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PubMed1994

Eotaxin: a potent eosinophil chemoattractant cytokine detected in a guinea pig model of allergic airways inflammation.

Eosinophil accumulation is a prominent feature of allergic inflammatory reactions, such as those occurring in the lung of the allergic asthmatic, but the endogenous chemoattractants involved have not been identified. We have investigated this in an established model of allergic inflammation, using in vivo systems both to generate and assay relevant activity. Bronchoalveolar lavage (BAL) fluid was taken from sensitized guinea pigs at intervals after aerosol challenge with ovalbumin. BAL fluid was injected intradermally in unsensitized assay guinea pigs and the accumulation of intravenously injected 111In-eosinophils was measured. Activity was detected at 30 min after allergen challenge, peaking from 3 to 6 h and declining to low levels by 24 h. 3-h BAL fluid was purified using high performance liquid chromatography techniques in conjunction with the skin assay. Microsequencing revealed a novel protein from the C-C branch of the platelet factor 4 superfamily of chemotactic cytokines. The protein, "eotaxin," exhibits homology of 53% with human MCP-1, 44% with guinea pig MCP-1, 31% with human MIP-1 alpha, and 26% with human RANTES. Laser desorption time of flight mass analysis gave four different signals (8.15, 8.38, 8.81, and 9.03 kD), probably reflecting differential O-glycosylation. Eotaxin was highly potent, inducing substantial 111In-eosinophil accumulation at a 1-2 pmol dose in the skin, but did not induce significant 111In-neutrophil accumulation. Eotaxin was a potent stimulator of both guinea pig and human eosinophils in vitro. Human recombinant RANTES, MIP-1 alpha, and MCP-1 were all inactive in inducing 111In-eosinophil accumulation in guinea pig skin; however, evidence was obtained that eotaxin shares a binding site with RANTES on guinea pig eosinophils. This is the first description of a potent eosinophil chemoattractant cytokine generated in vivo and suggests the possibility that similar molecules may be important in the human asthmatic lung.

Amino Acid Sequence↗
PubMed1973

Blood changes in experimental arthritis in two types of genetically different rats.

1. Rats genetically resistant to dextran and other agents producing the anaphylactoid reaction (NR rats), have a higher polymorph count than do rats which react to these agents (R rats).2. NR rats do not develop polyarthritis when a hind paw is injected intradermally with Freund's adjuvant.3. The polyarthritis produced by an intravenous injection of Mycoplasma arthritidis culture develops more slowly in NR rats than in R rats.4. It is not clear whether the higher polymorph count in NR rats is a main factor in determining their resistance to adjuvant-induced arthritis.

Animals↗
PubMed2001

Depletion of plasma factor XIII prevents disseminated intravascular coagulation-induced organ damage.

The impact of clot stability affecting the vasculopathy and tissue necrosis in Shwartzman reaction was investigated using plasma Factor XIII A2-depleted rabbit (FXIII-DR). Plasma Factor XIIIA2 (FXIIIA2) was depleted by infusion of the mono-specific goat anti-rabbit FXIIIA2 IgG. Generalized Shwartzman reaction (GSR) was induced by priming and challenged by i.v. injection of LPS and local Shwartzman reaction (LSR) was primed by intradermal injection of LPS and challenged by i.v. injection of LPS. Histological examination of the GSR animals showed, extensive thrombi accumulation in renal tubules and bilateral cortical necrosis of kidney in 8 out of 10 rabbits but none in the FXIII-DR. Fibrinogen levels were elevated to 3 approximately 4 fold at 24 h and lowered at 48 h whereas a steady rise was seen in the FXIII-DR. FDP levels in GSR animals were significantly elevated at 24 h and further increased at 48 h but only slightly elevated in the FXIII-DR. Examination of the LSR tissues after 48 h showed an acute onset of progressive cutaneous vascular thrombosis, purpura, and secondary hemorrhagic necrosis whereas neither fibrin deposit nor necrosis of tissue were detected in FXIII-DR despite of an early edema formation. Fibrinogen levels were also increased two fold at 24 h but returned to basal levels at 48 h in control LSR animals but not affected at all in FXIII-DR. These results suggest that during the severe inflammatory conditions such as sepsis, the fibrinolytic system is functionally sufficient to dissipate the pathogenic accumulation of disseminated intravascular clots and exudated fibrin clots if those clots were prevented from getting crosslinked in plasma.

Animals↗
PubMed1982

Evaluation of the intradermal allergy test in normal dogs.

In 45 normal dogs, serial dilutions of different allergens were injected intradermally to determine the skin threshold concentrations. For housedust, housedust mite (Dermatophagoides pteronyssinus) and human dandruff extracts these were found to be the same in the dog as in man, while those for animal dandruffs, pollens and fungi were 10 times higher in the dog. The term 'histamine reactive value' (RH) is introduced for the dog. The mean (+/-SD) was found to be 49.0 +/- 2.5 in normal dogs, using histamine diphosphate solutions of 0.01, 0.1 and 1 per cent.

Allergens↗
PubMed2004

Lack of effect of two oral sodium channel antagonists, lamotrigine and 4030W92, on intradermal capsaicin-induced hyperalgesia model.

Preclinical studies have emphasized that persistent small afferent input will induce a state of central facilitation, which can be regulated by systemically administered sodium channel blockers. We have extended these preclinical studies to the human volunteers by examining the effects of lamotrigine and 4030W92, two structurally related voltage-sensitive sodium channel antagonists, on acute sensory thresholds and facilitated processing induced by intradermal capsaicin. Fifteen healthy subjects received 4030W92, lamotrigine, and placebo in a randomized order using double-blinded crossover design methodology in three sessions each separated by a 7-day washout period. In each session, baseline neurosensory testing was performed on the volar aspect of the subject's left forearm. Subjects were then dosed with either lamotrigine (300 mg), 4030W92 (100 mg), or placebo, followed 2 h later by capsaicin (100 microg) injected intradermally on the volar aspect of the left forearm. Pain scores, blood pressure, heart rate, and respiratory rate were measured at the time of injection and every 5 min for 15 min. Fifteen minutes after the capsaicin injection, the hyperalgesic area was determined by von Frey hair, stroking, and heat; the flare response was outlined; and neurosensory testing again was performed halfway between the edge of the hyperalgesic area and the capsaicin injection site. While capsaicin significantly decreased the hot pain and VF pain thresholds, oral lamotrigine and 4030W92 failed to alter this response to capsaicin, relative to placebo treatment. Similarly, oral lamotrigine or 4030W92 did not alter the pain scores reported from mechanical pain stimuli at any time postcapsaicin. This study showed a lack of effect of two structurally similar sodium channel antagonists on a human experimental pain model using intradermal capsaicin, which is consistent with other studies on the effects of sodium channel antagonists of capsaicin-induced pain and hyperalgesia. This lack of effect stands in contrast to reported effects of sodium channel antagonists on preclinical models of cutaneous hyperalgesia or effects of lamotrigine on clinical neuropathic pain.

Administration, Oral↗
PubMed1980

Characteristics of prostaglandin E1 potentiation of inflammatory activity of some agents.

In rats pretreated with indomethacin, injection of PGE1 (prostaglandin E1) with carrageenan potentiated the carrageenan paw oedema. This effect of PGE1, was maximal when it was injected together with carrageenan, there being a reduction in the action of PGE1 if carrageenan injection was delayed after PGE1 injection. PGE1 induced potentiation of increase in plasma protein leakage induced by intradermal injections of bradykinin and histamine also depended on the injection of PGE1 along with these agents. Thus oedema enhancement by PGE1 differs from its action in pain, where PGs cause a long lasting sensitization of the injected area for the actions of other algesics. Since vasodilation may be a mechanism of oedema enhancement by PGs, the ability of adenosine and papaverine to mimic PGE1 in paws and skins of rats were examined. Adenosine was active whereas papaverine was inactive in this respect. To clarify this difference, the vasodilatory properties of PGE1, adenosine and papaverine were assessed by their ability to antagonize NA response in perfused rat mesenteric blood vessels. Only papaverine was effective in antagonising the NA response. Thus, PGE1 and adenosine which potentiated the oedema inducing actions of other agents showed no vasodilatory properties and papaverine, a vasodilator, had no oedema potentiating actions.

Adenosine↗
PubMed1977

Responses of tumors induced in inbred guinea pig strain JY=1 and strain Hartley/F to BCG.

A transplantable fibrosarcoma induced in inbred JY-1 guinea pig strain by 3-methylcholanthrene (MCA) and designated J4, an allotransplantable subline of J4 (JH4) which was obtained by the transplantation of J4 into the inbred Hartley/F guinea pig strain and maintained by passages in this strain, and a syngeneic liposarcoma H10 induced in a Hartley/F guinea pig by MCA were tested for their immunotherapeutic response with BCG. The growth of J4 and H10 tumors was suppressed in most of the animals when tumor cells were mixed with BCG before being injected sc into BCG-immune or BCG-nonimmune recipients. The growth of the JH4 tumor was suppressed at the sites of injection with a mixture of tumor cells and BCG in BCG-immune recipients but not in nonimmune animals. All guinea pigs surviving the injection of a tumor cell-BCG mixture resisted a second tumor cell challenge. When subcutaneous sarcomas grew to about 8-15 mm in diameter, BCG was injected into the tumors. The growth of JH4 tumor was not influenced by the injection in either BCG-immune or BCG-nonimmune animals, while the regression of the established J4 transplants was produced in 2 of 3 nonimmune recipients. The growth of the H10 tumor was not inhibited with an intratumor injection into nonimmune guinea pigs, while the H10 tumor regressed in BCG-immune animals for 4-5 weeks after intratumor injection and thereafter grew progressively. Skin reactions in animals that received repeated intradermal injections of the tumor cells and BCG were tested with 10(6) viable tumor cells as eliciting antigens. Typical delayed-type hypersensitivity reactions that were specific to the homologous antigens were observed. The possible reasons for the different responses to BCG among the guinea pig tumors, including line-10 hepatocarcinoma in strain-2 guinea pigs, were discussed.

Animals↗
PubMed1997

T-lymphocyte dependence of psoriatic pathology in human psoriatic skin grafted to SCID mice.

Considerable indirect evidence suggests that T lymphocytes have a role in the pathogenesis of psoriasis. The goal of this study was to directly test the ability of T cells to maintain psoriasis pathology. Psoriatic skin was transplanted onto SCID mice, which were then injected with autologous T cells. T cells were cultured from either psoriatic skin lesions or peripheral blood and injected intradermally or intravenously. Control SCID mice transplanted with psoriasis grafts were not injected with T cells. After 10 wk, control psoriatic skin grafts not injected with T cells lost many of the features of psoriasis. Injection of peripheral blood T cells was not able to maintain these psoriatic features. In contrast, the injection of T cells derived from psoriatic skin was able to maintain the psoriatic phenotype. Psoriatic features that were maintained included epidermal thickness and labeling index and expression of HLA-DR, involucrin, and ICAM-1, as well as loss of expression of filaggrin. Injection of skin infiltrating T cells into skin of normal donors on SCID mice did not induce changes of psoriasis. The ability of T cells from lesional skin, but not peripheral blood, to maintain psoriasis suggests that psoriasis is mediated by an autoantigen reactive T cell, which is present at a higher frequency in the psoriatic lesion.

Adoptive Transfer↗
PubMed1991

Dermal and serological response against Pseudomonas aeruginosa in sheep bred for resistance and susceptibility to fleece-rot.

Genetically select lines of Merino sheep have been bred at Trangie (NSW Agriculture and Fisheries) for resistance (R) or susceptibility (S) to fleece-rot and flystrike. It is believed that fleece characters are primarily responsible for the R or S phenotype. When transferred to the wetter coastal environment of Sydney, R and S sheep with no more than 6 weeks wool cover, continued to show significant differences in the incidence and severity of fleece-rot dermatitis. To test the hypothesis that these sheep might also exhibit differences in their local skin reactions and immune responsiveness, 3 intradermal injections of killed Pseudomonas aeruginosa were administered at monthly intervals. After primary intradermal challenge, R sheep had a higher incidence of skin induration and a stronger inflammatory response (increased induration diameter) than S sheep. Compared to S sheep, R sheep also developed higher levels of circulating antibodies against whole cell antigen and both inner and outer membrane proteins of P. aeruginosa. These responses were maintained in R sheep with each consecutive challenge while S sheep showed a decline in their immune responsiveness. Differences in antibody response against outer membrane proteins were also detected when antigenically naive sheep from each genetic line were sensitised by epicutaneous challenge with P. aeruginosa under experimental wetting conditions. Intradermal challenge of these animals 6 months later with outer membrane proteins, revealed a late maximum (72 h) in the development of induration diameters for R sheep while S animals showed maximal induration diameters by 24 h. However, there was no significant difference in induration response between 24 h and 72 h within each group of sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2007

Lactoferrin, a glycoprotein with immunomodulatory and mast cell stabilising properties, in skin of horses suffering from Culicoides hypersensitivity.

Lactoferrin (LF), a glycogen of the transferrin family with anti-bacterial and immunomodulatory properties, is expressed in various secretions and tissues. Cutaneous LF serves as a mast cell stabilising compound, modulates T cell activity and is found during IgE-mediated late phase reactions at allergen challenged sites. Culicoides hypersensitivity (CHS) in horses is a common IgE-mediated allergic dermatitis, characterised by an early and late phase cutaneous reaction upon allergen challenge. The aim of the study presented here was to examine whether LF mRNA expression in skin biopsies from horses affected by CHS prior to and 4h following intradermal challenge with a commercial C. nubeculosus extract is modified in comparison to skin biopsies from non-affected horses. In order to obtain reliable data, real time PCR was performed and genes of interest were normalized using three different housekeeping genes, beta-actin, GAPDH, beta-2-microglobulin. In comparison to non-affected horses, higher variation in LF mRNA levels both prior to and post-intradermal challenge with C. nubeculosus extract was seen in horses affected by CHS. However, the statistical analysis demonstrated that LF mRNA expression was not significantly different between CHS affected and non-affected horses prior to intradermal challenge with C. nubeculosus extract. Intradermal injection of C. nubeculosus extract did not result in local upregulation of LF mRNA at 4h post-injection. LF mRNA expression was therefore not significantly different pre- or post-intradermal challenge with C. nubeculosus extract in either group. Our data indicate that clinically normal skin of horses affected by CHS is not characterized by modified maintenance levels of LF mRNA. In contrast to human skin allergen challenged sites, LF mRNA levels in horses affected by CHS are not significantly different to that of control sites at 4h post-injection of C. nubeculosus extract.

Animals↗
PubMed1988

Early burn wound excision and skin grafting postburn trauma restores in vivo neutrophil delivery to inflammatory lesions.

This study assessed the effect of early vs delayed postburn wound excision and skin grafting on the in vivo neutrophil delivery to a delayed-type hypersensitivity (DTH) reaction and a bacterial skin lesion (BSL). Male Lewis rats were presensitized to keyhole-limpet hemocyanin. Group 1 comprised sham controls. Groups 2 through 4 were given a 30% 3 degrees scald burn, but the burn wounds were excised, and skin was grafted on days 1, 3, and 7, respectively, after the burn. Group 5 comprised burn controls. Twelve days after burn trauma, all rats were injected at different intervals (during a 24-hour period) with a trio of intradermal injections of keyhole-limpet hemocyanin, Staphylococcus aureus 502A, and saline at different sites. In vivo neutrophil delivery to these dermal lesions was determined by injecting indium in 111 oxyquinoline-labeled neutrophils isolated from similarly treated groups of rats. Neutrophil delivery to DTH and BSL lesions was restored to normal by excision and skin grafting of the burn wound one day after burn trauma. Waiting three days after burn trauma to excise and skin graft the wound partially, but not completely, restored the in vivo neutrophil delivery to DTH and BSL lesions. Waiting one week to excise and skin graft a burn wound resulted in no improvement in neutrophil delivery to DTH and BSL dermal lesions. It was concluded that burn wound excision and skin grafting immediately after burn trauma restored in vivo neutrophil delivery to a BSL and DTH dermal lesion. This may, in part, explain the beneficial effect of early aggressive burn wound debridement in patients with burn injuries.

Animals↗
PubMedDate not supplied

The characterization of Leishmania from patients with lymphadenopathy in Shiraz, Iran.

Leishmania were cultured from enlarged lymph nodes of 6 of 18 patients with localized lymphadenitis and no other sign or symptom of leishmaniasis in Shiraz, Iran. The organisms failed to produce visible lesions when injected intradermally or intraperitoneally into Swiss outbred white or Balb/c mice. Golden hamsters similarly injected appeared well 16 weeks later, but histological examination of their spleens and livers revealed a few amastigotes in sections of the liver of one. Lectin agglutination profiles of promastigotes cultured from 2 of the patients were identical with those obtained with the World Health Organization reference strain of L. tropica (MHOM/SU/74/K27). Isoenzyme characterization of one of the isolates showed it to be L. tropica zymodeme LON18.

Adolescent↗
PubMed2003

Sentinel node identification and the ability to detect metastatic tumor to inguinal lymph nodes in squamous cell cancer of the vulva.

OBJECTIVES: The goal of this study was to identify one or more inguinal sentinel nodes in patients with primary squamous cell carcinoma of the vulva and to determine the ability of the sentinel node to predict metastasis to the inguinal lymphatic basin. METHODS: Techniques employing technetium-99m (Tc-99m) sulfur colloid and isosulfan blue dye were utilized to identify sentinel nodes in the inguinal lymphatic beds. Technetium-99m sulfur colloid was injected intradermally at the tumor margins 90-180 min preoperatively followed by a similar injection of isosulfan blue dye 5-10 min before the groin dissection. A handheld collimated gamma counter was employed to identify Tc-99m-labeled sentinel nodes. Lymphatic tracts that had taken up blue dye and their corresponding sentinel node were also identified and retrieved. A completion inguinal dissection was then performed. Each sentinel node was labeled as hot and blue, hot and nonblue, or cold and blue. The sentinel nodes were subjected to pathologic examination with step sections and nonsentinel nodes were evaluated in the standard fashion. RESULTS: Twenty-one patients with a median age of 79 were entered onto protocol and a total of 31 inguinal node dissections were performed. A sentinel node was identified in 31/31 (100%) groin dissections with the use of Tc-99m. Isosulfan blue dye identified a sentinel node in 19/31 (61%) groin dissections. Surgical staging revealed 7 patients with stage I disease, 5 with stage II disease, 5 with stage III disease, and 4 with stage IV disease. Lymph nodes in 9 groin dissections were found to have metastatic disease, and in 4 of these dissections, the sentinel node was the only positive node. Lymph nodes in 22 groin dissections had no evidence of metastasis. No false-negative sentinel lymph nodes were obtained (sentinel node negative and a nonsentinel node positive). CONCLUSION: Tc-99m sulfur colloid is superior to isosulfan blue dye in the detection of sentinel nodes in inguinal dissections of patients with vulvar cancer. A sentinel node dissection utilizing Tc-99m alone can identify a sentinel node in all inguinal dissections. Pathologic examination with step sections has shown the sentinel node to be an accurate predictor of metastatic disease to the inguinal nodal chain.

Carcinoma, Squamous Cell↗
PubMed1999

Evidence that mast cell degranulation, histamine and tumour necrosis factor alpha release occur in LPS-induced plasma leakage in rat skin.

1. In the present study we investigated the role of mast cells during inflammation in rat skin. As the release of several pro-inflammatory mediators, such as histamine and tumour necrosis factor alpha (TNFalpha), occurs following mast cell activation we studied whether mast cell degranulation and the release of both histamine (H) and TNFalpha occurred in a model of lipopolysaccharide (LPS)-induced plasma leakage in rat skin. 2. Plasma leakage in the rat skin was measured over a period of 2 h as the local accumulation of intravenous injection of 125I-human serum albumin (125I-HSA) in response to intradermal injection of LPS. LPS (10 microg site-1) produced an increase of plasma leakage (50.1+/-2.3 microl site-1) as compared to saline (9.0+/-3.2 microl site-1). Histological analysis of rat tissue showed that LPS induced a remarkable mast cell degranulation (59.8+/-2.1%) as compared to saline (13.5+/-2.2%). 3. Ketotifen (10-9 - 10-7 mol site-1), a well-known mast cell-membrane stabilizer, produced a dose-related inhibition of LPS-induced plasma leakage by 36+/-3.5%, 47+/-4.0%, 60+/-3.3% respectively. In addition, ketotifen (10-7 mol site-1) inhibited mast cell degranulation by 59. 2+/-2.7%. 4. Chlorpheniramine maleate (CPM) (10-9 - 10-7 mol site-1), an H1 histamine receptor antagonist only partially inhibited LPS-induced plasma leakage in rat skin (38+/-1.1% at the highest dose). Furthermore, CPM (10-7 mol site-1) did not prevent mast cell degranulation. 5. A polyclonal antibody against TNFalpha (1:500, 1:100, 1:50 v v-1 dilution), locally injected, decreased LPS-induced plasma leakage in the skin by 15+/-2.0%, 24+/-2.1% and 50+/-3.0% respectively. 6. Taken together these results suggest that LPS-induced plasma leakage in rat skin is mediated, at least in part, by mast cell degranulation and by the release of histamine and TNFalpha from these cells.

Animals↗
PubMed1992

Immunization of cancer patients using autologous cancer cells modified by insertion of the gene for tumor necrosis factor.

When tumor is resected from patients as part of the natural course of their treatment, an attempt will be made to establish a tissue culture line of the tumor. The gene coding for tumor necrosis factor will be introduced into these tumor cells and the integration and expression of this gene will be tested. Patients will become eligible for this study only if they develop metastatic cancer that has failed all standard effective treatment and have no other effective treatment options available to them. Tumor cells will be injected intradermally and subcutaneously into the thigh of these patients. The amount of tumor injected will be less than 1/50th the total tumor burden of the patient. In previous studies we have shown that these gene-modified tumor cells are more immunogenic than the native unaltered tumor. Attempts will then be made to grow immune lymphocytes either from the tumor site or from the draining lymph nodes of these patients in order to use these lymphocytes for adoptive immunotherapy as detailed in previous protocols. The direct effect of the immunization with these immunogenic tumor cells will also be measured by assessing the impact on established tumor at other sites. Fifty patients receiving tumor inoculation will be included in this study.

Adolescent↗
PubMed1992

Immunization of cancer patients using autologous cancer cells modified by insertion of the gene for interleukin-2.

When tumor is resected from patients as part of the natural course of their treatment, an attempt will be made to establish a tissue culture line of the tumor. The gene coding for interleukin-2 will be introduced into these tumor cells and the integration and expression of this gene will be tested. Patients will become eligible for this study only if they develop metastatic cancer that has failed all standard effective treatment and have no other effective treatment options available to them. Tumor cells will be injected intradermally and subcutaneously into the thigh of these patients. The amount of tumor injected will be less than 1/50th the total tumor burden of that patient. In previous studies we have shown that these gene modified tumor cells are more immunogenic than the native unaltered tumor. Attempts will then be made to grow immune lymphocytes either from the tumor site or from the draining lymph nodes of these patients in order to use these lymphocytes for adoptive immunotherapy as detailed in previous protocols. The direct effect of the immunization with these immunogenic tumor cells will also be measured by assessing the impact on established tumor at other sites. Fifty patients receiving tumor inoculation will be included in this study.

Adult↗
PubMed1984

Participation of mast cells and complement in the immediate phase of hematoporphyrin-induced phototoxicity.

We have investigated the roles of mast cells and the complement system in the immediate phase of hematoporphyrin-induced phototoxicity in guinea pigs. Clinically, i.v. injection of hematoporphyrin, followed by irradiation with a light source containing 400-405 nm wavelength, resulted in the immediate onset of erythema and edema, which subsided partially in 30-60 min. This was followed by the appearance of delayed erythema and edema, which peaked at 6-12 h after irradiation. Histologic examination of the response of the immediate phase, using a 1 micron-thick section, revealed eosinophil infiltration and mast cell degranulation. The immediate phase of the clinical response was further quantitated by the extravasation of intravenously injected [125I]bovine serum albumin. Pretreatment of the guinea pig skin with the intradermal injection of compound 48/80 significantly suppressed the increase in vascular permeability induced by hematoporphyrin and irradiation (p less than 0.05). This hematoporphyrin-induced alteration in vascular permeability was also significantly inhibited by antihistamines, either H1 receptor antagonist alone (p less than 0.05) or a combination of H1 and H2 receptor antagonists (p less than 0.05). Guinea pigs depleted of complement also showed significantly less vascular permeability changes (p less than 0.05). These results indicate that functionally intact mast cells, and the complement system, are required for the full development of the immediate phase of phototoxicity induced by hematoporphyrin.

Animals↗
PubMed1978

A report on clinical aspects and histopathology of sweet itch.

Sweet itch is an intensely pruritic dermatitis of horses recurring annually in Ireland from April to November. The tissue changes of sweet itch have similarities to immediate-type hypersensitivity reactions which occur in skin sensitised to the saliva of bloodsucking insects. There was subepidermal oedema, and marked eosinophilia; the blood vessels were tortuous and enlarged. Microfilaria were not found in serial sections of lesions of 5 affected horses. The histopathology of the immediate dermal remal reaction to the intradermal injection of Culicoides extract shows dermal vasodilation and eosinophil diapedesis. Seven horses challenged intradermally with whole extract of Culicoides, Stomoxys calcitrans, Tabanidae and saline, gave immediate reactions to Culicoides, 3 gave immediate reactions to Stomoxys calcitrans. Immediate and delayed reactions only occurred at the sites of challenge with Culicoides extract. Three normal ponies when challenged intradermally with extracts of biting flies, showed minimal dermal reactions.

Animals↗