 analyzer. Manual leukocyte differential counts were performed. Based on the treatment protocol, the dogs were divided into a blood transfusion group, and a non blood transfusion group. A slightly to moderately regenerative normocytic normochromic anaemia occurred throughout the study period for both treatment groups. The anaemia was very severe at presentation in dogs that received a blood transfusion and moderate at presentation in dogs that did not receive a blood transfusion. Anaemia was still present by the end of the study period in both treatment groups. The regenerative response was moderate in severely anaemic dogs and mild in moderately anaemic dogs. A mild inflammatory leukocytic response was found in both treatment groups. The median segmented neutrophil count for both treatment groups was within the reference interval throughout the study period. A left shift occurred more commonly in dogs that received a blood transfusion, and was significantly influenced by the degree of anaemia at presentation. In dogs with a left shift, a degenerative left shift, not influenced by the degree of anaemia at presentation, was found more commonly. Severe thrombocytopaenia for both treatment groups, which resolved within a week in both groups, was found. Treatment with a blood transfusion reduced the anaemia, but had no significant effect on white blood cell or platelet responses. Blood cell responses were not significantly influenced by age, previous infection with babesiosis or duration of illness. / Dissertation (MSc (Veterinary Science))--University of Pretoria, 2008. / Companion Animal Clinical Studies / unrestricted