The development of comprehension and reading-related skills in children learning English as an additional language and their monolingual, English-speaking peers.

BACKGROUND: A significant number of pupils in UK schools learn English as an additional language (EAL). Relative differences between the educational attainment of this group and monolingual, English-speaking pupils call for an exploration of the literacy needs of EAL learners. AIMS: This study explores the developmental progression of reading and listening comprehension skills and a range of reading-related skills in EAL learners, whose first language is of South Asian origin, and their monolingual peers. SAMPLE: Participants were 39 children learning EAL and 39 monolingual, English-speaking children who were all in school Year 3 at the start of the study. METHOD: Children completed standardized measures of comprehension, vocabulary, reading accuracy, and reading fluency in school Year 3 and again in Year 4. RESULTS: The results suggest that, although children learning EAL often demonstrate fast and accurate reading accuracy skills, lower levels of vocabulary knowledge place significant constraints on EAL learners' comprehension of spoken and written texts. CONCLUSIONS: Reciprocal relationships between vocabulary and comprehension may lead to increasing gaps in reading comprehension between monolingual and EAL pupils over time. It is proposed that support for the development of vocabulary skills in children learning EAL is needed in early years' classrooms.

The comprehension skills of children learning English as an additional language.

BACKGROUND: Data from national test results suggests that children who are learning English as an additional language (EAL) experience relatively lower levels of educational attainment in comparison to their monolingual, English-speaking peers. AIMS: The relative underachievement of children who are learning EAL demands that the literacy needs of this group are identified. To this end, this study aimed to explore the reading- and comprehension-related skills of a group of EAL learners. SAMPLE: Data are reported from 92 Year 3 pupils, of whom 46 children are learning EAL. METHOD: Children completed standardized measures of reading accuracy and comprehension, listening comprehension, and receptive and expressive vocabulary. RESULTS: Results indicate that many EAL learners experience difficulties in understanding written and spoken text. These comprehension difficulties are not related to decoding problems but are related to significantly lower levels of vocabulary knowledge experienced by this group. CONCLUSIONS: Many EAL learners experience significantly lower levels of English vocabulary knowledge which has a significant impact on their ability to understand written and spoken text. Greater emphasis on language development is therefore needed in the school curriculum to attempt to address the limited language skills of children learning EAL.

Murine cytomegalovirus infection alters Th1/Th2 cytokine expression, decreases airway eosinophilia, and enhances mucus production in allergic airway disease.

Concomitant infection of murine CMV (MCMV), an opportunistic respiratory pathogen, altered Th1/Th2 cytokine expression, decreased bronchoalveolar lavage (BAL) fluid eosinophilia, and increased mucus production in a murine model of OVA-induced allergic airway disease. Although no change in the total number of leukocytes infiltrating the lung was observed between challenged and MCMV/challenged mice, the cellular profile differed dramatically. After 10 days of OVA-aerosol challenge, eosinophils comprised 64% of the total leukocyte population in BAL fluid from challenged mice compared with 11% in MCMV/challenged mice. Lymphocytes increased from 11% in challenged mice to 30% in MCMV/challenged mice, and this increase corresponded with an increase in the ratio of CD8(+) to CD4(+)TCRalphabeta lymphocytes. The decline in BAL fluid eosinophilia was associated with a change in local Th1/Th2 cytokine profiles. Enhanced levels of IL-4, IL-5, IL-10, and IL-13 were detected in lung tissue from challenged mice by RNase protection assays. In contrast, MCMV/challenged mice transiently expressed elevated levels of IFN-gamma and IL-10 mRNAs, as well as decreased levels of IL-4, IL-5, and IL-13 mRNAs. Elevated levels of IFN-gamma and reduced levels of IL-5 were also demonstrated in BAL fluid from MCMV/challenged mice. Histological evaluation of lung sections revealed extensive mucus plugging and epithelial cell hypertrophy/hyperplasia only in MCMV/challenged mice. Interestingly, the development of airway hyperresponsiveness was observed in challenged mice, not MCMV/challenged mice. Thus, MCMV infection can modulate allergic airway inflammation, and these findings suggest that enhanced mucus production may occur independently of BAL fluid eosinophilia.

Changes in susceptibility to acetaminophen-induced liver injury by the organic anion indocyanine green.

The non-metabolizable organic anion indocyanine green (ICG) has been shown previously to reduce markedly the biliary secretion of acetaminophen, particularly the glutathione conjugate of APAP (APAP-GSH), suggesting that this APAP metabolite may compete with other xenobiotics for excretion into the bile via a canalicular organic anion transport process. This study was conducted to determine whether changes in the biliary disposition of APAP induced by ICG could lead to alterations in susceptibility to APAP hepatotoxicity. To investigate this, groups of overnight-fasted male CD-1 mice received 30 micromol ICG/kg, intravenously, immediately prior to APAP dosing (500 mg/kg, ip). Controls were given propylene glycol vehicle. Mice were killed at 4 h after APAP challenge for immunochemical analysis of cytosolic protein arylation and determination of non-protein sulfhydryl (NPSH) depletion, or at 12 and 24 h for biochemical and histological assessment of liver injury. Elevated plasma sorbitol dehydrogenase activity and centrilobular hepatocellular necrosis was present in control mice receiving APAP at 12 and 24 h. Treatment with ICG did not alter susceptibility to APAP toxicity when measured at 12 h after challenge. However, the severity of histologic lesions in the ICG-APAP group was significantly lower at 24 h after challenge. Furthermore, treatment with ICG did not alter APAP-induced glutathione depletion or cytosolic protein arylation. These data suggest that the organic anion ICG has a protective effect on APAP toxicity that promotes a faster recovery from liver injury.

Ribose cysteine protects against acetaminophen-induced hepatic and renal toxicity.

Ribose cysteine (RibCys) is a cysteine prodrug that increases both hepatic and renal glutathione with documented antagonism of acetaminophen (APAP)-induced hepatotoxicity. To determine if RibCys could also protect against APAP-induced kidney damage, mice were injected with APAP (600 mg/kg) or APAP and RibCys (1.0 g/kg) (APAP/RIB) followed by additional RibCys injections 1 and 2 hours later. Mice were euthanatized 10-12 hours after APAP administration, and liver and kidney toxicity were assessed by plasma sorbitol dehydrogenase (SDH) activity and blood urea nitrogen (BUN), respectively, and by histopathology. APAP treatment resulted in elevation of SDH activity and BUN to 2,490 U/ml and 47 mg/dl, respectively. By contrast, SDH and BUN values for APAP/RIB-treated mice were not different from controls, 0 U/ml and 31 mg/dl, respectively. Histopathologic examination revealed moderate to severe hepatic centrilobular necrosis in 9/11 and renal proximal tubular necrosis in 10/11 APAP-treated mice. However, no evidence of hepatic or renal toxicity was noted in any of the 12 APAP/RIB-treated mice. Utilizing the same treatment regimen, APAP covalent binding to hepatic and renal cytosolic proteins was assessed 4 hours after APAP challenge. RibCys cotreatment decreased covalent binding to the 58-kDa acetaminophen-binding protein in both liver and kidney. RibCys decreased both toxicity and covalent binding after APAP administration, and in addition to protecting the liver, this cysteine prodrug can also effectively protect the kidney from APAP-induced injury.

Peroxisome proliferator-activated receptor alpha-null mice lack resistance to acetaminophen hepatotoxicity following clofibrate exposure.

The purpose of this study was to investigate whether activation of the nuclear receptor PPARalpha is needed for protection from acetaminophen (APAP) hepatotoxicity produced by repeated administration of the peroxisome proliferator clofibrate (CFB). Female wild-type and PPARalpha-null mice received corn oil vehicle or 500 mg CFB/kg, ip, daily for 10 days. They were then fasted overnight (18 h) and either killed at 4 or 24 h after challenge with 400 mg APAP/kg. Controls received 50% propylene glycol vehicle only. In this model of CFB hepatoprotection, liver injury was assessed by measuring plasma sorbitol dehydrogenase activity and by histopathology at 24 h after APAP challenge. Significant hepatocellular necrosis was evident in both corn oil-pretreated PPARalpha-null and wild-type mice at 24 h after APAP challenge. In agreement with previous studies, CFB-pretreated wild-type mice showed marked protection against APAP toxicity. In contrast, CFB did not provide protection against APAP hepatotoxicity in the PPARalpha-null mice. Similarly, at 4 h after APAP challenge, hepatic glutathione depletion and selective arylation of cytosolic proteins were reduced significantly in CFB-pretreated wild-type mice, but not in PPARalpha-null mice. The lack of changes in APAP binding and NPSH depletion in CFB-pretreated, PPARalpha-null mice is consistent with the presence of significant liver injury at 24 h in this treatment group. These findings demonstrate that the protection against APAP hepatotoxicity by peroxisome proliferator treatment is mediated by the activation of PPARalpha.

Evaluation of short-term increased intraocular pressure on flash- and pattern-generated electroretinograms of dogs.

OBJECTIVE: To determine the electrodiagnostic and histologic response of short-term increases of intraocular pressure (IOP) on transient pattern electroretinograms (PERG) and flash electroretinograms (FERG) in the eyes of dogs. ANIMALS: 8 healthy mixed-breed dogs. PROCEDURE: Transient PERG and FERG waveforms were recorded from dogs (while anesthetized) as IOP was increased from baseline (7 to 19 mm Hg) to 90 mm Hg. One hundred mean PERG responses and a single FERG response were recorded at each step during 3 recording sessions. Globes of each dog were enucleated after euthanasia on posttreatment day 7 and evaluated by a pathologist. RESULTS: Increases in spatial frequency resulted in decreased amplitudes of N2 (second negative PERG peak). Increases in IOP resulted in decreases in all 3 PERG waveforms and the FERG waveform. All values began to return to baseline after short-term increases in IOP on day 0, and waveforms were not significantly different on posttreatment days 3 and 7 CONCLUSIONS: Data suggest that short-term increases in IOP affect PERG and FERG waveforms, and PERG waveforms are more sensitive to increases in IOP Differences were not detected between treated and control eyes on histologic examination. Further studies are necessary to determine at what IOP permanent damage to ganglion and photoreceptor cells will develop and whether PERG is a reliable clinical diagnostic technique for use in dogs to reveal retinal damage that is secondary to increased IOP prior to changes in waveforms generated by FERG in dogs.

Sequential and morphological analyses of aberrant crypt foci formation in mice of differing susceptibility to azoxymethane-induced colon carcinogenesis.

Aberrant crypt foci (ACF), putative preneoplastic lesions, are early morphological changes induced by the colon carcinogen azoxymethane (AOM). Although inbred mice differ markedly in their susceptibility to AOM carcinogenesis, we have previously shown that ACF develop in both resistant and sensitive mouse strains after AOM treatment. The purpose of this study was to examine the sequential development and identify the morphological characteristics of ACF induced by AOM in the distal colon of sensitive and resistant mice. A/J (highly susceptible), SWR/J (relatively susceptible) and AKR/J (resistant) mice were treated with 10 mg/kg AOM or saline i.p. once a week for 6 weeks and were killed at 1, 2, 4, 6, 9 and 24 weeks after the last injection. The distal colons were stained with methylene blue and the numbers of ACF and tumors determined. Tumors were present as early as 4 weeks after AOM exposure in SWR/J and A/J mice and increased in frequency throughout the study in both strains. No tumors developed in the AKR/J mice. ACF, however, formed in all strains of mice. The greatest difference between susceptible and resistant strains was in the number of large ACF that developed at later time points. Furthermore, morphometric analysis revealed that A/J mice had the highest percentage of dysplastic ACF, followed by SWR/J mice. These data indicate that the difference in cancer risk from AOM may be due to the lack of progression of smaller ACF in the resistant mice and to the development of dysplasia in a higher percentage of ACF from susceptible strains.

Proinflammatory roles of T-cell receptor (TCR)gammadelta and TCRalphabeta lymphocytes in a murine model of asthma.

The role of lymphocytes bearing alphabeta or gammadelta T-cell receptors (TCRs) was assessed during the acute allergic response in a mouse model of asthma. The inflammatory immune response to ovalbumin (OVA) was characterized in wild-type C57BL/6J mice and congenic TCRbeta(-/-) and TCRdelta(-/-) mice by evaluation of airway eosinophilia, histopathology, serum immunoglobulin (Ig)E levels, and in vivo airway responsiveness to methacholine. OVA-challenged wild-type mice demonstrated marked pulmonary inflammation, evidenced by airway eosinophilia (68 +/- 7 x 10(4) cells), peribronchial lympho-plasmocytic infiltration, and elevated serum IgE (4.9 +/- 0.6 microg/ml). These responses were markedly attenuated in TCRdelta(-/-) animals (5.0 +/- 1.0 x 10(4) eosinophils and 1.6 +/- 0. 3 microg/ml IgE) and were completely absent in TCRbeta(-/-) mice (< 1 x 10(3) eosinophils and 0.38 +/- 0.21 microg/ml IgE). Similar results were observed in mice treated with anti-TCRgammadelta or anti-TCRalphabeta monoclonal antibodies. Airway responsiveness to aerosolized methacholine was also reduced in challenged TCRdelta(-/-) animals relative to challenged wild-type mice. These results demonstrate that acute allergic airway responses are dependent upon intact TCRalphabeta and TCRgammadelta lymphocyte function and that TCRgammadelta cells promote acute airway sensitization.

The PPAR activator docosahexaenoic acid prevents acetaminophen hepatotoxicity in male CD-1 mice.

Acetaminophen (APAP)-induced hepatocellular necrosis can be prevented by treatment with peroxisome proliferators. This protection is associated with lowered protein arylation and glutathione depletion in mice. Peroxisome proliferators have been shown to activate nuclear receptors. These receptors, termed peroxisome proliferator activated receptors (PPARs), can also be activated by free fatty acids. This study was designed to determine if treatment with the PPAR activator docosahexaenoic acid (DHA) would also lower APAP toxicity. Male CD-1 mice received 250 mg DHA/kg or 500 mg clofibrate (CFB)/kg, i.p., for 5 d. Controls received corn oil vehicle, i.p. After overnight fasting, mice received 800 mg APAP/kg, p.o. At 24 h after APAP, hepatotoxicity was evident in control mice by elevated plasma sorbitol dehydrogenase activity (SDH) and histologic evidence of hepatic degeneration and necrosis. As expected, CFB pretreatment significantly decreased this. Similarly, DHA protected against APAP-induced hepatotoxicity at 24 h after challenge. However, treatment with DHA did not increase hepatic glutathione prior to APAP, as previously shown with CFB. Interestingly, DHA did not increase palmitoyl coenzyme A (CoA) oxidase activity or other biochemical parameters associated with peroxisome proliferation after 5 d of treatment at 250 mg/kg. No significant alterations in microsomal APAP glucuronidation or cytochrome P-450-mediated bioactivation were detected either. Collectively, these results show that DHA also prevents APAP-induced hepatotoxicity at 24 h after challenge. However, the association between resistance against APAP-induced liver injury, PPAR activation, and peroxisome proliferation is not clearly understood.

Shifts in lung lymphocyte profiles correlate with the sequential development of acute allergic and chronic tolerant stages in a murine asthma model.

T lymphocytes have a central regulatory role in the pathogenesis of asthma. We delineated the participation of lymphocytes in the acute allergic and chronic tolerant stages of a murine model of asthma by characterizing the various subsets of lymphocytes in bronchoalveolar lavage and lung tissue associated with these responses. Acute (10-day) aerosol challenge of immunized C57BL/6J mice with ovalbumin resulted in airway eosinophilia, histological evidence of peribronchial and perivascular airway inflammation, clusters of B cells and TCRgammadelta cells in lung tissue, increased serum IgE levels, and airway hyperresponsiveness to methacholine. In mice subjected to chronic (6-week) aerosol challenge with ovalbumin, airway inflammation and serum IgE levels were significantly attenuated and airway hyperresponsiveness was absent. The marked increases in lung B and T cell populations seen in the acute stage were also significantly reduced in the chronic stage of this model. Thus, acute ovalbumin challenge resulted in airway sensitization characteristic of asthma, whereas chronic ovalbumin challenge elicited a suppressed or tolerant state. The transition from antigenic sensitization to tolerance was accompanied by shifts in lymphocyte profiles in the lung and bronchoalveolar lavage fluid.

Quantitative assessment of azoxymethane-induced aberrant crypt foci in inbred mice.

Heritable differences in tumor susceptibility are observed in mice after repetitive exposures to the organotropic colon carcinogen azoxymethane (AOM). The following study was undertaken to determine whether early morphological alterations within the colonic epithelium correlate with subsequent cancer risk. A/J and SWR/J (susceptible) and AKR/J (resistant) mice were injected once a week with AOM at a dose of 10 mg/kg, i.p., for a total of 6 weeks. Four weeks after the last injection, methylene blue-stained whole-mount colons were examined for the presence of colonic epithelial lesions referred to as aberrant crypt foci (ACF). Putative lesions identified under low magnification were further characterized by H&E staining of corresponding sections. AOM produced a treatment-related increase in ACFs in each of the mouse lines examined. The tumor-susceptible SWR/J and A/J mice developed on average between three- and sixfold more ACFs in the distal colon (32 and 15/cm of colon, respectively) than the resistant AKR/J mice (5/cm colon). The size distribution of ACFs was further analyzed in each of the strains. In SWR/J and A/J, 20-35% of lesions were classified as large ACFs, consisting of 5 or more aberrant crypts per focus. This is in striking contrast to the size distribution of lesions identified in the AKR/J colons, where fewer than 5% of grossly identified lesions were classified as large. In fact, the majority (> 80%) of ACFs in AKR/J mice consisted of only 1-2 aberrant crypts@focus. In addition, there was no evidence of dysplasia in any of the AKR/J lesions examined, whereas the lesions in susceptible mice were dysplastic (adenomas). Our data indicate that tumorigenic response is associated with the extent and multiplicity of ACFs that form within the colonic epithelium at an early time point after carcinogen exposure. These studies further support the use of this morphological biomarker as a short-term endpoint of colon tumorigenesis.

Repeated dosing with the peroxisome proliferator clofibrate decreases the toxicity of model hepatotoxic agents in male mice.

Pretreatment of mice with clofibrate (CFB) has been shown to protect against acetaminophen (APAP) hepatotoxicity. To determine if pretreatment with CFB prevents the toxicity of other model hepatotoxicants, male C57BL6J or CD-1 mice received 500 mg CFB/kg, i.p., daily for 10 days, and then were challenged with either 250 mg bromobenzene (BrB)/kg, 0.025 ml carbon tetrachloride (CCl4)/kg or 0.5 ml chloroform (CHCl3)/kg. Liver and kidney injury was assessed by plasma sorbitol dehydrogenase activity (SDH) and blood urea nitrogen (BUN), respectively and histopathology. Challenge with BrB significantly elevated plasma SDH activity in C57Bl6J mice. This was prevented in CFB pretreated mice receiving the same dose of BrB. Changes in BUN were not detected in either group of BrB treated mice. Similarly, pretreatment of male CD-1 mice with CFB significantly reduced CCl4-induced elevation in plasma SDH activity, with no BUN elevation detected in either group. CFB pretreatment also diminished elevation in plasma SDH activity produced by CHCl3 in CD-1 mice, while BUN was significantly elevated in both groups, indicating that CFB did not protect against CHCl3-induced nephrotoxicity. Histopathological examination of liver and kidney sections confirmed these results. This study shows that mice pretreated with CFB were protected from toxicity at 24 h after challenge with other model hepatotoxic agents besides APAP.

The representation of nonstructural information in visual memory: evidence from image combination.

Two experiments investigated the differential representation of the figure and ground of a picture in visual short-term and long-term memory. It is known (Hitch, Brandimonte, & Walker, 1995) that subjects find it more difficult to combine mental images of two separately presented pictures in order to identify a novel form when the two pictures are incongruent in color (i.e., when a black-on-white line drawing has to be combined with a white-on-black drawing). In the present experiments, the figures were depicted in solid form to allow color congruity to be varied independently for figure and ground. Results showed a clear impairment in image combination when the to-be-combined figures were incongruent in color (black-on-gray and white-on-gray) but not when their grounds were incongruently colored (gray-on-black and gray-on-white). In this way, image combination was seen to be supported by a representation of the object depicted in the picture rather than by a literal representation of the picture itself (i.e., a pictorial code). In line with previous findings, the same representation was seen to support image combination based on short-term memory (Experiment 1) and long-term memory (Experiment 2), provided that in the latter case verbal recoding was precluded. When verbal recoding was allowed, image combination based on long-term memory was insensitive to color congruity, implying the involvement of a more abstract structural representation.

Comparison of unilateral arytenoid lateralization and ventral ventriculocordectomy for the treatment of experimentally induced laryngeal paralysis in dogs.

This study evaluated changes in respiratory function in dogs with experimentally induced laryngeal paralysis treated with either unilateral arytenoid lateralization or ventral ventriculocordectomy, and compared the effectiveness of these procedures. Evaluation consisted of clinical assessment and tidal breathing flow volume loop and upper airway resistance measurements. Carbon dioxide and doxapram hydrochloride were used as respiratory stimulants. Initially, all dogs improved clinically after corrective surgery. However, by the end of the study, laryngeal collapse had developed in 2 of 5 dogs corrected by ventral ventriculocordectomy. No statistical differences in upper airway mechanics testing were seen between the surgical procedures. With both groups combined, many measurements of upper airway obstruction improved after surgical correction. Based on this study, these surgical procedures yield comparable results, although additional studies are needed to evaluate both the cause of laryngeal collapse and the role of upper airway mechanics testing in the evaluation of canine laryngeal paralysis.

Evaluation of fetal infection and abortion in pregnant ponies experimentally infected with Ehrlichia risticii.

Fetal infectivity of Ehrlichia risticii was investigated in 19 ponies that were E risticii negative on the basis of results of an indirect fluorescent antibody (IFA) test. Thirteen pregnant ponies were infected by IV administration of E risticii between 90 and 180 days of gestation. Six pregnant ponies served as noninfected controls. Each infected pony had clinical signs of equine monocytic ehrlichiosis, was confirmed to be ehrlichemic, and developed an IFA titer to E risticii. Two infected ponies became recumbent, were unresponsive to supportive care, and were euthanatized. After recovery from clinical illness, the remaining ponies were observed throughout gestation for reproductive abnormalities. On abortion, each fetus was necropsied and tissue specimens from the liver, bone marrow, spleen, colon, and mesenteric lymph nodes were inoculated into canine monocyte cell cultures. Six infected ponies aborted at a mean 217 days of gestation, which was between postinoculation days 65 and 111. Five fetuses were recovered for evaluation, and E risticii was isolated from 4 of them. All 5 fetuses recovered had similar histologic finding, including enterocolitis, periportal hepatitis, and lymphoid hyperplasia with necrosis of the mesenteric lymph nodes and spleen. All 5 fetuses tested negative for IgG to E risticii, although 3 had low IgM titer to E risticii. The remaining 5 infected ponies had normal parturition. Presuckle IFA titer to E risticii was measured in 4 of the term foals, and results for 3 were positive. Two foals from infected ponies were monitored for 6 months and daily gain in body weight was comparable to that of a control foal. None of the control ponies became ill or seroconverted during the clinical illness phase, and none aborted throughout gestation Two control ponies seroconverted to E risticii 6 weeks before parturition. Results of this study indicate that E ristcii is a primary abortifacient under experimental conditions.

Preneoplastic and neoplastic lesions of rat hereditary renal cell tumors express markers of proximal and distal nephron.

Long-Evans (Eker) rats carry a mutation that predisposes them to develop spontaneous renal cell tumors of two morphologic patterns: solid chromophilic masses or cystic lesions lined by eosinophilic cells. Previous studies have suggested that these tumors arise from the proximal tubules. In the present study, lectin-binding characteristics and cytokeratin expression of various stages of hereditary rat renal epithelial neoplasia were examined to localize the portion of the nephron from which tumors arise. Lectin-binding histochemistry has been used as a marker of cell surface glycoprotein expression, thought to be important in the differentiation of benign from malignant epithelial lesions and in the determination of their cell of origin. The presence or absence of keratin intermediate filaments in the rat nephron has been used to identify nephron segments. The polyclonal antibody to high- and low-molecular-weight cytokeratin stained the cells of the collecting ducts but not the proximal or distal tubules. Binding to the proximal tubules by the lectins Conavalia ensiformis (Con A), Dolichas biflorus, Ricinus communis (RCA-1), and Triticum vulgare and to the distal tubules by Con A, RCA-1, Arachis hypogaea (PNA) with and without neuraminidase, and the antibody for cytokeratins was demonstrated. The lectin binding and cytokeratin staining patterns of rat hereditary renal cell carcinoma, adenoma and the preneoplastic lesions of atypical tubules and hyperplasias suggest that cystic adenomas arise from the distal nephron, principally the collecting duct, whereas the solid atypical tubules, hyperplasias, and adenomas arise from the proximal nephron, principally the proximal tubule.

Identification of Ehrlichia risticii as the causative agent of two equine abortions following natural maternal infection.

Two pregnant mares diagnosed as having equine monocytic ehrlichiosis based on history, clinical signs, and high serum antibody titers to Ehrlichia risticii aborted subsequent to recovery from illness. Mare 1 and mare 2 experienced clinical illness at 120 and 143 days of gestation and aborted at 203 and 226 days of gestation, respectively. The fetuses were expelled in fresh condition, and both mares retained their placentas upon abortion. Gross findings for the fetuses included meconium staining and petechiation of external surfaces. Internally, there was increased volume of feces within the small and large intestines and liver discoloration with enlargement. Microscopic findings included lymphohistiocytic enterocolitis, hepatitis, and myocarditis. Lymphoid hyperplasia and depletion were present in spleen, thymus, and lymph nodes. Ehrlichia risticii was recovered from bone marrow, spleen, lymph node, colon, and liver of the first fetus and bone marrow and colon of the second fetus. Electron microscopic evaluation of the organism isolated in cell culture revealed morphology consistent with E. risticii. The isolated organism was inoculated into a naive pony, and this pony developed high levels of antibody against E. risticii, became ehrlichemic, and developed clinical signs of depression, anorexia, and mild diarrhea. These findings confirm that E. risticii is an abortifacient under conditions of natural infection and should be considered as a differential diagnosis of equine abortions.

Eosinophilic keratoconjunctivitis in a horse.

An 11-year-old Quarter Horse gelding was evaluated because of a persistent, raised band of 1- to 2-mm subepithelial plaques of the left cornea. Cytologic examination of corneal scrapings revealed numerous eosinophils and segmented neutrophils, with few mast cells, plasma cells, and lymphocytes. Bacteriologic culture yielded sparse growth of alpha-hemolytic Streptococcus and Staphylococcus spp. Histologically, the plaques consisted of subepithelial foci of fragmented and degenerated collagen fibers infiltrated by eosinophils and neutrophils, with few lymphocytes, plasma cells, and macrophages. Plaques were surrounded by a layer of brightly eosinophilic, acellular, granular material. Distribution of inflammatory cells in the conjunctiva was similar to cells in the cornea. After reepithelialization of the cornea, corticosteroid ointment was administered topically. Twenty-eight days after treatment with corticosteroids, the plaques had completely resolved. Histologic and cytologic diagnoses in this horse were similar to reports of eosinophilic keratitis in cats.

Hydrallantois in a caprine doe.

Hydrallantois was diagnosed in a 5-year-old Toggenburg doe. Clinical signs included bilateral abdominal distention, anorexia, and recumbency. Ultrasonographically, excessive fluid and live fetuses were detected in the uterus. At the time of cesarean section, the fluid (approx 12 L) was determined to be in the allantoic cavities; concentrations of electrolytes in the fluid were similar to concentrations in allantoic fluid from cows with hydrallantois. Two viable fetuses and 1 nonviable fetus were delivered. The doe retained its placentas for 60 hours, but made a good recovery. Hydrallantois should be considered in the differential diagnosis of abdominal distention in caprine does in late gestation.