Marine-based electrochemical Carbon Dioxide Removal (mCDR) is a rapidly evolving subject area. Technology is being developed that facilitates atmospheric CO2 removal by extracting Dissolved Inorganic Carbon (DIC) from seawater. Decarbonated seawater, that also has a high pH, is released into the marine environment, facilitating the drawdown of atmospheric CO­2 into the surface ocean. Chemical perturbations also include low levels of carbon dioxide (CO2) and bicarbonate (HCO3-), and increased levels of carbonate (CO32-). There is no literature that investigates the impact of low carbon seawater with elevated pH on marine ecosystems. Understanding and cataloguing the effect of mCDR is fundamental for: i) determining potential impact on vulnerable systems; ii) supporting the development of any necessary mitigating actions; iii) confirming overall mCDR effectiveness; and iv) engaging the public and harnessing their support. This work presents results from laboratory experiments that examine the physiological response of keystone organisms to decarbonated and high pH seawater. Decarbonated high pH seawater released into the environment will be diluted by mixing with ambient seawater, such that the chemical perturbations become less extreme with distance from source. Intertidal mussels (Mytilus edulis) are a keystone species that utilize DIC for major cellular functions and have poor acid-base balance. Mussels were exposed to three different dilutions of decarbonated high pH seawater (generating pH values of approximately, 10, 9.2 and 8.7). Mortality, oxygen consumption rate and filtering rate were measured after short-term (48 hr) exposure and then 48 hrs after returning to ambient seawater. Initial experiments indicate that undiluted decarbonated high pH seawater has a significant short-term impact on the physiological response of Mytilus edulis, but the species shows signs of recovery following a week in ambient seawater. Data from these and other experiments will be used to generate a risk gradient that illustrates how physiological response(s) change with dilution of low carbon, high pH seawater discharge.

Due to its position at the air-sea interface, the sea-surface microlayer (SML) modulates the exchange of gases, including the deposition of ozone to the ocean. While ozone deposition to the ocean is a large sink of ozone from the troposphere, the processes involved are not well understood. Previous work has focussed on seawater iodide as a driver of ozone uptake to the ocean, however the SML contains a complex mixture of organic material, which could also impact ozone uptake. The contribution of this organic material to ozone uptake remains particularly unclear.During this project, ozone uptake to seawater was measured by eddy covariance from coastal towers near Penlee Point (Plymouth, UK) and Tudor Hill (Bermuda), and at sea aboard the RV Atlantic Explorer, operating at and around the Bermuda Atlantic Time-series Study site in the Sargasso Sea. Additionally, the chemical component of ozone uptake to seawater was measured using a flow reactor during a trans-Atlantic cruise. This suite of observations has been combined to investigate the driving forces of oceanic ozone uptake. We present data that demonstrate that iodide was not a strong predictor of ozone uptake, despite its fast chemical reaction with ozone and the ubiquitous presence of iodide in the surface ocean.Organic compounds in the SML are of interest to this work because some organic compounds have ozone-reactive functional groups. An example of this is carbon-carbon double bonds, present in some oceanic fatty acids. By increasing chemical reactivity, organic material can therefore augment ozone uptake to the ocean. The contribution of chemical reactions between ozone and organic material to ozone uptake was investigated using the kinetic multilayer model of surface and bulk chemistry (KM-SUB). A simplified system of a monolayer of an unsaturated fatty acid (oleic acid) over seawater was modelled and demonstrated that a monolayer of ozone-reactive surfactants on the ocean surface could contribute substantially more to ozone uptake, compared to environmental levels of aqueous iodide.This work indicates that the commonly applied iodide-based parameterisation for ozone uptake to seawater may not accurately represent the chemical processes involved in ozone deposition to the sea surface. This has implications not only for predicted spatial and temporal variations in the magnitude of ozone deposition, but also for the chemical profile of oxidised gases emitted from the sea surface to the remote marine troposphere.

<p>Atmospheric methane (CH<sub>4</sub>) is a potent greenhouse gas with natural and anthropogenic sources. Concentrations have been significantly increasing over the past few decades, which poses a problem for future climate change goals. The contribution of oceans to the global atmospheric CH<sub>4</sub> cycle is largely uncertain. It is accepted that oceans act as a small net source of atmospheric CH<sub>4</sub>. As the polar regions are warming faster than the global average, it is important that we can better quantify CH<sub>4</sub> emissions from the polar oceans. </p> <p><br />In this study, we combine various forms of shipborne data (ambient atmospheric methane concentrations, sea-air CH<sub>4</sub> fluxes and isotopic composition of atmospheric CH<sub>4</sub>) taken during cruises in the Arctic and Southern Oceans to present a more complete picture of atmospheric CH<sub>4</sub> above polar oceans, including addressing the question of how much the oceanic component is contributing towards the atmospheric budget in these regions. Measurements  were made around the Barents Sea and Greenland Sea in the Arctic, and in the Atlantic sector of the Southern Ocean, including the Scotia Sea.</p> <p><br />Sea-air CH<sub>4</sub> fluxes are measured using the eddy covariance method; indeed, this the first study to use this technique to directly measure how much CH<sub>4</sub> is released from the ocean into the atmosphere in both the Southern and Arctic Oceans. Atmospheric CH<sub>4</sub> measurements are then investigated in order to understand the impact that CH<sub>4</sub> released from the ocean has on the atmospheric burden. We also measure the isotopic composition of CH<sub>4</sub> (δ<sup>2</sup>H and δ<sup>13</sup>C) in air samples taken onboard polar cruises, to understand the sources of atmospheric CH<sub>4</sub> above these oceans. The isotope measurements can indicate if the CH<sub>4</sub> comes from a biogenic or thermogenic source, which can help determine if anthropogenic or natural processes are behind the production.</p> <p><br />We investigate the potential sources of CH<sub>4</sub> released by the polar ocean by looking at areas of known seabed CH<sub>4</sub> seepages, investigating phytoplankton abundance, and investigating the isotopic composition of atmospheric CH<sub>4</sub> in areas of elevated CH<sub>4</sub>. </p> <p><br />We find that the region of the Arctic Ocean investigated in this study is a slight atmospheric CH<sub>4</sub> source in boreal summer, while the region of the Southern Ocean investigated is a CH<sub>4</sub> source in areas of shallower water/continental shelves and a CH<sub>4</sub> sink in region of open ocean, in austral summer. This finding is consistent with previous studies that have detected seabed CH<sub>4</sub> emission. Seabed CH<sub>4</sub> seepage at shallower depths is more likely to penetrate the sea-air interface, while CH<sub>4</sub> produced at the seabed at deeper depths gets oxidised as it travels through the water column, making it less likely to reach the surface . We also find evidence of localised “hot spots” of methane emission which will be described. </p>

Since 1st January 2020 the legal sulphur content of shipping fuel was decreased – from 3.5% to 0.5% by mass outside of the Sulphur Emission Control Areas (SECAs) to improve coastal air quality. A possible downside of this change was acceleration of climate change since sulphur is believed to be a negative climate forcer and sipping is one of its main sources. Further question was the level of compliance to the new rules, especially in the open waters. Another climate related aspect of shipping is recent growth in the liquified natural gas (LNG) tanker fleets. LNG is considered the greenest of the fossil fuels, however there are few empirical studies of methane emissions from marine LNG transport.The Atmospheric Composition and Radiative forcing changes due to UN International Ship Emissions regulations (ACRUISE) project aims to address the above considerations. During three field campaigns the FAAM Airborne Laboratories’ large research aircraft was deployed to target ships in coastal shipping lanes and open waters. First measurements were performed in July 2019 (before regulation change) in shipping lanes along the Portuguese coast, the English Channel SECA and the Celtic Sea. Further two campaigns were delayed by the COVID-19 pandemic until September 2021 and April 2022, targeting ships in the Bay of Biscay, the English Channel SECA and the Celtic Sea. Throughout the project, nearly 300 ships were measured during 30 research flights, varying from plume aging and cloud interaction studies, through collecting bulk statistics in busy shipping lanes to comparing emissions in and out of SECA. This work focuses on the gaseous species measurements (SO2, CO2, CH4 and VOCs from whole air samples). They are used to study changes in apparent sulphur fuel content of the ships observed throughout ACRUISE, plume composition and methane emissions from LNG tankers.

Ship exhausts have historically been significant sources of sulfur dioxide and aerosols to the marine atmosphere and some global models suggest the emissions cause a large negative radiative forcing by modifying cloud properties. International Maritime Organisation (IMO, an agency of the UN) regulations require that ships in international waters reduce their sulfur emissions from a maximum of 3.5% to 0.5% from January 2020. The ACRUISE project, taking advantage of this unique large-scale aerosol perturbation, investigates the impacts of the IMO’s 2020 sulfur regulations on aerosols, clouds, and radiation in the North Atlantic and globally. Here I summarise our findings so far from intensive aircraft observations, high-resolution model simulations, and deep learning-based satellite cloud analysis. Aerosol-cloud interaction near shipping lanes was studied from an aircraft in the northeast Atlantic in 2019 as well as in 2021. Aerosol chemical and physical properties were markedly different between the two years, with much lower sulfur content, smaller, and less hygroscopic aerosols in 2021. A detailed analysis of the aerosol and cloud microphysics observations within/immediately outside the ship plumes will be performed to determine whether some clouds appeared to be strongly impacted by ship plumes, while other clouds were not. To help interpret the aircraft data and provide context, we ran nested regional domain simulations of the Met Office Unified Model for all flight campaigns. These high-resolution simulations (few hundred metres) show a generally diffuse pattern of perturbed trace gases and aerosols that are not apparent as individual ship tracks, suggesting that analysis of tracks alone may underestimate the climatic effects of ship emissions. We have trained a deep learning model to detect ship-tracks in satellite imagery with good skill and applied it to the whole MODIS mission in order to develop a global climatology. We will discuss the spatial and temporal distribution of shiptracks relative to the underlying ship emissions, and particularly focus on the effects of the IMO regulation as well as the global COVID-19 pandemic. Ongoing work that combines airmass trajectory modelling with known positions of ships will enable us to assess the impact of ship emissions on all pixels, and not just those identified as ship tracks.

Uncertainty in the CO2 gas transfer velocity (K660) severely limits the accuracy of air-sea CO2 flux calculations and hence hinders our ability to produce realistic climate projections. Recent field observations have suggested substantial variability in K660, especially at low and high wind speeds. Laboratory experiments have shown that naturally occurring surface active organic materials, or surfactants, can suppress gas transfer. Here we provide direct open ocean evidence of gas transfer suppression due to surfactants from a ~11,000 km long research expedition by making measurements of the gas transfer efficiency (GTE) along with direct observation of K660. GTE varied by 20% during the Southern Ocean transect and was distinct in different watermasses. Furthermore GTE correlated with and can explain about 9% of the scatter in K660, suggesting that surfactants exert a measurable influence on air-sea CO2 flux. Relative gas transfer suppression due to surfactants was ~30% at a global mean wind speed of 7 m s-1 and was more important at lower wind speeds. Neglecting surfactant suppression may result in substantial spatial and temporal biases in the computed air-sea CO2 fluxes.

Air-sea carbon dioxide (CO2) flux is often indirectly estimated by the bulk method using the in-situ air-sea difference in CO2 fugacity and a wind speed dependent parameterisation of the gas transfer velocity (K). In the summer, sea-ice melt in the Arctic Ocean generates strong shallow stratification with significant gradients in temperature, salinity, dissolved inorganic carbon (DIC) and alkalinity (TA), and thus a near-surface CO2 fugacity (fCO2w) gradient. This gradient can cause an error in bulk air-sea CO2 flux estimates when the fCO2w is measured by the ship’s underway system at ~5 m depth. Direct air-sea CO2 flux measurement by eddy covariance (EC) is free from the impact of shallow stratification because the EC CO2 flux does not rely on a fCO2w measurement. In this study, we use summertime EC flux measurements from the Arctic Ocean to back-calculate the sea surface fCO2w and temperature and compare them with the underway measurements. We show that the EC air-sea CO2 flux agrees well with the bulk flux in areas less likely to be influenced by ice melt (salinity > 32). However, in regions with salinity less than 32, the underway fCO2w is higher than the EC estimate of surface fCO2w and thus the bulk estimate of ocean CO2 uptake is underestimated. The fCO2w difference can be partly explained by the surface to sub-surface temperature difference. The EC estimate of surface temperature is lower than the sub-surface water temperature and this difference is wind speed-dependent. Upper-ocean salinity gradients from CTD profiles suggest likely difference in DIC and TA concentrations between the surface and sub-surface water. These DIC and TA gradients likely explain much of the near-surface fCO2w gradient. Accelerating summertime loss of sea ice results in additional meltwater, which enhances near-surface stratification and increases the uncertainty of bulk air-sea CO2 flux estimates in polar regions.

There is a pressing need to globally inventory and assess coastal and inland aquatic habitats; extremely valuable and productive regions that are vulnerable to global anthropogenic pressures and climatic change. Basic information about sessile communities (wetlands, coral reefs, and sea grasses) includes mapping their extent and distribution, which can be gleaned from spectral surface reflectance imagery at high spatial resolution, but moderate temporal resolution. Moderate to high temporal resolution is also required for detailed observations of sessile community change (e.g., phenology, disturbance) and high temporal resolution is required for environmental changes in the surrounding water, phytoplankton concentration and composition, and concentrations of sediment or chromophoric dissolved organic matter (CDOM). Current and upcoming satellite missions and technology could meet spatial and spectral challenges. Multiple orbiting and airborne platforms, along with a network of in situ measurements, could provide a more complete picture of how these vital resources are changing. This paper provides an overview of these resources.

OBJECTIVE:To determine whether viral involvement with platelets obtained from cattle persistently infected (PI) with bovine viral diarrhea virus (BVDV) is associated with altered platelet function or decreased platelet counts.SAMPLE POPULATION:Platelets obtained from 8 cattle PI with BVDV and 6 age-, sex-, and breed-matched uninfected control cattle.PROCEDURE:Manual platelet counts were determined, and platelet function was assessed through optical aggregometry by use of the aggregation agonists ADP and platelet-activating factor. Identification of BVDV in serum and preparations of purified platelets was determined by use of virus isolation tests.RESULTS:No significant difference in platelet counts was detected between cattle PI with BVDV and control cattle. In response to the aggregation agonists, maximum aggregation percentage and slope of the aggregation curve were not significantly different between cattle PI with BVDV and control cattle. We isolated BVDV from serum of all PI cattle and from purified platelets of 6 of 8 PI cattle, but BVDV was not isolated from serum or platelets of control cattle.CONCLUSIONS AND CLINICAL RELEVANCE:Isolation of BVDV from platelets in the peripheral circulation of cattle immunotolerant to BVDV does not result in altered platelet function or decreases in platelet counts.

Previously, spontaneous genetic immunodeficiencies in mice, Arabian foals, and recently in Jack Russell terriers have been ascribed to defects in DNA-PKcs (catalytic subunit of the DNA dependent protein kinase) expression. In severe combined immunodeficiency (SCID) foals, a 5 bp deletion at codon 9480 results in a frameshift and a 967 amino acid deletion from the C terminus (including the entire PI3 kinase domain) and an unstable mutant protein. In SCID mice, a single base pair mutation results in a premature stop codon and deletion of 83 amino acids; as in SCID foals, the mutant protein is unstable. Here, we define the mutation within the canine DNA-PKcs gene that results in SCID. In this case, a point mutation results in a stop codon at nucleotide 10,828 and premature termination at a position 517 amino acids before the normal C terminus resulting in a functionally null allele. Thus, this is the third documentation of a spontaneous germline mutation in the C terminus of DNA-PKcs. Emerging data implicate DNA repair factors as potential tumor suppressors. Here, we have ascertained the carrier frequency of the defective DNA-PKcs genes in Arabian horses and in Jack Russell terriers. Our data indicate (in good agreement with a previous report) that the carrier frequency of the equine SCID allele is approximately 8%; in contrast, the carrier frequency of the canine SCID allele is less than 1.1%. We also assessed the frequency of the equine SCID allele in a series of 295 tumors from Arabian horses. We find a statistically significant correlation between the development of a virally induced tumor (sarcoid) and heterozygosity for the equine SCID allele. These data provide further support for an emerging consensus: that DNA-PK may normally act as a tumor suppressor through its caretaker role in maintaining chromosomal stability.

Because of unexplained mortality among 33 sibling offspring of a single pair of dogs, a family of Jack Russell Terriers was investigated. Twelve pups, 5 male and 7 female, died between 8 and 14 weeks of age. Six of those animals died in the field within 50 hours following vaccination with modified live vaccines. Subsequent histopathologic examination revealed the absence of splenic white pulp in 4 dogs and hepatic inclusions diagnostic for adenoviral infection in 2 dogs. Two additional litters yielded 2 pups with the same splenic and hepatic lesions. These observations led to a detailed study of 7 siblings whelped specifically for this investigation. Four of these 7 siblings had a profound lymphopenia and a decrease in serum immunoglobulins. Six of these dogs were necropsied at 7 weeks of age, and 4 of them had marked hypoplasia of all lymphoid tissue. The affected pups had an 86% decrease in mean thymic weight, with poor corticomedullary differentiation, and very few CD3-positive (T cell) thymocytes were detected immunohistochemically. However, the affected thymic tissue stained intensely with a immunochemical stain for cytokeratin. The other affected lymphoid tissues were identified histologically only by stromal architectural characteristics. Lymph nodes lacked both CD3 and CD79a (B cell) positive cells. The analyzed breeding data were consistent with an autosomal recessive mode of inheritance. This canine severe combined immunodeficiency has immunologic and pathologic features similar to those observed in immunodeficient C.B-17 mice and Arabian horses.

We recently described the incidence of a SCID disease in a litter of Jack Russell terriers. In this study, we show that the molecular defect in these animals is faulty V(D)J recombination. Furthermore, we document a complete deficit in DNA-dependent protein kinase activity that can be explained by a marked diminution in the expression of the catalytic subunit DNA-dependent protein kinase catalytic subunit (DNA-PKcs). We conclude that as is the case in C.B-17 SCID mice and in Arabian SCID foals, the defective factor in these SCID puppies is DNA-PKcs. In mice, it has been clearly established that DNA-PKcs deficiency produces an incomplete block in V(D)J recombination, resulting in "leaky" coding joint formation and only a modest defect in signal end ligation. In contrast, DNA-PKcs deficiency in horses profoundly blocks both coding and signal end joining. Here, we show that although DNA-PKcs deficiency in canine lymphocytes results in a block in both coding and signal end joining, the deficit in both is intermediate between that seen in SCID mice and SCID foals. These data demonstrate significant species variation in the absolute necessity for DNA-PKcs during V(D)J recombination. Furthermore, the severity of the V(D)J recombination deficits in these three examples of genetic DNA-PKcs deficiency inversely correlates with the relative DNA-PK enzymatic activity expressed in normal fibroblasts derived from these three species.

Altered platelet function has been reported in calves experimentally infected with type II bovine viral diarrhea virus (BVDV). The purpose of the present study was to further evaluate the ability of BVDV isolates to alter platelet function and to examine for the presence of a virus-platelet interaction during BVDV infection. Colostrum-deprived Holstein calves were obtained immediately after birth, housed in isolation, and assigned to 1 of 4 groups (1 control and 3 treatment groups). Control calves (n = 4) were sham inoculated, while calves in the infected groups (n = 4 for each group) were inoculated by intranasal instillation with 10(7) TCID50 of either BVDV 890 (type II), BVDV 7937 (type II), or BVDV TGAN (type I). Whole blood was collected prior to inoculation (day 0) and on days 4, 6, 8, 10, and 12 after inoculation for platelet function testing by optical aggregometry by using adenosine diphosphate and platelet activating factor. The maximum percentage aggregation and the slope of the aggregation curve decreased over time in BVDV-infected calves; however, statistically significant differences (Freidman repeated measures ANOVA on ranks, P < 0.05) were only observed in calves infected with the type II BVDV isolates. Bovine viral diarrhea virus was not isolated from control calves, but was isolated from all calves infected with both type II BVDV isolates from days 4 through 12 after inoculation. In calves infected with type I BVDV, virus was isolated from 1 of 4 calves on days 4 and 12 after inoculation and from all calves on days 6 and 8 after inoculation. Altered platelet function was observed in calves infected with both type II BVDV isolates, but was not observed in calves infected with type I BVDV. Altered platelet function may be important as a difference in virulence between type I and type II BVDV infection.

OBJECTIVE:To compare degree of viremia and disease manifestations in calves with type-I and -II bovine viral diarrhea virus (BVDV) infection.ANIMALS:16 calves.PROCEDURE:Colostrum-deprived calves obtained immediately after birth were assigned to 1 control and 3 treatment groups (4 calves/group). Calves in treatment groups were inoculated (day 0) by intranasal instillation of 10(7) median tissue culture infective dose BVDV 890 (type II), BVDV 7937 (type II), or BVDV TGAN (type I). Blood cell counts and virus isolation from serum and leukocytes were performed daily, whereas degree of viremia was determined immediately before and 4, 6, 8, and 12 days after inoculation. Calves were euthanatized on day 12, and pathologic, virologic, and immunohistochemical examinations were performed.RESULTS:Type-II BVDV 890 induced the highest degree of viremia, and type-I BVDV TGAN induced the lowest. Virus was isolated more frequently and for a longer duration in calves inoculated with BVDV 890. A parallel relationship between degree of viremia and rectal temperature and an inverse relationship between degree of viremia and blood cell counts was observed. Pathologic and immunohistochemical examinations revealed more pronounced lesions and more extensive distribution of viral antigen in calves inoculated with type-II BVDV.CONCLUSIONS AND CLINICAL RELEVANCE:Degree of viremia induced during BVDV infection is associated with severity of clinical disease. Isolates of BVDV that induce a high degree of viremia may be more capable of inducing clinical signs of disease. Strategies (eg, vaccination) that reduce viremia may control clinical signs of acute infection with BVDV.

Thrombocytopenia has been associated with type II bovine viral diarrhea virus (BVDV) infection in immunocompetent cattle, but the mechanism is unknown. The purpose of the present study was to develop and characterize a model of type II BVDV-induced thrombocytopenia. Colostrum-deprived Holstein calves were obtained immediately after birth, given a BVDV-negative and BVDV antibody-negative plasma transfusion, housed in an isolation facility, and randomly assigned to either control (n = 4) or infected (n = 5) groups. Infected calves were inoculated by intranasal instillation on day 3 of age with 10(7) TCID50 of the prototype type II isolate, BVDV 890, whereas control calves were sham inoculated. Blood counts and virus isolations from serum, white blood cells, and platelets were performed daily until day 12 after infection, at which time all experimental calves were euthanatized, and pathologic, virologic, and immunohistochemical examinations were performed. On physical examination, the control calves remained normal, but the infected calves developed pyrexia and diarrhea characteristic of type II BVDV infection. The platelet count decreased in all infected calves, and a statistically significant difference in the platelet count between control and infected calves was observed on days 7-12 after infection. In addition, the mean platelet volume and white blood cell counts also decreased. Examination of the bone marrow from the infected calves revealed immunohistochemical staining for BVDV antigen in megakaryocytes and evidence of concurrent megakaryocyte necrosis and hyperplasia.

OBJECTIVE:To evaluate platelet aggregation responses in calves experimentally infected with a thrombocytopenia-inducing type II bovine viral diarrhea virus (BVDV) isolate (BVDV 890).ANIMALS:9 neonatal male Holstein calves.PROCEDURE:5 calves were inoculated with BVDV 890, and 4 were used as controls. Platelet aggregation studies and attempts to isolate BVDV from platelets were performed 2 days before, the day of, and every 2 days for 12 days after inoculation. Platelet function was assessed by means of optical aggregometry, using adenosine diphosphate and platelet-activating factor as agonists. Bovine viral diarrhea virus was isolated from purified platelet preparations by use of an immunoperoxidase monolayer assay.RESULTS:Maximum percentage aggregation and slope of the aggregation curve decreased over time in calves infected with BVDV. Bovine viral diarrhea virus was not isolated from platelets from control calves, but it was isolated from infected calves from 4 through 12 days after inoculation.CONCLUSIONS AND CLINICAL RELEVANCE:Results suggest that platelet function may be depressed in calves infected with type II BVDV. Although the mechanism for altered platelet function was not determined, it likely involved an increase in the percentage of aged platelets in the circulation, a direct virus-platelet interaction, or an indirect virus-platelet interaction. Platelet dysfunction, in addition to thrombocytopenia, may contribute to the hemorrhagic syndrome associated with acute type II BVDV infection in calves.

for Brucella abortus strain RB5. Vet Pathol 33:615. [Abstr.] 4. Chitwood MB, Lichtenfels JR: 1972, Identification of parasitic metazoa in tissue sections. Exp Parasitol 32:461-464. 5. Ewalt DR: 1989, Comparison of three culture techniques for the isolation of Brucella abortus from bovine supramammary lymph nodes. J Vet Diagn Invest 1:227-230. 6. Ewalt DR, Payeur JP, Martin MB, et al.: 1994, Characteristics of a Brucella species from a bottlenose dolphin (Tursiops truncatus). J Vet Diagn Invest 6:448-452. 7. Farrell ID: 1974, The development of a new selective medium for the isolation of Brucella abortus from contaminated sources. Res Vet Sci 16:280-286. 8. Fleischman RW, Squire RA: 1970, Verminous pneumonia in the California sea lion (Zalophus californianus). Pathol Vet 7:89101. 9. Foster G, Jahans KL, Reid RJ, et al.: 1996, Isolation of Brucella species from cetaceans, seals, and an otter. Vet Rec 138:583586. 10. Howard EB, Britt JO, Matsumoto G: 1983, Parasitic diseases. In: Pathobiology of marine mammal diseases, ed. Howard EB, pp. 128-213. CRC Press, Boca Raton, FL. 11. Kennedy PC, Miller RB: 1993, Brucellosis. In: Pathology of domestic animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., pp. 396-402. Academic Press, San Diego, CA. 12. Lambourn DM, Jeffries SJ, Hall PB, et al.: 1996, Evidence of brucellosis in Pacific harbor seals (Phoca vitulina richardsi) and California sea lions (Zalophus californianus) from Puget Sound, Washington. Annu Conf Wildl Dis Assoc 45:000. [Abstr.] 13. Luna LG: 1960, Manual of histologic and special staining technics, 2nd ed. McGraw-Hill, New York, NY. 14. Migaki G, Van Dyke D, Hubbard RC: 1971, Some histopathological lesions caused by helminths in marine mammals. J Wildl Dis 2:281-289. 15. Morales GA, Helmboldt CF: 1970, Verminous pneumonia in the California sea lion (Zalophus californianus). J Wildl Dis 7:22-27. 16. Morgan WJB, Corbel MJ: 1976, Recommendation for the description of a species and biotypes of the genus Brucella. Dev Biol Stand 31:27-37. 17. Palmer MV, Cheville NF, Tatum FM: 1996, Morphometric and histopathologic analysis of lymphoid depletion in murine spleens following infection with Brucella abortus strains 2308, RB51, or an htrA deletion mutant. Vet Pathol 33:282-289. 18. Ross HM, Foster G, Reid RJ, et al.: 1994, Brucella species infection in sea-mammals. Vet Rec 134:359. 19. Ross HM, Jahans IU, MacMillan AP, et al.: 1996, Brucella species infection in North Sea and cetacean populations. Vet Rec 138:647-648. 20. Rhyan JC, Wilson ISL, Burgess DE, et al.: 1995, Immunohistochemical detection of Tritrichomonas foetus in formalin-fixed, paraffin-embedded sections of bovine placenta and fetal lung. J Vet Diagn Invest 7:98-101.