Efficacy of commercial vaccines for protecting guinea pigs against Bordetella bronchiseptica pneumonia

Autogenous bacterins are recommended to protect guinea pigs (Cavia porcellus) against pneumonia due to Bordetella bronchiseptica. Bordetella vaccines are available commercially for several other animal species. The substantial antigenic cross-reactivity among Bordetella isolates from various animal species suggests that immunity resulting from use of these vaccines might protect guinea pigs. Groups of ten individually housed Hartley guinea pigs from a colony free of Bordetella were vaccinated with one of two commercial porcine B. bronchiseptica vaccines, a human DPT vaccine (which includes a Bordetella pertussis component), or an autogenous B. bronchiseptica bacterin. Twenty-one days following vaccination, the animals were challenged with an intranasal dose of 10(6) virulent B. bronchiseptica cells. The animals were euthanized and necropsied 15 days after challenge. The nares, nasopharynx, distal trachea and lungs were cultured. All nonvaccinated control animals developed acute signs of pneumonia, while none of the vaccinated animals developed clinical signs of disease or gross lesions. The frequency of B. bronchiseptica isolation from the lungs of animals in each vaccine group was reduced. However, approximately 70% of all animals in each vaccine group harbored B. bronchiseptica in the trachea, and almost all harbored B bronchiseptica in the nares and nasopharynx. The porcine vaccines appeared to afford protection against acute pulmonary disease in the guinea pig.     

Determination of an antigen suitable for enzyme-linked immunosorbent assay of the antibody to Bordetella bronchiseptica in guinea pigs

To establish an enzyme-linked immunosorbent assay (ELISA) technique for the serological diagnosis of infections caused by Bordetella bronchiseptica (B. bronchiseptica) in guinea pigs, the authors recently assessed the usefulness of three antigen preparations derived from the bacterial cell components: sonication antigen (S-Ag), cell surface antigen (C-Ag) and lipopolysaccharide antigen (L-Ag). The use of S-Ag for ELISA resulted in the most sensitive detection of the antibody to B. bronchiseptica from guinea pig sera immunized with killed bacteria and sera derived from naturally infected guinea pigs. Like C-Ag, S-Ag was highly specific, showing no cross-reactivity with Pasteurella multocida. Assessment of antibody formations in animals with experimentally induced infection using the three antigen preparations revealed that the antibody to S-Ag was formed earlier than antibodies to the other two antigen preparations following growth of the bacterium in the lungs. These results indicate that ELISA with S-Ag as an antigen is a useful tool for the serological diagnosis of infection by B. bronchiseptica.     

Efficacy of a commercial bacterin in protecting strain 13 guineapigs against Bordetella bronchiseptica pneumonia

Bordetella bronchiseptica is known to be endemic in many guineapig (Cavia porcellus) colonies, and periodically is the aetiological agent of fatal epizootics of bronchopneumonia. A commercial, non-adjuvant B. bronchiseptica bacterin, which is approved for use in canines, was evaluated for induction of a protective immune response in Strain 13/N guineapigs against an airborne challenge of virulent B. bronchispeptica in small-particle aerosol. Seronegative animals were vaccinated on days 0 and 21 with intramuscular injections of 0.2 ml of bacterin. Humoral antibody titres of the vaccinated animals, as determined by ELISA, ranged from 128-1024 on day 49. On day 30 following the second dose of bacterin (study day 51), 12 vaccinated and 12 PBS sham-vaccinated animals were exposed to an inhaled dose of 4.3 x 10(5) CFU of B. bronchiseptica (325 LD50). Vaccinated, challenged animals remained clinically normal, although each guineapig did develop a localized upper respiratory infection. The rate of weight gain as well as rectal temperature of these animals were analogous to those exhibited by the control groups. Examination of 4 of the vaccinated, challenged animals on day 7 after exposure showed bacteria present in moderate to high numbers in the larynx and trachea but only minimally detectable in the lungs; by 30 days after exposure, the numbers of bacteria in the larynx and trachea were diminished, with none being detected in the lungs. Pathological alterations induced by B. bronchiseptica were not detected at either day 7 or day 30 after challenge in any of the vaccinated, challenged animals. Protection induced in Strain 13/N guineapigs by the commercial canine bacterin was sufficient to preclude the development of pulmonary disease, even in animals presented with a massive challenge of virulent bacteria in a small-particle aerosol.     

Microbiological monitoring of Guinea pigs reared conventionally at two breeding facilities in Korea.

In this study, microbiological monitoring of guinea pigs reared conventionally in two facilities was performed twice in 2004, with a three-month-interval between surveys. This study was based on the recommendations of the FELASA Working Group, with some modifications. In serological tests in the first survey, some animals from facility A showed positive results for Encephalitozoon cuniculi, Sendai virus, pneumonia virus of mice (PVM), and Reovirus-3 (Reo-3); facility B showed a positive result only for E. cuniculi. The results of the second survey were similar to the first, except for the presence of Sendai virus; all animals from the two facilities were Sendai virus-negative in the second experiment. No pathogenic bacteria were cultured in the organs of any of the animals in the first survey. However, in the second survey, Bordetella bronchiseptica was cultured from the lung tissue of two 10-week-old animals from facility A. Chlamydial infection was examined by the Macchiavello method, but no animal showed positive results. Tests using fecal flotation or the KOH wet mount method showed no infection of endoparasites, protozoa, ectoparasites, or dermatophytes in any animal in both surveys. However, in the histopathological examination, an infection of protozoa-like organisms was observed in the cecum of some animals from facility A. The present study revealed that microbiological contamination was present in guinea pigs reared conventionally in two facilities in Korea, suggesting that there is a need to improve environmental conditions in order to eradicate microbial contamination.     

A survey of Streptococcus pneumoniae, Streptococcus zooepidemicus, Salmonella spp., Bordetella bronchiseptica and Sendai virus in guinea pig colonies in Japan

S. pneumoniae, S. zooepidemicus, Salmonella spp., B. bronchiseptica and Sendai virus were examined in a total of 45 guinea pig colonies (17 institutional and 28 breeder's colonies) of Hartley strain, and found to be positive in 6, 3, 5, 20 and 14 colonies, respectively. Sendai virus was highly prevalent among guinea pigs, showing so high rates positive as 80 to 100% of animals obtained from 11 of the 14 contaminated colonies. B. bronchiseptica was also shown to be prevalent within contaminated colonies by indication of rates positive more than 40% of animals examined in 14 of the 20 colonies. Infection rates of other 3 pathogens, however, ranged from lower than 20% to higher than 80% according to colonies. All strains of Salmonella isolated in this survey were identified as S. typhimurium and those of S. pneumoniae as serotype 19F.     

Comparative evaluation of different immunoassays for the detection of Taenia solium cysticercosis in swine with low parasite burden

Seven swine were experimentally infected with Taenia solium eggs and blood samples from each animal were periodically collected. At the end of the experiment (t140) the animals did not show clinical aspects of cysticercosis or parasites in tongue inspection. All animals were slaughtered and cut into thin slices in searching for cysts. The number of cysts found in each animal varied from 1 to 85. Enzyme-linked immunosorbent assay (ELISA) tests for antibody (Ab) detection and for antigen (Ag) detection were performed, which presented respectively 71 and 57% of positivity. By immunoblot (IB), using 18/14(T. crassiceps Ag) or lentil-lectin-purified glycoproteins from T. solium Ag (LLGP) as Ag, five (71%) and six (86%) animals were positive, respectively. The association between Ag-ELISA with any IB (18/14 or LLGP) allowed the detection of all animals at 140 days post-experimental infection (days p.e.i.). The use of IB 18/14 combined to the Ag-ELISA allowed the detection of all animals since 70 days p.e.i., and the association between IB LLGP and Ag-ELISA allowed the detection of all animals since 112 days p.e.i. While all animals could be considered healthy by conventional screening tests, the use of immunoassays for detecting Ab and Ag showed better accuracy; therefore it would be more useful than usual clinical examination for screening cysticercosis in slightly infected pigs.     

Whole ricin and recombinant ricin A chain idiotype-specific immunotoxins for therapy of the guinea pig L2C B cell leukemia

The therapeutic efficacy of whole ricin, or recombinant ricin A chain, coupled to a monoclonal antibody that reacts with the idiotype of the surface IgM expressed on guinea pig L2C lymphoblasts, was assessed. In vitro studies were done to characterize the immunotoxins (IT) and to demonstrate their specificity before use in vivo. The concentration of whole ricin IT (M6-Ricin) that inhibited protein synthesis by 50% (IC50) in L2C cells was 1.4 X 10(-9) M, in a 5-hr assay, in the presence of lactose to block non-antibody-directed toxicity. M6-Ricin did not inhibit protein synthesis in two control guinea pig cell lines that did not express the idiotype, nor did a whole ricin IT prepared with an isotype-matched monoclonal antibody of irrelevant specificity inhibit protein synthesis in L2C cells. Two recombinant ricin A chain IT, which differed from one another by a factor of 2 to 3 in the number of A chains conjugated per antibody molecule, were less effective in vitro than M6-Ricin (IC50 of greater than 5 X 10(-8) M). For in vivo experiments, the IT were given by the i.p. route 24 hr after the i.p. inoculation of 1 X 10(5) L2C cells. The highest doses of M6-Ricin and M6-Ricin A chain IT tested, 30 micrograms/kg and 3000 micrograms/kg, respectively, were within fourfold to fivefold of their maximum tolerated doses; no deaths or ill effects due to ricin toxicity were noted. These doses increased the median survival time of L2C-bearing guinea pigs to 31 to 34 days, compared with 15 days for untreated animals. This magnitude of increase in survival indicates that 99.999% (5 logs) of injected tumor cells were eliminated, thus accounting for the 12% long-term survival rate obtained. Median survival times for guinea pigs treated with 30 micrograms/kg of the A chain IT were 18 and 21 days for the two conjugates tested, and the median survival for guinea pigs treated with 3000 micrograms/kg of unconjugated antibody was 18 days. Our data demonstrate that recombinant A chain IT are active in vivo and that the B chain of ricin can potentiate IT activity in vivo. Although the potency differs by 100-fold, the therapeutic index of the intact ricin IT is similar to that of the ricin A chain IT.     

The fate of cyclamate in man and other species

1. (14)C-labelled cyclamate has been administered to guinea pigs, rabbits, rats and humans. When given orally to these species on a cyclamate-free diet, cyclamate is excreted unchanged. In guinea pigs some 65% of a single dose is excreted in the urine and 30% in the faeces, the corresponding values for rats being 40 and 50%, for man, 30-50% and 40-60%, and for rabbits, 90 and 5%, the excretion being over a period of 2-3 days. 2. Cyclamate appears to be readily absorbed by rabbits but less readily by guinea pigs, rats and humans. 3. If these animals, including man, are placed on a diet containing cyclamate they develop the ability to convert orally administered cyclamate into cyclohexylamine and consequently into the metabolites of the latter. The extent to which this ability develops is variable, the development occurring more readily in rats than in rabbits or guinea pigs. In three human subjects, one developed the ability quite markedly in 10 days whereas two others did not in 30 days. Removal of the cyclamate from the diet caused a diminution in the ability to convert cyclamate into the amine. 4. In rats that had developed the ability to metabolize orally administered cyclamate, intraperitoneally injected cyclamate was not metabolized and was excreted unchanged in the urine. The biliary excretion of injected cyclamate in rats was very small, i.e. about 0.3% of the dose. 5. The ability of animals to convert cyclamate into cyclohexylamine appears to depend upon a continuous intake of cyclamate and on some factor in the gastrointestinal tract, probably the gut flora.     

Ebola GP-specific monoclonal antibodies protect mice and guinea pigs from lethal Ebola virus infection

Ebola virus (EBOV) causes acute hemorrhagic fever in humans and non-human primates with mortality rates up to 90%. So far there are no effective treatments available. This study evaluates the protective efficacy of 8 monoclonal antibodies (MAbs) against Ebola glycoprotein in mice and guinea pigs. Immunocompetent mice or guinea pigs were given MAbs i.p. in various doses individually or as pools of 3-4 MAbs to test their protection against a lethal challenge with mouse- or guinea pig-adapted EBOV. Each of the 8 MAbs (100 μg) protected mice from a lethal EBOV challenge when administered 1 day before or after challenge. Seven MAbs were effective 2 days post-infection (dpi), with 1 MAb demonstrating partial protection 3 dpi. In the guinea pigs each MAb showed partial protection at 1 dpi, however the mean time to death was significantly prolonged compared to the control group. Moreover, treatment with pools of 3-4 MAbs completely protected the majority of animals, while administration at 2-3 dpi achieved 50-100% protection. This data suggests that the MAbs generated are capable of protecting both animal species against lethal Ebola virus challenge. These results indicate that MAbs particularly when used as an oligoclonal set are a potential therapeutic for post-exposure treatment of EBOV infection.     

New animal model of shigellosis in the Guinea pig: its usefulness for protective efficacy studies

It has been difficult to evaluate the protective efficacy of vaccine candidates against shigellosis, a major form of bacillary dysentery caused by Shigella spp. infection, because of the lack of suitable animal models. To develop a proper animal model representing human bacillary dysentery, guinea pigs were challenged with virulent Shigella flexneri serotype 2a (strains 2457T or YSH6000) or S. flexneri 5a (strain M90T) by the intrarectal (i.r.) route. Interestingly, all guinea pigs administered these Shigella strains developed severe and acute rectocolitis. They lost approximately 20% of their body weight and developed tenesmus by 24 h after Shigella infection. Shigella invasion and colonization of the distal colon were seen at 24 h but disappeared by 48 h following i.r. infection. Histopathological approaches demonstrated significant damage and destruction of mucosal and submucosal layers, thickened intestinal wall, edema, erosion, infiltration of neutrophils, and depletion of goblet cells in the distal colon. Furthermore, robust expression of IL-8, IL-1beta, and inducible NO synthase mRNA was detected in the colon from 6 to 24 h following Shigella infection. Most importantly, in our new shigellosis model, guinea pigs vaccinated with an attenuated S. flexneri 2a SC602 strain possessing high levels of mucosal IgA Abs showed milder symptoms of bacillary dysentery than did animals receiving PBS alone after Shigella infection. In the guinea pig, administration of Shigella by i.r. route induces acute inflammation, making this animal model useful for assessing the protective efficacy of Shigella vaccine candidates.     

Rearing of germfree guinea pigs and establishment of an SPF guinea pig colony]

New born guinea pigs of Hartley strain derived by hysterectomy were fed commercial pellets, cow's milk, egg yolk and vitamin mixture since 0 days of age, when they were kept at 31 +/- 1 degrees C. Out of 33 animals, 30 were reared for 40 days under aseptic state and they were transfered to a barrierred facility to establish an SPF colony free from Bordetella bronchiseptica, Streptococcus zooepidemicus (Animal C), Salmonella spp., Tyzzer's organisms, Mycoplasma spp., Reo 3 virus, Sendai virus, Eimeria spp., Chirodiscoides caviae and Gliriocola porcelli.     

Development of an animal model of late asthmatic response in guinea pigs and effects of anti-asthmatic drugs.

We developed an animal model of late asthmatic response (LAR) in guinea pigs and examined the effects of anti-asthmatic drugs and peptide leukotriene antagonist, MCI-826, on this model. Bronchial challenge of DNP-As (Dinitrophenylated-Ascaris suum extract)-sensitized guinea pigs induced a biphasic increase in pulmonary resistance (RL) with the maximal increase being observed immediately (IAR, immediate asthmatic response) and 3 to 5 hr after antigen inhalation (LAR). Twelve of 22 guinea pigs showed both IAR and LAR. The average increases in RL for all 22 guinea pigs at IAR and LAR, were 168 +/- 13 and 207 +/- 16 (% of baseline value), respectively. Bronchoalveolar lavage (BAL) fluid of guinea pigs that received antigen, revealed increases in the numbers of eosinophils (7.3-fold compared to animals receiving saline) and neutrophils (5.3-fold compared to animals receiving saline) 4 hr after antigen inhalation. When DSCG (disodium cromoglycate) was administered (10 mg/kg, i.v.) before antigen challenge, DSCG significantly inhibited IAR (p less than 0.05) and slightly inhibited LAR (p less than 0.2). Theophylline (30 mg/kg, p.o.) administered before antigen, slightly inhibited both IAR and LAR (p less than 0.2). Salbutamol (3 mg/kg, i.p.) administered before antigen, significantly inhibited IAR (p less than 0.05), but did not affect LAR. These results were correlated with clinical trials. Moreover, peptide leukotriene antagonist, MCI-826, (E)-2,2-Diethyl-3'-[2-[2-(4- isopropyl)thiazolyl] ethenyl]succinanilic acid (0.1 mg/kg, p.o.) administered 1 hr before antigen challenge, significantly inhibited both IAR and LAR (p less than 0.05). MCI-826 (0.1 mg/kg, p.o.) administered 1.5 hr after antigen inhalation, also inhibited LAR (p less than 0.05). Analysis of BAL fluid revealed that DSCG and MCI-826 significantly inhibited the increase in eosinophils (p less than 0.05). These data suggest that leukotriene plays an important role in the development of the pathogenesis of LAR, and that our model is an useful experimental model for investigating the mechanisms of LAR and examining the effects of several anti-asthmatic drugs on LAR.     

Biochemical and pharmacological activities of SSR 146977, a new potent nonpeptide tachykinin NK3 receptor antagonist

SSR 146977 is a potent and selective antagonist of the tachykinin NK3 receptor. In Chinese hamster ovary cells expressing the human tachykinin NK3 receptor, SSR 146977 inhibited the binding of radioactive neurokinin B to NK3 receptors (Ki = 0.26 nM), senktide (10 nM) induced inositol monophosphate formation (IC50 = 7.8-13 nM), and intracellular calcium mobilization (IC50 = 10 nM). It antagonized [MePhe7]neurokinin B induced contractions of guinea pig ileum (pA2 = 9.07). Senktide (30 nM) induced firing rate increase of noradrenergic neurons in the guinea pig locus coeruleus and dopaminergic neurons in the guinea pig substantia nigra was also blocked by SSR 146977 (50 and 100 nM, respectively). In vivo, in the respiratory system, SSR 146977 inhibited bronchial hyperresponsiveness to acetylcholine, bronchial microvascular permeability hypersensitivity to histamine (doses of 0.1-1 mg/kg i.p.), and cough (doses of 0.03-1 mg/kg i.p.) provoked by citric acid in guinea pigs. In the central nervous system, SSR 146977 inhibited turning behaviour (ID50 = 0.2 mg/kg i.p. and 0.4 mg/kg p.o.) and prevented the decrease of locomotor activity (10 and 30 mg/kg i.p) mediated by the stimulation of NK3 receptors in gerbils. In guinea pigs, SSR 146977 antagonized senktide-induced acetylcholine release in the hippocampus (0.3 and 1 mg/kg i.p) and norepinephrine release in the prefrontal cortex (0.3 mg/kg i.p.). It also prevented haloperidol-induced increase of the number of spontaneously active dopamine A10 neurons (1 and 3 mg/kg i.p.).     

Non-specific antimicrobial cellular resistance in sensitized guinea pigs.

Specific delayed-type hypersensitivity was induced in guinea pigs with bovine albumin + complete Freund adjuvant, bovine gamma globulin + complete Freund adjuvant and BCG vaccine. The animals were subsequently tested for nonspecific antimicrobial resistance. Sensitized and control groups were challenged intraperitoneally with Listeria monocytogenes 2 hr after reinjection with the sensitizing antigen. The listeria content of the spleens was determined 1 or 5 days after the infection. The number of organisms recovered from the spleen one day after infection was significantly less in guinea pigs sensitized with bovine gamma globulin and BCG than in the control group; after 5 days no such difference was recorded. There was no difference between the bovine albumin sensitized and the control group 1 day after infection, while on the 5th postinfection day listeria counts were higher in the sensitized than in the control animals.     

Guinea pig model of Mycobacterium tuberculosis latent/dormant infection

Although guinea pigs are considered one of the best animal models of tuberculosis, little data exist describing latent or dormant tuberculosis infection in these animals. Here we address this issue using a streptomycin auxotrophic mutant of Mycobacterium tuberculosis. This mutant grows unimpaired in the presence of streptomycin but in its absence shifts to latency/dormancy (lack growth and over-expression of alpha-crystallin). To establish infection animals are inoculated with the mutant followed by daily administration of streptomycin (three weeks), which allows initial microbial multiplication in the animal's tissues. Withdrawal of streptomycin establishes latency/dormancy and few viable organisms are recovered from the animals' lungs and spleen six months later. During the infectious process guinea pigs steadily gained weight and presented no clinical signs (scuff fur and lethargy) of disease. Histopathology of organs mimicked tuberculous lesions in humans and PBMC from infected animals strongly responded to stimulation with PPD. Finally, tuberculin skin test (a hallmark of latent infection diagnosis) performed in infected animals was strongly positive (>or=15 mm induration). These results point to an interesting and reliable model of latent/dormant tuberculosis infection in guinea pigs.     

Enhanced multiplication and transmission of Streptococcus pneumoniae in guinea pigs by Sendai virus infection

It was demonstrated that the transmission S. pneumoniae in guinea pigs was remarkably promoted by the combined infection with Sendai virus in the following experiments. When guinea pigs infected with S. pneumoniae alone (infector) were cagemated with non-treated guinea pigs (contact) for 2 and 4 weeks, only 2 of 30 contacts were infected with the organism. On the contrary, when the contact guinea pigs were infected with Sendai virus and immediately cage-mated with the infectors, the pneumococcal infection occurred in 25 of 30 contacts during 2 to 4 weeks period. In the experiment in which 30 non-treated contacts were cage-mated with pneumococcal infectors for 4 weeks and then infected with Sendai virus, no pneumococcal infection was demonstrated in the contacts, suggesting no presence of latent infection of the organism in the contact guinea pigs. Twenty-five of 30 contacts suffered from pneumococcal infection when they were exposed to Sendai virus for 2 weeks and then cage-mated with infectors. The multiplication of S. pneumoniae in the respiratory tract of the guinea pigs was remarkably enhanced by combined infection with Sendai virus. Namely, a 1000-fold increase in the number of organism resulted in the guinea pigs suffered from combined infection as compared with that in the animals received pneumococcal single infection.     

急性巨细胞病毒感染导致新生豚鼠脾细胞亚群的定量改变

新生豚鼠皮下接种豚鼠巨细胞病毒(GPCMV)后,导致脾脏GPCMV急性感染,脾脏肿大,脾细胞增生,计算表明,脾T淋巴细胞,B淋巴细胞、吞噬细胞数显著高于正常动物,接种病毒后第5天即可在脾细胞检出高滴度感染性病毒(达2.5 log10 TCID50/10~7细胞),其中,主要是脾B淋巴细胞、T淋巴细胞和巨噬细胞携带病毒。     

Recombinant IgA Is Sufficient To Prevent Influenza Virus Transmission in Guinea Pigs

A serum hemagglutination inhibition (HAI) titer of 40 or greater is thought to be associated with reduced influenza virus pathogenesis in humans and is often used as a correlate of protection in influenza vaccine studies. We have previously demonstrated that intramuscular vaccination of guinea pigs with inactivated influenza virus generates HAI titers greater than 300 but does not protect vaccinated animals from becoming infected with influenza virus by transmission from an infected cage mate. Only guinea pigs intranasally inoculated with a live influenza virus or a live attenuated virus vaccine, prior to challenge, were protected from transmission (A. C. Lowen et al., J. Virol. 83:2803–2818, 2009.). Because the serum HAI titer is mostly determined by IgG content, these results led us to speculate that prevention of viral transmission may require IgA antibodies or cellular immune responses. To evaluate this hypothesis, guinea pigs and ferrets were administered a potent, neutralizing mouse IgG monoclonal antibody, 30D1 (Ms 30D1 IgG), against the A/California/04/2009 (H1N1) virus hemagglutinin and exposed to respiratory droplets from animals infected with this virus. Even though HAI titers were greater than 160 1 day postadministration, Ms 30D1 IgG did not prevent airborne transmission to passively immunized recipient animals. In contrast, intramuscular administration of recombinant 30D1 IgA (Ms 30D1 IgA) prevented transmission to 88% of recipient guinea pigs, and Ms 30D1 IgA was detected in animal nasal washes. Ms 30D1 IgG administered intranasally also prevented transmission, suggesting the importance of mucosal immunity in preventing influenza virus transmission. Collectively, our data indicate that IgG antibodies may prevent pathogenesis associated with influenza virus infection but do not protect from virus infection by airborne transmission, while IgA antibodies are more important for preventing transmission of influenza viruses.     

Therapy of experimental staphylococcal infection with a hyperimmune antistaphylococcal plasma

Generalized nonlethal infection was induced in guinea pigs by the intramuscular injection of 10(10) S. aureus cells, and on days 1, 3 and 5 after inoculation a half of the animals received antistaphylococcal hyperimmune human plasma intraperitoneally in a dose of 2 ml (6 AU/ml) per animal. This plasma decreased the number of staphylococcal colonies in the spleen and affected mainly the system of phagocytes (neutrophils): on day 3 the percentage of neutrophils with Fc gamma R increased in the treated guinea pigs in comparison with the controls and with the initial level; from day 6 the percentage of active neutrophils with Fc gamma R increased in the treated animals in comparison with the controls; on day 14 the percentage of such neutrophils increased in comparison with the initial level as well, and the treated guinea pigs also showed an increase in the content of lymphocytes with receptors for staphylococci in comparison with the controls. There was little difference in the content of neutrophils with CR, as well as in the percentage of active phagocytes with these receptors, in the treated animals and in the controls. By the moment of the resolution of generalization (day 14) the content of active T-lymphocytes increased in the treated guinea pigs in comparison with the controls and with the initial level; simultaneously the levels of B-lymphocytes and B-lymphocytes with receptors for mouse red blood cells returned to their initial values.