The InSight HP3 Penetrator (Mole) on Mars: Soil Properties Derived from the Penetration Attempts and Related Activities.

The NASA InSight Lander on Mars includes the Heat Flow and Physical Properties Package HP3 to measure the surface heat flow of the planet. The package uses temperature sensors that would have been brought to the target depth of 3-5 m by a small penetrator, nicknamed the mole. The mole requiring friction on its hull to balance remaining recoil from its hammer mechanism did not penetrate to the targeted depth. Instead, by precessing about a point midway along its hull, it carved a 7 cm deep and 5-6 cm wide pit and reached a depth of initially 31 cm. The root cause of the failure - as was determined through an extensive, almost two years long campaign - was a lack of friction in an unexpectedly thick cohesive duricrust. During the campaign - described in detail in this paper - the mole penetrated further aided by friction applied using the scoop at the end of the robotic Instrument Deployment Arm and by direct support by the latter. The mole tip finally reached a depth of about 37 cm, bringing the mole back-end 1-2 cm below the surface. It reversed its downward motion twice during attempts to provide friction through pressure on the regolith instead of directly with the scoop to the mole hull. The penetration record of the mole was used to infer mechanical soil parameters such as the penetration resistance of the duricrust of 0.3-0.7 MPa and a penetration resistance of a deeper layer ( > 30 cm depth) of 4.9 ± 0.4 MPa . Using the mole's thermal sensors, thermal conductivity and diffusivity were measured. Applying cone penetration theory, the resistance of the duricrust was used to estimate a cohesion of the latter of 2-15 kPa depending on the internal friction angle of the duricrust. Pushing the scoop with its blade into the surface and chopping off a piece of duricrust provided another estimate of the cohesion of 5.8 kPa. The hammerings of the mole were recorded by the seismometer SEIS and the signals were used to derive P-wave and S-wave velocities representative of the topmost tens of cm of the regolith. Together with the density provided by a thermal conductivity and diffusivity measurement using the mole's thermal sensors, the elastic moduli were calculated from the seismic velocities. Using empirical correlations from terrestrial soil studies between the shear modulus and cohesion, the previous cohesion estimates were found to be consistent with the elastic moduli. The combined data were used to derive a model of the regolith that has an about 20 cm thick duricrust underneath a 1 cm thick unconsolidated layer of sand mixed with dust and above another 10 cm of unconsolidated sand. Underneath the latter, a layer more resistant to penetration and possibly containing debris from a small impact crater is inferred. The thermal conductivity increases from 14 mW/m K to 34 mW/m K through the 1 cm sand/dust layer, keeps the latter value in the duricrust and the sand layer underneath and then increases to 64 mW/m K in the sand/gravel layer below. Supplementary Information: The online version contains supplementary material available at 10.1007/s11214-022-00941-z.

Postweaning multisystemic wasting syndrome (PMWS) in Sweden from an exotic to an endemic disease.

Postweaning multisystemic wasting syndrome (PMWS) is causally associated with porcine circovirus type 2 (PCV2) infection of pigs. PCV2 was first demonstrated in Swedish pigs in 1993, although the virus was almost certainly present in pigs in the country before that. Despite this, no signs of PMWS were observed in pigs of Sweden until the first outbreak was reported in 2003. The accumulated number of PMWS-affected herds have increased via 16 (2004) and 41 (2005) to 123 in December 2006. Of these herds, 30 (25%) have now been declared free from PMWS. However, a number of other herds have had individual pigs that have fulfilled the demands for PMWS at necropsy and 52 of these herds have been declared negative on herd basis after treatment for intestinal or respiratory diseases, and/or by correcting shortcomings in management of the herd including feed. Thus, individual cases of the disease have been observed in around 200 herds by the end of 2006 and PMWS is now regarded as an endemic disease in Sweden. The pig population of Sweden is geographically isolated, the density of pigs and the pathogen load in the country is low and the use of growth promoters (low dose antibiotics in feed) was prohibited in 1986. Additionally, the trade of animals in Sweden is organised in a restricted way. Because of these factors it is possible to conduct meaningful real-time studies on the transformation of PMWS in Sweden from being an exotic to an endemic disease in a three year time scale. Initially the PMWS cases were concentrated in the southern part of Sweden, but have gradually spread north. The PMWS-positive herds have, in general, had an effective production, but some management errors have constantly been observed in affected herds. Physical links between affected herds are often missing, and the data generated to date on the PMWS outbreaks in Sweden do not suggest an introduction of a new contagious microbe into the country that is responsible for the PMWS outbreaks, nor does PMWS appear to be spread via semen. In Sweden, intensity in rearing, disease preventing measures and immaturity of the piglets appear to be important as predisposing factors to PMWS and, as such, are discussed in this article.

Postweaning multisystemic wasting syndrome--PMWS. the first year with the disease in Sweden.

Postweaning multisystemic wasting syndrome (PMWS) is causally associated with porcine circovirus type 2 (PCV2) infection of pigs. PCV2 has been present in the Swedish pig population for at least ten years. Despite this, no signs of PMWS were observed in pigs of Sweden until 2003. Since then the disease has spread slowly in Sweden. The pig population of Sweden is geographically isolated, the density of pigs and the pathogen load in the country is low and the trade of animals is organised in a restricted way. To date, there has been little information placed in the peer-reviewed literature on the study of the spread of PMWS in a country during the early phase of the disease outbreak, mainly because diagnosis of PMWS has only occurred after the disease has been recognised on a number of farms. This manuscript documents the studies to date on the PMWS outbreak in Sweden which has been closely monitored since the initial outbreak of diseases on a single farm in 2003 was diagnosed. In Sweden PMWS was officially reported for the first time at a progeny test station during December 2003. One year later sixteen herds have been diagnosed and reported to the authorities: one progeny test station, one nucleus herd, thirteen piglet producers or integrated herds and one specialised fattening herd. Fifteen suspected cases have been deemed negative for PMWS with disease scenarios associated with Lawsonia intracellularis, Brachyspira pilosicoli, Mycoplasma hyopneumoniae, shortcomings in feed composition etc. To date, one year after the index case was reported ten other herds suspected for PMWS are under observation. The PMWS cases are concentrated into the southern part of Sweden. However, the disease is spreading slowly, and in general there are no obvious physical links between affected herds. The data generated to date in Sweden suggest that introduction of a new contagious microbe into the country that is responsible for the PMWS outbreaks appears unlikely, as does the spread of PMWS via semen.

Detection of pseudorabies virus genomic sequences in apparently uninfected 'single reactor' pigs.

With a pseudorabies virus (PrV) gB ELISA, performed on 480,000 pigs on 8,900 Swedish farms, approximately 1,300 cases were observed with only one single animal reacting positively. These animals were termed 'single reactors' (SR). In order to find explanations for this peculiar phenomenon, the presence of PrV was investigated in organs of immunosuppressed and non-immunosuppressed SR animals. The virus was not detected by immunohistochemistry, virus isolation or co-cultivation. An in situ DNA hybridization test detected PrV gC gene sequences in the olfactory bulb of one sow. A nested polymerase chain reaction (PCR) assay revealed gB, gE and gD gene sequences of PrV in the tissues of trigeminal ganglia, olfactory bulb, tonsils and brain. The nucleotide sequences of the amplicons revealed 98 to 100% homology with the corresponding sequences of PrV. The large latency transcript (LLT) was not detected in the organs of the SR pigs. Transmission of the SR phenomenon to animals in contact or to the next generation was not observed. Considering the present observations and the facts that (i) PrV vaccination is not applied in Sweden; (ii) the SR animals occur not only in the South, but also in Northern Scandinavia, which has no history of PrV infection and (iii) viral reactivation was not observed under natural conditions or after experimental immunosuppression, it is concluded that the SR phenomenon should hardly be considered as a typical PrV latency. The present findings show that certain herpesviral genomic sequences exist in apparently uninfected individuals.

Agricultural policy and social returns to eradication programs: the case of Aujeszky's disease in Sweden.

Economic-welfare analysis of animal disease prevention programs frequently ignore the constraints of the agricultural policy environment. Prevention programs affect producers, consumers and the government. The policy environment to a large extent determines the magnitude as well as the distribution of benefits of the program among these groups. The Swedish hog industry has been exposed to three major policy changes during the 1990-1995 period. These scenarios involve various degrees of government intervention in the agricultural sector including internal market deregulation and EU-membership. Aujeszky's disease is a virus disease with swine as the natural infection reservoir. Piglets are the most fragile and an outbreak of the disease results in symptoms such as shaking, cramps and convulsions with an increase in the mortality rate. Slaughter hogs suffer from coughing, fever and reduce their feed consumption. During the last 20-25 years the incidence of Aujeszky's disease (AD) has been increasing in Sweden. In 1989 an eradication program was undertaken. A model is developed to analyze social benefits of an eradication program given variations in agricultural policy. The model refers to the specifics of the AD-program implemented in Sweden. The expected benefits of the program are evaluated using a welfare-economic analysis applying cost-benefit analysis. Total benefits of the program are evaluated across herd and size categories and different regions. Data concerning the frequency of the virus among various categories of herds prior to enacting the program were used (Wahlström et al., 1990). In addition, data from an agricultural insurance company were used to estimate the conditional probability of an outbreak given that the herd is infected. Biological and technical parameter values were collected from a variety of sources. The results of the analysis indicate that the program is economically viable given a social rate of discount in the range of 3-5% without considering non-monetary aspects such as animal ethics. A scenario where the Swedish agricultural sector is deregulated provides the maximum benefits of the program. Consumers obtain about 50% of the benefits excluding program costs. The deregulation scenario would correspond closely to a case where a reformed Common Agricultural Policy (CAP) is applied across member countries. In the current case where Sweden is a member of the EU, the benefits are reduced mainly due to lower prices of inputs and pork.

Testing of remedial measures in fattening pig herds affected with subclinical infections of Actinobacillus pleuropneumoniae serotype 2.

The present investigation comprised 5 specialized herds of slaughter pigs, each with a production of 1,500 to 4,000 fatteners per year. High prevalence of pleuritis was demonstrated in all herds at slaughter. Serological investigations by means of ELISA were carried out to determine antibody titres to Actinobacillus pleuropneumoniae (A. pl.) serotype 2 during the fattening period and at slaughter. The investigations showed that this agent was a predominant cause of the subclinical pleuritis although A. pl. was difficult to isolate. An environment study was performed in all herds and major environmental deficiencies were corrected during the course of the investigation. Similarly, all herds changed to a strict routine of batch rearing. In 4 herds out of 5, the animals were vaccinated on arrival to the growing-finishing units and again generally 3-4 weeks later with an inactivated vaccine against A. pl. serotype 2. The prevalence of pleuritis decreased with 25-75% during the three-year observation period. Also the prevalence of pneumonia decreased at the same time. Conversely, daily weight gain and feed conversion improved. The prevalence of pleuritis and pneumonia registered at slaughter was lower in three-breed crosses (including Hampshire, Landrace and Yorkshire) than in the two-breed crosses with Landrace and Yorkshire.

Salmonella typhimurium infection in calves: cell-mediated and humoral immune reactions before and after challenge with live virulent bacteria in calves given live or inactivated vaccines.

Groups of six calves, 4 to 5 weeks old, were vaccinated either orally with a live auxotrophic Salmonella typhimurium (O-antigen 1,4,12) SL1479 vaccine (10(8) bacteria on day zero, 10(10) bacteria on days 7 and 14) or subcutaneously with a heat-inactivated (56 degrees C, 30 min) S. typhimurium SVA1232 vaccine (10(10) bacteria suspended in 30% [vol/vol] aluminum hydroxide on days zero, 7, and 14). The calves were then orally challenged with either 10(6) (approximately 100 X the 25% lethal dose) or 10(9) (approximately 100,000 X the 25% lethal dose) live bacteria of the calf-virulent S. typhimurium SVA44 strain. The immune reactivity of these calves and of nonvaccinated control calves was followed before and after the challenge infection up to 42 days by (i) intradermal injection of S. typhimurium crude extract, outer membrane protein preparation (porins), and lipopolysaccharide (LPS), (ii) in vitro stimulation of peripheral blood lymphocytes estimated by using uptake of [3H]thymidine, with S. typhimurium crude extract, porins, LPS, and polysaccharide (O-antigenic polysaccharide chain free of lipid A), and Salmonella sp. serotype thompson (O-antigen 6,7) strain IS40 LPS and polysaccharide, and (iii) estimation of the class-specific immunoglobulin G (IgG) and IgM antibody responses against S. typhimurium LPS and porins, and Salmonella sp. serotype thompson LPS. The immune studies showed that in calves given the live vaccine orally, the skin test reactivity and lymphocyte stimulation indices were significantly higher (P values ranging from less than 0.025 to less than 0.0005) against homologous, but not heterologous, antigens than those seen in calves given the heat-inactivated vaccine subcutaneously. In contrast, the IgG and IgM antibody titers against homologous LPS and porins were significantly higher (P less than 0.0005) in sera collected on day 21 from calves given the heat-inactivated vaccine than in calves given the live vaccine. After the oral challenge, calves given the live vaccine showed reduced cell-mediated immune reactions, in agreement with the observation that the host defense could eradicate the challenge organism, whereas calves given the heat-inactivated vaccine showed significantly increased cell-mediated immune reactions (P values ranging from less than 0.025 to less than 0.005), in agreement with the observation that in these calves, the challenge strain caused enteritis as well as systemic invasion. The increased cell-mediated immune reactivity in calves given the live vaccine correlated well with the excellent protection against challenge infection seen in these animals.

Salmonella typhimurium infection in calves: protection and survival of virulent challenge bacteria after immunization with live or inactivated vaccines.

Salmonella typhimurium SL1479, an auxotrophic mutant strain having a complete block in the aromatic biosynthetic pathway and therefore requiring p-aminobenzoic acid and 2,3-dihydroxybenzoate not available in mammalian tissues, was given orally in a dose of 10(10) live bacteria to 4- to 5-week-old calves. Only a mild transient fever response was seen. Strain SL1479 was unable to colonize and persist in the calves for more than 2 weeks. In a vaccination experiment, groups of six calves were (i) orally vaccinated with the live S. typhimurium SL1479 strain, (ii) subcutaneously vaccinated with a heat-inactivated S. typhimurium SVA1232 strain with aluminum hydroxide as adjuvant, or (iii) not vaccinated, to serve as controls. Calves were orally challenged with the live, calf-virulent S. typhimurium SVA44 strain: either 10(6) bacteria (equivalent to 100 25% lethal doses [LD25S]) or 10(9) bacteria (100,000 LD25S doses). The live oral vaccine gave significantly better protection than the heat-vaccinated, subcutaneously injected vaccine since (i) only control calves and calves given the killed vaccine developed profuse diarrhea, (ii) clinically, the mild fever responses seen after challenge in calves given the live vaccine were significantly lower (P less than 0.0005), (iii) autopsies performed 21 days after the challenge infection revealed normal findings in calves given the live vaccine, whereas calves given the killed vaccine showed signs of acute enteritis and chronic salmonellosis, (iv) all 12 calves given either 100 X or 100,000 X the LD25 survived the 21-day observation period; the mean survival time in nonvaccinated calves was 8.0 days; in calves given heat-inactivated vaccine and 100 X the LD25 it was 21.0 days, and in calves given 100,000 X the LD25 it was 11.5 days, (v) the fecal bacterial counts of the challenge S. typhimurium SVA44 strain were significantly lower (P less than 0.0005) in both groups given the live vaccine, and (vi) upon autopsy followed by culture, the qualitative recovery of the challenge strain from the alimentary canals and tissues of calves given the live vaccine was significantly lower (P less than 0.005).

Defined salmonella antigens for detection of cellular and humoral immune responses in salmonella infected calves.

Intracutaneous injection of a crude supernatant fraction from homogenised Salmonella typhimurium SVA 44 (O 4, 5, 12) or S dublin SVA 47 (O 9, 12) elicited highly significant (P less than 0.005) double skin-fold thickness increases in calves spontaneously infected with salmonella and verified as excretors. The use of isolated structurally defined outer membrane components from salmonella bacteria established that the delayed skin reactions could be elicited by either the lipopolysaccharide which contains O-antigenic polysaccharide chains homologous to the infecting strain, or an outer membrane protein fraction (porin). The porin preparation gave rise to skin reactions regardless of which salmonella serotype the calf was infected with. Histological examination of biopsy material indicated a delayed skin reaction. No such reactions were seen in biopsies from control calves. The use of lipopolysaccharide permitted a salmonella serogroup specific skin test although the endotoxic side effects were marked in doses above 50 micrograms. Purified O-antigen specific polysaccharides devoid of lipid A from S typhimurium (O 4, 12) or S enteritidis (O 9, 12) failed however to elicit skin reactions. Infected calves had humoral antibody titres against the O antigen of the infecting strain which were significantly (P less than 0.005) higher than those found in control calves.

Salmonella typhimurium infection in calves: specific immune reactivity against O-antigenic polysaccharide detectable in in vitro assays.

Peripheral blood lymphocytes collected from calves infected experimentally with Salmonella typhimurium (O antigens 4,5,12) or Salmonella sp. serotype dublin (O 9,12) were stimulated with various bacterial cell envelope components, and their [3H]thymidine incorporation was measured. It was found that peripheral blood lymphocytes from infected calves incorporated significantly more [3H]thymidine than peripheral blood lymphocytes from uninfected controls (P values ranged from less than 0.05 to less than 0.0005). The responder cell type was found in a B-cell-depleted and T-cell-enriched population. The Salmonella infections elicited T-cell responses against at least two cell envelope components: (i) a specific response against the O-antigenic polysaccharide chain of the lipopolysaccharide (This was evident in that a polysaccharide from S. enteritidis [O 9,12] which shares a trisaccharide structure [O antigen 12 determinant] with S. typhimurium stimulated [3H]thymidine uptake, which, although lower than in the homologous system, was significantly higher than that seen after incubation with unrelated Salmonella sp serotype thompson polysaccharide.) and (ii) a response against outer membrane proteins (porins), which are present in both S. typhimurium and Salmonella sp. serotype dublin. The experiments with peripheral blood lymphocytes from Salmonella sp. serotype dublin-infected calves gave results in excellent agreement with those obtained in S. typhimurium-infected calves.

Salmonella typhimurium infection in calves: delayed specific skin reactions directed against the O-antigenic polysaccharide chain.

Specific delayed skin reactions developed after intradermal injection of Salmonella typhimurium lipopolysaccharide in 12-week-old calves which had been orally infected with S. typhimurium 5 weeks earlier. Uninfected calves showed no delayed skin reactions. Skin biopsies from skin swellings showed a massive infiltration of mononuclear cells in the skin of infected calves but not in those of uninfected calves. Persistence of infection in infected calves was confirmed by isolation of S. typhimurium from fecal specimens. The delayed skin reactions could be shown to be specific and directed against the O-polysaccharide chain of the lipopolysaccharide since none of the lipopolysaccharide chain of the lipopolysaccharide since none of the lipopolysaccharide preparations from a rough mutant of S. typhimurium, two strains with different O-polysaccharide chains, or lipid A elicited skin reactivity. To cause a reaction, the O-polysaccharide had to be in a macromolecular complex, since skin swellings were seen only after injections of either O-polysaccharide chains cross-linked by 1,2,3,4-diepoxybutane or octasaccharides from the O chain covalently linked to a straight 12-carbon aliphatic chain forming an artificial glycolipid. Injection of the pure octasaccharides of O-polysaccharide chains failed to elicit delayed skin reactions.

Delayed hypersensitivity skin test for detection of immune responses against Salmonella in cattle.

Intracutaneous injection of a crude supernatant fraction from homogenised Salmonella typhimurium (O antigens 4, 5, 12) or S dublin (O antigens 9, 12) in 250 cattle or calves from salmonella infected herds elicited in 27 per cent and 42 per cent, respectively, a local dermal reaction. Both the time course and histological examinations of biopsy materials indicated a delayed type of hypersensitivity reaction. No local dermal reactions were seen in any of 250 heads of cattle or calves from control herds. The immunological characterisation of the S typhimurium and S dublin crude extracts revealed that they contained O antigens (ie, lipopolysaccharides) and outer membrane proteins, porins. A Yersinia enterocolitica serotype O3 extract did not evoke skin reactions in any of 70 tested animals. Fifteen calves infected with S typhimurium and five with S dublin exhibited increased ELISA titres against the O antigenically homologous lipopolysaccharides.

Ingestion of Yersinia pseudotuberculosis into human fibroblasts in vitro.

The ingestion into human fibroblasts of different strains (avirulent and virulent) of Yersinia pseudotuberculosis was investigated. The kinetics of ingestion was studied with the addition of 10(7) bacteria to human lung fibroblast cultures. The number of ingested bacteria after 0.5-3 h was measured with viable count technique. All strains were ingested except for one avirulent strain. The other strains were ingested at roughly the same rate. The bacterial uptake seemed to be mediated by a phagocytic-like procedure and the intracellular bacteria resided in vacuoles. The bacteria survived and also multiplied in the cells (for at least 7 days).

Frequency of latent bovine leukosis in Sweden.

The enzootic bovine leukosis occurs in Sweden especially in the south-eastern part of the country. An orientating serological survey was carried out on various categories of dairy cattle predominantly from this area. Serological and haematological examinations were also carried out on beef cattle herds connected to a volontary control program for bovine leukosis.