No description available.

Doctor of Philosophy / Pup mortality is reported to be a significant problem in the dog. The purpose of this thesis was to identify the extent and causes of the mortality and the risk factors. Mortality was classified according to the clinical condition of the pup at birth and the pathological investigation was designed to investigate the validity of this classification. Total pup mortality, excluding elective euthanasia for show reasons, was 18.5%. Perinatal mortality, that is, stillbirths and deaths that occurred in the first week, accounted for 90.9% of these losses. Each breed surveyed exhibited a specific mortality pattern and the results of one breed could not be used to anticipate the outcome in another breed. As a consequence of this, there was a marked difference in the predictor variables, or risk factors, identified for each breed. Birth weight and inter-pup whelping intervals were the most consistent variables that increased the odds of a pup dying. The principal cause of pup mortality was attributed to foetal asphyxia, that is, apparently normal pups subjected to excessive hypoxia during the birth process and they were either still born or born in a distressed condition and subsequently died. Death attributed to foetal asphyxia accounted for 7.8% of all pups born and 42.5% of the total mortality. The majority of these pups (82.2%) died during whelping or in the first 24 hours after birth. The death of just over half of these pups could be directly attributed to dystocia. The remaining pups were compromised during what appeared to be a normal whelping. Neonatal atelectasis, pulmonary congestion, inhalation of amniotic fluid and meconium, leptomeningeal and generalised systemic congestion were the principal pathological findings in these pups. Average birth weights, inter-pup whelping intervals, parity, pup presentation and litter position were all significant predictors of mortality due to foetal asphyxia. The abnormal pup was defined as a pup at birth that was mummified, had died prior to birth, was small for date or had gross congenital defects present. These accounted for the death of 4.9% of all pups born and 26.3% of all losses. The only significant predictors of mortality due to the birth of an abnormal pup were the inter-pup interval and birth weight. Since the abnormality occurred in utero and was not related to the birth process this result had no bearing on the outcome. The death of live born, apparently normal pups, in the neonatal period accounted for 5.7% of all pups born and 31.2% of the total mortality. Over half these losses were attributed to fading puppy syndrome. The remainder were due to mismothering / mismanagement and other miscellaneous causes. The majority of fading pups examined were not normal at birth. Growth retardation and the consequent increased susceptibility to foetal hypoxia, lung pathology indicative of foetal asphyxia and intrauterine and/or very early neonatal infections were the principal causes of mortality attributed to fading puppy syndrome identified in this study. The canine perinate is totally dependent on the bitch both in the uterus and in the immediate post partum period. The investigation of pup mortality can not be divorced from the assessment of maternal health, the influence of the whelping process and the post whelping care of the immature pups by the bitch. These factors must be correlated with gross and histological changes identified in dead pups to determine the sequence of events that contributed to the death of the whelp.

Doctor of Philosophy / Pup mortality is reported to be a significant problem in the dog. The purpose of this thesis was to identify the extent and causes of the mortality and the risk factors. Mortality was classified according to the clinical condition of the pup at birth and the pathological investigation was designed to investigate the validity of this classification. Total pup mortality, excluding elective euthanasia for show reasons, was 18.5%. Perinatal mortality, that is, stillbirths and deaths that occurred in the first week, accounted for 90.9% of these losses. Each breed surveyed exhibited a specific mortality pattern and the results of one breed could not be used to anticipate the outcome in another breed. As a consequence of this, there was a marked difference in the predictor variables, or risk factors, identified for each breed. Birth weight and inter-pup whelping intervals were the most consistent variables that increased the odds of a pup dying. The principal cause of pup mortality was attributed to foetal asphyxia, that is, apparently normal pups subjected to excessive hypoxia during the birth process and they were either still born or born in a distressed condition and subsequently died. Death attributed to foetal asphyxia accounted for 7.8% of all pups born and 42.5% of the total mortality. The majority of these pups (82.2%) died during whelping or in the first 24 hours after birth. The death of just over half of these pups could be directly attributed to dystocia. The remaining pups were compromised during what appeared to be a normal whelping. Neonatal atelectasis, pulmonary congestion, inhalation of amniotic fluid and meconium, leptomeningeal and generalised systemic congestion were the principal pathological findings in these pups. Average birth weights, inter-pup whelping intervals, parity, pup presentation and litter position were all significant predictors of mortality due to foetal asphyxia. The abnormal pup was defined as a pup at birth that was mummified, had died prior to birth, was small for date or had gross congenital defects present. These accounted for the death of 4.9% of all pups born and 26.3% of all losses. The only significant predictors of mortality due to the birth of an abnormal pup were the inter-pup interval and birth weight. Since the abnormality occurred in utero and was not related to the birth process this result had no bearing on the outcome. The death of live born, apparently normal pups, in the neonatal period accounted for 5.7% of all pups born and 31.2% of the total mortality. Over half these losses were attributed to fading puppy syndrome. The remainder were due to mismothering / mismanagement and other miscellaneous causes. The majority of fading pups examined were not normal at birth. Growth retardation and the consequent increased susceptibility to foetal hypoxia, lung pathology indicative of foetal asphyxia and intrauterine and/or very early neonatal infections were the principal causes of mortality attributed to fading puppy syndrome identified in this study. The canine perinate is totally dependent on the bitch both in the uterus and in the immediate post partum period. The investigation of pup mortality can not be divorced from the assessment of maternal health, the influence of the whelping process and the post whelping care of the immature pups by the bitch. These factors must be correlated with gross and histological changes identified in dead pups to determine the sequence of events that contributed to the death of the whelp.

No description available.

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

Please read the abstract in the section 00front of this document / Canine babesiosis, caused by the tick-borne protozoan Babesia canis rossi, is an economically important and potentially fatal disease of dogs in South Africa. The host's response to many infectious diseases is mediated (at least in part) by intercellular messengers called cytokines. One of the most important cytokines released is tumour necrosis factor (TNF). A study was designed to measure serum concentrations of TNF in dogs naturally infected with canine babesiosis and to relate TNF concentrations to clinical severity, mortality, rectal temperature and parasitaemia. There was a statistically significant difference in TNF concentrations between groups of differing disease severity, with a general trend of increasing mean 10g(TNF) with increasing severity of disease. A noteworthy finding was that dogs with hypoglycaemia had very high TNF (mean 15.03 nglml compared to a mean of 2.32 nglml for other sick dogs without hypoglycaemia). When TNF values were compared between survival and non-survival groups, there was no significant difference. The rectal temperature of the dogs in this study did not show any statistically significant association with TNF concentrations. When parasitaemia and TNF were examined within groups of infected dogs, there was no significant relationship. However, when the sample size was increased by pooling all infected dogs and treating them as a single group, there was a highly significant positive correlation (p = 0.003) between parasitaemia and serum TNF concentrations. The results ofthis study were encouraging and indicate that canine babesiosis may share a similar pathophysiology with human malaria in terms ofTNF being associated with disease severity. One ofthe most significant findings in this study was the presence ofvery high TNF values in two ofthree dogs with hypoglycaemia. Hypoglycaemia has not been previously recorded in dogs with babesiosis and is a potentially important finding particularly in view ofthe hypoglycaemia associated with malaria in humans. Malarial hypoglycaemia is correlated with a higher mortality in humans, especially in pregnant women and children. If the findings ofthis study can be Vl confinned and expanded, they may lend further support to the use of canine babesiosis as a model for some ofthe problems encountered in human malaria research. / Dissertation (MMed Vet (Med))--University of Pretoria, 2001. / Companion Animal Clinical Studies / unrestricted

A hypercoagulable state has been demonstrated in human falciparum malaria in mild and complicated forms of the disease. Disseminated intravascular coagulation (DIC) was implicated by some authors, but deemed a rare occurrence by others. The possibility of coagulopathy in Babesia canis rossi infections in the canine patient has also been suggested in the literature, but minimal work has been done to evaluate the clinicopathological nature of it in further detail. In the canine babesiosis (CB) pathogenesis thought-process, DIC has been implicated. A DIC-like syndrome, as evidenced by intravascular fibrin deposition and haemorrhage into muscles and tissues was found at post mortem in one study. On the basis of these findings, it was postulated that DIC might be a serious complication of severe Babesia infection in the dog. Clinical DIC (haemorrhagic diathesis) is however seldom seen. It was also hypothesised in the literature that the multiple organ dysfunction syndrome (MODS) demonstrated in the complicated form of Babesia was caused, in addition to tissue damage due to local hypoxia, by microthrombi as a result of a coagulopathy. This needs to be further investigated. Pulmonary thromboembolism (PTE) has not been implicated in CB, however thromboemboli in the lungs were found in dogs with immune-mediated haemolytic anaemia (IMHA) for which a similar mechanism of venous stasis, hypercoagulability and endothelial damage (as found in CB) is proposed. In humans, PTE is believed to be a major underdiagnosed contributor to mortality in 5 to 15% of hospitalised adults. If early diagnosis of PTE can be achieved, the mortality rate can certainly be decreased. A similar situation with resultant serious implications in complicated CB cases may exist. Clinically, PTE is suspected if a patient with a known prothrombotic condition develops sudden dyspnoea and tachypnoea. These clinical symptoms are frequently seen in complicated CB patients and may, in addition to being a compensatory mechanism for the metabolic acidosis and anaemia, be attributed to thrombus-induced mechanical changes in lung function. Pulmonary scintigraphy provides a sensitive means of diagnosing PTE. It was (and some authors still do) believed that a ventilation scintigraphic scan should be done in association with a perfusion scan to increase the specificity and accuracy of diagnoses. However, authors of the recent PISA-PED study in humans proposed that the sensitivity and specificity of a perfusion scan, without a ventilation scan, in patients with suspected PTE was sufficient. The incidence of PTE or the use of pulmonary perfusion scintigraphy in CB dogs has never been studied. The objective of this study was to prospectively evaluate the scintigraphic pulmonary perfusion pattern in hospitalised Babesia dogs in an attempt to ascertain whether a scintigraphic pattern consistent with PTE does indeed occur in these patients. The study consisted of a normal control group of nine mature healthy Beagle dogs aged 36 – 43 months and weighing 9.9 – 15kg and a Babesia group with 14 dogs of a variety of breeds that were naturally infected with Babesia, aged 6 – 103 months and weighing 6.3 – 25.5kg. Pulmonary perfusion scintigraphy was performed after making thoracic radiographs and performing a blood gas analysis in both groups. The scintigraphic images were visually inspected for changes suggestive of PTE. Surprisingly, not a single dog in the Babesia group had segmental or wedge-shaped perfusion defects which would have resulted in a high probability for PTE. The scintigraphic pulmonary perfusion pattern demonstrated was not significantly different between the two groups (p = 1.00). Many dogs in both groups had a mottled appearance on the right and left dorsal oblique images, which was not believed to be consistent with clinically relevant PTE. This study provides baseline data that may be used to further investigate the pulmonary perfusion pattern in Babesia dogs. / Dissertation (MMedVet (Diagnostic Imaging))--University of Pretoria, 2007. / Companion Animal Clinical Studies / unrestricted

Background and objecttives: The aims of this study were to determine whether: i) diseases in hospitalised South African dogs with leukocyte counts ≥35x109/l were different from, ii) hospitalisation time longer than and mortality rate higher than control dogs; iii) glucocorticoid treatment contributed to significant leukocytosis; iv) hypoalbuminaemia and thrombocytopaenia added prognostic value, v) high leukocyte counts predict complicated babesiosis. Methods: Records were examined from 182 hospitalized dogs with a WBC ≥35Χ109/l (LCG) and 179 hospitalized dogs with 3.0 ≤ WBC ≤30Χ109/l and immature neutrophil count ≤0.5Χ109/l (CG). Diagnoses were assigned to groups Infection, Immune-mediated; Necrosis; Neoplasia; Babesiosis; Other. Results: WBC, neutrophil count, lymphocyte count and monocyte count were higher in LCG than CG (p<0.0001) while eosinophil count was lower in LCG than CG (p<0.0001). Hct, platelet count, and serum albumin concentration were lower in LCG than CG (p<0.0001). There was no difference in neutrophil count, lymphocyte or monocyte count between glucocorticoid-treated and non-glucocorticoid-treated dogs in LCG. Disease frequencies differed significantly (LCG > CG) in Infection, Necrosis, Babesiosis and immune mediated haematological disease groups. The frequency of complicated babesiosis cases was higher in LCG in than in CG (p < 0.0001). Time of hospitalization was significantly (p<0.0001) longer for LCG than for CG. There was a significant relationship between total and immature neutrophil count and survival (p=0.01) Conclusions: Leukocytosis is more likely to indicate infection, complicated babesiosis, immune mediated hematological disease or necrosis in the population of dogs examined. Hypoalbuminaemia and thrombocytopaenia in an animal with significant leukocytosis is not prognostically useful, while the combination of total and immature neutrophil count is. In hospitalized animals with severe leukocytosis, glucocorticoid treatment does not increase the leukocyte count. / Dissertation (MMedVet)--University of Pretoria, 2007. / Companion Animal Clinical Studies / unrestricted

Studies comparing canine distemper virus (CDV) strains from Africa with that of previously described lineages have been hampered due to a lack of field strains for in vitro experiments. There are no reports of CDV isolations in southern Africa, and although CDV is said to have geographically distinct lineages, molecular information of African strains has not yet been documented. Clinical specimens consisting of whole blood, spleen, lungs, brain and cerebrospinal fluid from dogs with clinical signs suggestive of distemper were obtained from private veterinary practices and diagnostic laboratories in Gauteng province, South Africa. One hundred and sixty two specimens from 124 dogs were inoculated into Vero cells expressing canine signalling lymphocyte activation molecule (Vero.DogSLAM). Cytopathic effects (CPE) in the form of syncytia formation and cell necrosis were observed in 33 (20.4%) specimens within 24 hours of inoculation and the presence of CDV was confirmed with the aid of the direct fluorescent antibody test and electronmicroscopy (EM). Viruses isolated in cell cultures were subjected to reverse transcription – polymerase chain reaction (RT-PCR), and the complete H gene was sequenced and phylogenetically analysed with other strains from GenBank. The animals all displayed the catarrhal, systemic, or nervous signs of the disease. Four of the dogs positive for CDV by viral isolation had a history of prior vaccinations to canine distemper. Seventy three percent of all positive dogs were less than 12 months old. There was no breed or sex predisposition to CDV infection in domestic dogs. Phylogenetic comparisons of the complete H gene of CDV isolates from different parts of the world (available in GenBank) with wild-type South African isolates revealed nine clades. All South African isolates form a separate African clade of their own and thus are clearly separated from the American, European, Asian, Arctic and vaccine virus clades. It is likely that only the ‘African lineage’ of CDV may be circulating in South Africa currently, and the viruses isolated from dogs vaccinated against CDV are not the result of reversion to virulence of vaccine strains, but infection with wild-type strains. Copyright / Dissertation (MSc)--University of Pretoria, 2008. / Veterinary Tropical Diseases / unrestricted

Canine parvoviral enteritis is an economically important disease in South Africa and globally. Although treatment of dogs with parvoviral enteritis is often successful, many dogs die of complications related to septicaemia or are euthanized because of anticipated high costs. More effective prediction of the outcome of this disease will have an economic impact if a prognosis can be determined early in the course of the disease. Although leukocyte responses seldom are pathognomonic for a specific disease, they can provide clinical information to establish a fairly reliable prognosis. A prospective study was performed on 62 puppies presented to the OVAH with typical clinical signs of canine parvoviral enteritis that subsequently was confirmed on electron microscopy. Full haematology was performed at admission as well as every consecutive day until death or discharge. Of the 11 puppies that died (18%), nine died due to complications of the disease and two were euthanized due to financial restrictions and a poor prognosis. The puppies that died due to the disease died within the first three days of hospitalization. All the puppies that died were sent for a full post mortem examination and histopathological evaluation. Statistical analysis of the data showed that there was a definite difference between the puppies that died and those that survived in several of the leukocyte parameters. These parameters included the total leukocyte, lymphocyte, monocyte and eosinophil counts. In none of the puppies that died from the disease did the total leukocyte count rise above 2.0 × 10 9 /l (normal reference range: 6.0-15.0 × 10 9 /l). In the puppies that survived, the total leukocyte count started rising within 24 – 48 hours after admission and often resulted in a rebound leukocytosis. The puppies that died did not develop lymphocytosis to indicate an immune response, whereas the surviving puppies developed lymphocytosis within 24 – 48 hours after admission. The puppies that died also did not develop monocytosis and remained severely eosinopaenic during the course University of Pretoria etd – Goddard, A (2006) xii of the disease. Evidence of impaired leukocyte production was found on histopathology. Most of the puppies that died from the disease showed marked to severe thymic and lymphoid atrophy and marked to severe bone marrow hypocellularity. These results show that a reliable prognosis can be obtained at 24 and 48 hours after admission by evaluation of the leukocytes, specifically the total leukocyte, lymphocyte, monocyte and eosinophil counts. / Dissertation (Master in Veterinary Medicine(Clinical Laboratory Diagnostics))--University of Pretoria, 2006. / Companion Animal Clinical Studies / unrestricted