DOCSLIB.ORG

Isolated Arteritis of the Epididymis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Isolated Arteritis of the Epididymis J Clin Pathol: first published as 10.1136/jcp.38.7.797 on 1 July 1985. Downloaded from J Clin Pathol 1985;38:797-800 Isolated arteritis of the epididymis C WOMACK, ID ANSELL From the Departments ofHistopathology, University and City Hospitals, Nottingham SUMMARY The clinical, histological, and immunohistochemical features of two cases of appar- ently isolated arteritis of the epididymis are presented. The aetiology and pathogenesis of the condition are discussed. Immunoglobulin and complement were shown in the acute arterial lesions, but this is not conclusive evidence that isolated arteritis is either an immune complex disease or a forme fruste of polyarteritis nodosa. Necrotising arteritis apparently confined to one CASE 2 organ yet showing histological features similar to A 14 year old boy was noted to have an unde- those seen in polyarteritis nodosa is now well recog- scended right testicle at a routine school medical nised. Since the first description of isolated arteritis examination. There was no history of trauma, there in the appendix by Plaut' similar apparently isolated were no urogenital symptoms, and the patient was arteritis has been recorded in the gall bladder,2 otherwise fit and well. On examination the right tes- uterine cervix,34 uterine body,5 skin,6 and breast.' ticle was in the inguinal canal and was small and The British testicular tumour panel material8 non-mobile. The left testicle was clinically normal. included three cases of necrotising arteritis; in one The patient underwent a right orchidectomy patient the disease was present only in the testis, but because the cord was insufficient to perform copyright. his subsequent clinical history is unknown. We orchidopexy. He made an uneventful postoperative report two cases of apparently isolated arteritis of recovery and is in good physical health six months the epididymis in patients who have no clinical evi- later. The resected testis measured 3-5 x 2-0 x 2 0 dence of systemic disease. cm. The testis, epididymis, and cord appeared nor- mal macroscopically. Case reports Both patients were normotensive and neither was http://jcp.bmj.com/ taking any drugs before presentation. CASE 1 A 37 year old man presented with a tender mass in INVESTIGATIONS the left testicle which had appeared suddenly three Table 1 shows the results of relevant postoperative weeks previously. There was no history of recent haematological and biochemical investigations. All trauma. An injury to the same testicle some 20 years were within the normal ranges of the laboratory. before had preceded a similar tender mass, which Blood eosinophil counts were not performed. on September 26, 2021 by guest. Protected had disappeared spontaneously. There were no other urogenital symptoms and the patient was HISTOLOGY otherwise fit and well. On examination there was a Routine paraffin embedded tissue sections roughly hard, irregular, tender nodule at the lower pole of 7 ,um thick were stained by haematoxylin and eosin, the left epididymis; the right testicle was clinically Martius scarlet blue, and elastic Van Gieson. In normal. The patient underwent a left orchidectomy case 1 the testis showed no appreciable histological via an inguinal incision. He made an uneventful abnormality; in case 2 there was complete absence postoperative recovery and is in good physical of germ cells consistent with maldescent. There was health two and a half years later. The resected testis a multifocal necrotising arteritis affecting the measured 6 5 x 3-5 x 3-0 cm and showed no mac- medium and small muscular arteries of the roscopic abnormality. The lower pole of the epididymis in both cases and of the spermatic cord in epididymis contained a well defined, hard white case 2. The acute arteritic lesions were characterised mass 2 cm in diameter. by focal fibrinoid necrosis of the vessel wall with an associated infiltrate of neutrophil polymorphonu- clear leucocytes and lymphocytes (Fig. 1). Accepted for publication 14 March 1985 Eosinophil polymorphonuclear leucocytes were not 797 J Clin Pathol: first published as 10.1136/jcp.38.7.797 on 1 July 1985. Downloaded from 798 Womack, Ansell Table 1 Haematological and biochemical results Case Blood Serum Erythrocyte sedimentation Haemoglobin White cell count Urea concentration Creatinine concentration rate (mm in the first hour) concentration (gldl) (X109/1) (mmolNl) (pinolll) 1 7 13-8 5-7 4-3 82 2 1 15-0 5-6 4-5 87 Values are all within the laboratory normal ranges. seen and the fibrinoid material stained red with Mar- Discussion tius scarlet blue. In some arteries the acute lesions were circumferential. Some arterial lesions were The diagnosis of isolated arteritis depends on the characterised by pronounced intimal (fibrous) thick- clinical exclusion of systemic disease in a patient ening and an infiltrate of lymphocytes in the muscu- who has histological evidence of a necrotising lar wall without fibrinoid necrosis (Fig. 2). Around arteritis apparently limited to one organ. The his- all the abnormal arteries there was a lymphocytic tological picture is similar to that seen in classic infiltrate of variable intensity, which was most strik- polyarteritis nodosa, although there are some minor ing around the lesions showing fibrinoid necrosis. differences in cases of isolated arteritis, notably the lack of thrombosis, aneurysm formation, or infarc- IMMUNOHISTOCHEMISTRY tion.3 In some reports the lesions are described as Paraffin sections were stained for IgG, IgM, IgD, granulomatous,7 9 "' but the presence of multinucle- IgA, hepatitis B, and complement components Clq ated giant cells close to disrupted fragments of arter- and C3 using a standard peroxidase-antiperoxidase ial elastic lamina (a feature not specific to temporal was by Dako UK Ltd. technique. Antisera supplied arteritis) may occur secondarily to vessel wall dam-copyright. Positive staining was only seen in acute arteritic age." lesions (Table 2). To our knowledge isolated arteritis of the http://jcp.bmj.com/ on September 26, 2021 by guest. Protected Fig. 1 An acute arteritic lesion. Necrosis and fibrinoid change affects part ofthe circumference ofthis artery. There is a moderate inflammatory cell infitrate around the necrotic area and in a perivascular distribution (from case 1). Haematoxylin and eosin. Original magnification x135. J Clin Pathol: first published as 10.1136/jcp.38.7.797 on 1 July 1985. Downloaded from Isolated arteritis of the epididymis 799 ..,........... ..- .~~~~ $ t'i~~~~~~~~~~~~~~~~~i.4.... Fg x135 eoinOngna l~ti: .anJco not reported. Both regularly exposed to a wide variety of antigenic epididymis has been previously copyright. of our patients had evidence of necrotising arteritis material and an Arthus type reaction can reasonably of the epididymis without clinical evidence of sys- be proposed as a cause for isolated arteritis at these temic disease. The British testicular tumour panel8 sites. Similarly, the breasts may be exposed to new include three cases of necrotising arteritis: one antigens during pregnancy and lactation, although patient later developed renal lesions and another the recorded cases of isolated arteritis in this organ had rheumatoid arthritis. The third patient in the have occurred in middle aged and elderly women.7 panel series had a giant cell arteritis of the testis, but Potentially antigenic material may be localised in http://jcp.bmj.com/ his subsequent history is unknown. the epididymis following trauma or retrograde flow The aetiology of isolated arteritis is unknown. of urine down the vas deferens.8 In our two cases Necrotising arteritis is well recognised as a complica- there was no history of recent trauma that could tion of irradiation, but in our cases and in other explain the acute arterial lesions. Neither patient reports of isolated arteritis there was no history of complained of urinary symptoms, but we do not previous irradiation. Many forms of arteritis are know whether there was retrograde flow of urine considered to be mediated by immunological down the vasa, the likely mechanism of localisation on September 26, 2021 by guest. Protected mechanisms. Isolated arteritis may represent a local- of antigen to the epididymis if a type III hyper- ised type III hypersensitivity (Arthus) reaction." sensitivity reaction is entailed in the pathogenesis of Such hypersensitivity to an inhaled antigen has been the arterial lesions. The immunohistochemical suggested as one of the causes of the necrotising staining of our two cases is not, however, conclusive vasculitis, Wegener' s granulomatosis, although no evidence of an immune complex mediated disease. antigen has yet been identified." Sites such as skin, The presence of immunoglobulin and complement appendix, cervix, uterus, and gall bladder are in acute arteritic lesions may be due simply to Table 2 Immunohistological staining ofacute arteritic lesions Case lgG IgM IgA IgD Clq C3 Hepatitis B 1 + + - - + - - 2 - + - + + = staining in acute artentic lesions. - = no staining in acute arteritic lesions. J Clin Pathol: first published as 10.1136/jcp.38.7.797 on 1 July 1985. Downloaded from 800 Womack, Ansell passive diffusion of plasma constituents through References arterial walls damaged by another mechanism. Plaut A. Focal arteriolitis. Am J Pathol 1932; 8:620-1. We have already noted the histological similarities 2 Bohrod MG, Bodon GR. Isolated polyarteritis of the gall blad- between the lesions of isolated arteritis and polyar- der. Am Surg 1970; 36:681-5. teritis nodosa. Polyarteritis nodosa is considered to -Ansell ID, Evans DJ, Wright DGD. Asymptomatic arteritis of the uterine cervix. J Clin Pathol 1974; 27:664-8. be an immune complex mediated disease, and 30% Crow J, McWhinney N. Isolated arteritis of the cervix uteri. Br J of patients with the disorder have circulating Obstet Gynaecol 1979;86:393-8. hepatitis B antigen.'2 We were unable to show Lin CS, Brazza F. Focal arteritis of uterus. A case report. Mt Sinai J Med 1978;45:402-3. hepatitis B antigen immunohistochemically. The 6 Cupps TR, Fauci AS. The vasculitides.
Load more

Recommended publications
  • Early-Phase GVHD Gene Expression Profile in Target Versus Non
    Bone Marrow Transplantation (2013) 48, 284–293 & 2013 Macmillan Publishers Limited All rights reserved 0268-3369/13 www.nature.com/bmt ORIGINAL ARTICLE Early-phase GVHD gene expression profile in target versus non-target tissues: kidney, a possible target? B Sadeghi1, H Al-Chaqmaqchi1, S Al-Hashmi1, D Brodin2, Z Hassan1,3, M Abedi-Valugerdi4, A Moshfegh5 and M Hassan1,3 GVHD is a major complication after allo-SCT. In GVHD, some tissues like liver, intestine and skin are infiltrated by donor T cells while others like muscle are not. The mechanism underlying targeted tropism of donor T cells is not fully understood. In the present study, we aim to explore differences in gene expression profile among target versus non-target tissues in a mouse model of GVHD based on chemotherapy conditioning. Expression levels of JAK–signal transducers and activators of transcription (STAT), CXCL1, ICAM1 and STAT3 were increased in the liver and remained unchanged (or decreased) in the muscle and kidney after conditioning. At the start of GVHD the expression levels of CXCL9, ITGb2, SAA3, MARCO, TLR and VCAM1 were significantly higher in the liver or kidney compared with the muscle of GVHD animals. Moreover, biological processes of inflammatory reactions, leukocyte migration, response to bacterium and chemotaxis followed the same pattern. Our data show that both chemotherapy and allogenicity exclusively induce expression of inflammatory genes in target tissues. Moreover, gene expression profile and histopathological findings in the kidney are similar to those observed in the liver of GVHD mice. Bone Marrow Transplantation (2013) 48, 284–293; doi:10.1038/bmt.2012.120; published online 23 July 2012 Keywords: gene expression; GVHD; kidney; target tissues; mouse model INTRODUCTION none of these reports describe any changes in gene expression Allo-SCT is the treatment of choice for a variety of malignant and profile of non-target tissues like muscle.
    [Show full text]
  • Allergic Reactions After Vaccination: Translating Guidelines Into Clinical Practice
    R E V I E W EUR ANN ALLERGY CLIN IMMUNOL VOL 51, N 2, 51-61, 2019 A. RADICE1, G. CARLI2, D. MACCHIA1, A. FARSI2 Allergic reactions after vaccination: translating guidelines into clinical practice 1SOS Allergologia e Immunologia, Firenze, Azienda USL Toscana Centro, Italy 2SOS Allergologia e Immunologia, Prato, Azienda USL Toscana Centro, Italy KEYWORDS Summary vaccine; vaccination; allergic reactions; Vaccination represents one of the most powerful medical interventions on global health. anaphylaxis; vaccine hesitancy; vaccine Despite being safe, sustainable, and effective against infectious and in some cases also components; desensitization non-infectious diseases, it’s nowadays facing general opinion’s hesitancy because of a false perceived risk of adverse events. Adverse reactions to vaccines are relatively rare, instead, and those recognizing a hypersensitivity mechanism are even rarer. Corresponding author The purpose of this review is to offer a practical approach to adverse events after vaccina- Anna Radice Ospedale San Giovanni di Dio tion, focusing on immune-mediated reactions with particular regard to their recognition, Via Torregalli 3, 50143 Firenze diagnosis and management. Phone: +39 055 6932304 According to clinical features, we propose an algorythm for allergologic work-up, which E-mail: [email protected] helps in confirming hypersensitivity to vaccine, nonetheless ensuring access to vaccination. Finally, a screening questionnaire is included, providing criteria for immunisation in spe- Doi cialized care settings. 10.23822/EurAnnACI.1764-1489.86 Introduction The gain from vaccination is not just about human health, but it is also a matter of financial resources for health systems. “Smallpox is dead” stated the magazine of the World Health It has been calculated that for every dollar spent in vaccines, Organisation (WHO) in 1980.
    [Show full text]
  • Allergy, Hypersensitivity, Angioedema, and Anaphylaxis Episode Overview
    CrackCast Show Notes –Allergy and Anaphylaxis – October 2017 www.canadiem.org/crackcast Chapter 109 – Allergy, Hypersensitivity, Angioedema, and Anaphylaxis Episode Overview Key Points: 1. A history of sudden urticarial rash accompanied by respiratory difficulty, abdominal pain, or hypotension, strongly favors the diagnosis of anaphylaxis. 2. Epinephrine is the first-line treatment in patients with anaphylaxis: give it immediately. 3. There are no absolute contraindications to the use of epinephrine in the setting of anaphylaxis. 4. Antihistamines and corticosteroids are second- and third-line agents in the management of anaphylaxis and should not replace or precede epinephrine. 5. Consider prolonged observation or admission for patients who: a. Experience protracted anaphylaxis, hypotension, or airway involvement; b. Receive IV epinephrine or more than two doses of IM epinephrine; c. Or have poor outpatient social support. 6. Patients discharged after an anaphylactic event should be prescribed an EpiPen and instructed on its use. 7. Patients with refractory hypotension may require glucagon (receiving beta-blockage) or a continuous IV epinephrine infusion. 8. Non-histaminergic angioedema (non-allergic angioedema) does not typically respond to epinephrine and antihistamines. New drugs, including berinert, icatibant, ecallantide, and Ruconest have been approved for use in HAE. FFP has been used with varying success in HAE, ACID, and ACE inhibitor–induced angioedema. NOTE: ACID: acquired C1 esterase deficiency (ACED) Core Questions: 1. List the four types of Gell and Coombs classifications of immune reaction and give examples of each 2. List four etiologic agents causing anaphylaxis by immunologic mechanisms 3. List six mediators of anaphylaxis and their physiologic actions and clinical manifestations 4.
    [Show full text]
  • Hypersensitivity Reactions (Types I, II, III, IV)
    Hypersensitivity Reactions (Types I, II, III, IV) April 15, 2009 Inflammatory response - local, eliminates antigen without extensively damaging the host’s tissue. Hypersensitivity - immune & inflammatory responses that are harmful to the host (von Pirquet, 1906) - Type I Produce effector molecules Capable of ingesting foreign Particles Association with parasite infection Modified from Abbas, Lichtman & Pillai, Table 19-1 Type I hypersensitivity response IgE VH V L Cε1 CL Binds to mast cell Normal serum level = 0.0003 mg/ml Binds Fc region of IgE Link Intracellular signal trans. Initiation of degranulation Larche et al. Nat. Rev. Immunol 6:761-771, 2006 Abbas, Lichtman & Pillai,19-8 Factors in the development of allergic diseases • Geographical distribution • Environmental factors - climate, air pollution, socioeconomic status • Genetic risk factors • “Hygiene hypothesis” – Older siblings, day care – Exposure to certain foods, farm animals – Exposure to antibiotics during infancy • Cytokine milieu Adapted from Bach, JF. N Engl J Med 347:911, 2002. Upham & Holt. Curr Opin Allergy Clin Immunol 5:167, 2005 Also: Papadopoulos and Kalobatsou. Curr Op Allergy Clin Immunol 7:91-95, 2007 IgE-mediated diseases in humans • Systemic (anaphylactic shock) •Asthma – Classification by immunopathological phenotype can be used to determine management strategies • Hay fever (allergic rhinitis) • Allergic conjunctivitis • Skin reactions • Food allergies Diseases in Humans (I) • Systemic anaphylaxis - potentially fatal - due to food ingestion (eggs, shellfish,
    [Show full text]
  • Arthus Reaction
    The Journal of Emergency Medicine, Vol. 56, No. 4, pp. 450–451, 2019 Ó 2018 Elsevier Inc. All rights reserved. 0736-4679/$ - see front matter https://doi.org/10.1016/j.jemermed.2018.12.047 Visual Diagnosis in Emergency Medicine ARTHUS REACTION Mei-Hua Wang, RN,* Alvin Hu,† Yei-Soon Lee, MD,* and Chih-Cheng Lai, MD‡ *Department of Emergency Department, Chi Mei Medical Center, Liouying, Taiwan, †Poznan University of Medical Sciences, Poznan, Poland, and ‡Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Taiwan Reprint Address: Chih-Cheng Lai, MD, Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan CASE REPORT 0–4%), respectively, and a C-reactive protein level of 9.1 mg/L. Blood culture was collected but showed no bac- A 6-year-old boy presented to the emergency department terial growth. Physical examination showed an erythem- (ED) with fever and skin rash (Figure 1) over his left atous skin rash with swelling and severe pain over the thigh. He had just received a combination vaccine with vaccination site. Acetaminophen was given for pain relief diphtheria, tetanus, pertussis, and poliomyelitis (DTaP- and fever. Steroid (methylprednisolone 20 mg every 8 h) IPV) on his left thigh 12 h prior to his visit to the ED. and an antihistamine (cyproheptadine 2 mg three times a His vital signs were body temperature of 36.6C, respira- day) were prescribed for suspected allergic reaction. Af- tory rate of 20 breaths/min, blood pressure of 104/83 mm ter treatment, the fever subsided and the painful swelling Hg, and heart rate of 100 beats/min.
    [Show full text]
  • Reaction by Staphylococcal Protein a Cell Superantigen: Elicitation of An
    In Vivo Inflammatory Response to a Prototypic B Cell Superantigen: Elicitation of an Arthus Reaction by Staphylococcal Protein A This information is current as Lisa M. Kozlowski, Weiping Li, Michael Goldschmidt and Arnold of October 1, 2021. I. Levinson J Immunol 1998; 160:5246-5252; ; http://www.jimmunol.org/content/160/11/5246 Downloaded from References This article cites 50 articles, 28 of which you can access for free at: http://www.jimmunol.org/content/160/11/5246.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 1, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. In Vivo Inflammatory Response to a Prototypic B Cell Superantigen: Elicitation of an Arthus Reaction by Staphylococcal Protein A1 Lisa M. Kozlowski,2* Weiping Li,* Michael Goldschmidt,† and Arnold I. Levinson3* Staphylococcal protein A (SpA) is representative of a new class of Ags, the B cell superantigens (SAgs).
    [Show full text]
  • COVID-19 Vaccine and Allergy
    COVID Vaccine and Allergy Stephanie Leonard, MD Associate Clinical Professor Department of Pediatric Allergy & Immunology January 20, 2020 Safe and Impactful • Proper Screening COVID Vaccine • Monitoring Administration • Clinical Assessment • Vaccine Adverse Event Reporting System (VAERS) detected 21 cases of anaphylaxis after administration of a reported 1,893,360 first doses of the Pfizer-BioNTech COVID-19 vaccine • 11.1 cases per million doses (0.001%) • 1.3 cases per million for flu vaccines • 71% occurred within 15 min of vaccination, 86% within 30 minutes • Range = 2–150 minutes • Of 20 with follow-up info, all had recovered or been discharged home. • 17 (81%) with h/o allergies to food, vaccine, medication, venom, contrast, or pets. • 4 with no h/o any allergies • 7 with h/o anaphylaxis • Rabies vaccine • Flu vaccine • 19 (90%) diffuse rash or generalized hives Allergic Reactions Including Anaphylaxis After Receipt of the First Dose of Pfizer-BioNTech COVID-19 Vaccine — United States, December 14–23, 2020. MMWR Morb Mortal Wkly Rep 2021;70:46–51. Early Signs of Anaphylaxis • Respiratory: sensation of throat closing*, stridor, shortness of breath, wheeze, cough • Gastrointestinal: nausea*, vomiting, diarrhea, abdominal pain • Cardiovascular: dizziness*, fainting, tachycardia, hypotension • Skin/mucosal: generalized hives, itching, or swelling of lips, face, throat *these can be subjective and overlap with anxiety or vasovagal syndrome Labs that can help assess for anaphylaxis • Tryptase, serum (red top tube) • C5b-9 terminal complement complex Level, serum (SC5B9) (lavender top EDTA tube) Emergency Supplies Management of anaphylaxis at a COVID-19 vaccination site • If anaphylaxis is suspected, take the following steps: • Rapidly assess airway, breathing, circulation, and mentation (mental activity).
    [Show full text]
  • Immunological Exercises.Pdf
    Immunological Exercises Short Notes 1. Smallpox and Edward Jenner 2. Humoral Immunity and Cellular Immunity 3. Acquired Immunity 4. 2019-nCoV/SARS-CoV-2, COVID-19 5. Programmed cell death (apoptosis) 6. GALT (Gut-associated lymphoid tissue) 7. MIS (Mucosal lymphoid system) 8. APCs (antigen presenting cells) 9. Epitopes or antigenic determinants 10. T cell and B cell Epitopes 11. Common Ag and Cross Reaction 12. Heterophilic Ag and Autoantigen 13. Hapten 14.TD-Ag and TI-Ag 15. Heterophilic Ag and Autoantigen 16. Immunoglobulin (Ig) and Antibody (Ab) 17. Ig Isotype and Ig Allotype 18. Ig idotype 19. Monoclonal Ab and Polyclonal Ab 20. Neutralization 21. Opsonization 22. CDRs and VH 23. Fab and Fc 24. Noncovalent forces 25. Ig subtypes and sIgA 26. PAMPs/DAMPs (pathogen/danger/damage-associated molecular patterns) 27. PRRs (Pattern-recognition receptors) 28. NKG2D, MIC, KIR KLR 29. TLRs (Toll-like receptors ) 30. Regulatory T cells (Tregs), Tr1, Th3 31. Immunoregulation 32. Central T Cell Tolerance 33. Peripheral tolerance 34. Positive selection and Negative selection 35. Immune tolerance and Dizygotic twin cows 36. CD28 and B7 molecules 37. Activation-induced cell death (AICD) 38. NK cells and T cells 39. DCs and macrophages (Ms) 40. TCR-CD3 complex 1 41. Mature B cells 42. Recombination signal sequence (RSS) 43. MHC restriction 44. GM-CSF and INF- 45. Cytokine storm/cytokine release syndrome (CRS) 46. Affinity maturation 47. ITIM (immunoreceptor tyrosine-based inhibitory motif) and ITAM 48. BCR (B cell receptor) and TCR (T cell receptor) 49. CDRs, complementary-determining regions 50. Monoclonal antibody(mAb) 51.
    [Show full text]
  • LECTURE: 10 Title: IMMUNOLOGICAL MECHANISM in TISSUE DAMAGE TYPE-III IMMUNE-COMPLEX MEDIATED HYPERSENSITIVITY
    LECTURE: 10 Title: IMMUNOLOGICAL MECHANISM IN TISSUE DAMAGE TYPE-III IMMUNE-COMPLEX MEDIATED HYPERSENSITIVITY LEARNING OBJECTIVES: The student should be able to: • Define type III hypersensitivity reactions. • Identify the role of the immune complex in type III reactions, and indicate which cause more damage small or large immune complexes, and locate the possible deposition of each complex. • Compare type III and type I reactions. • List some of the immune complex diseases: - Autoimmune diseases: ♦ Systemic lupus erythematosus (SLE). ♦ Rheumatoid arthritis (RA). ♦ Hyperthyroidism. - Infectious agents: ♦ Infectious mononucleosis. ♦ Meningitis. ♦ Viral hepatitis (Chronic stage). ♦ Poststreptococcal glomerulonephritis. ♦ Streptokinase (bacterial enzymes) in cardiac patients. - Drugs: ♦ Sulfonamides + penicillin. • Determine either type III reactions act locally or systematically. • Explain the mechanism of local immune complex deposition and give one example. • Explain the mechanism of generalized immune complex deposition, and give one example. • Explain the main target organ (s) for type III reactions. • Describe the mechanism of activation of type III reaction. • List a diagnostic method, and some examples of clinical features of type III such as: - Arthus reactions (Local immune complex-deposition). - Serum sickness (Systemic immune complex-deposition). LECTURE REFRENCE: 1. TEXTBOOK: ROITT, BROSTOFF, MALE IMMUNOLOGY. 6th edition. Chapter 23. pp. 357-367. 2. HANDOUT. Hypersensitivity – Type III Immune complexes are formed every time antibody meets antigen and are removed by the mononuclear phagocyte system following complement activation. Persistence of antigen from continued infection or in autoimmune disease can lead to immune-complex disease. Immune complexes can form both in the circulation, leading to systemic disease, and at local sites such as the lung. Complement helps to disrupt antigen-antibody bonds and keeps immune complexes soluble.
    [Show full text]
  • Managing Adverse Events Following Immunization: Resource for Public Health
    Managing Adverse Events Following Immunization: Resource for Public Health By Special Immunization Clinic Network Investigators of the Canadian Immunization Research Network Version date: 09/01/2019 AEFI Management Resource for Public Health Contents INTRODUCTION .............................................................................................................. 3 LIST OF ABBREVIATIONS AND ACRONYMS ........................................................... 4 ALLERGIC-LIKE EVENTS (WITH OR WITHOUT ANAPHYLAXIS) ........................ 6 APNEA IN PRETERM INFANTS (APTI) ........................................................................ 9 ARTHRALGIA/ARTHRITIS........................................................................................... 10 FEVER .............................................................................................................................. 11 GUILLAIN-BARRÉ SYNDROME (GBS) ...................................................................... 12 HENOCH-SCHONLEIN PURPURA (HSP) ................................................................... 14 HYPOTONIC-HYPORESPONSIVE EPISODE (HHE) .................................................. 15 LOCAL REACTIONS AT THE INJECTION SITE (LRs) ............................................. 16 OCULO-RESPIRATORY SYNDROME (ORS) ............................................................. 19 PERSISTENT CRYING ................................................................................................... 20 SEIZURES .......................................................................................................................
    [Show full text]
  • Bronchial Lesions of Mouse Model of Asthma Are Preceded by Immune
    Laboratory Investigation (2015) 95, 886–902 © 2015 USCAP, Inc All rights reserved 0023-6837/15 Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT) Ian C Guest1 and Stewart Sell1,2 We systematically examined by immune histology the lungs of some widely used mouse models of asthma. These models include sensitization by multiple intraperitoneal injections of soluble ovalbumin (OVA) or of OVA with alum, followed by three intranasal or aerosol challenges 3 days apart. Within 24 h after a single challenge there is fibrinoid necrosis of arterial walls with deposition of immunoglobulin (Ig) and OVA and infiltration of eosinophilic polymorphonuclear cells that lasts for about 3 days followed by peribronchial B-cell infiltration and slight reversible goblet cell hypertrophy (GCHT). After two challenges, severe eosinophilic vasculitis is present at 6 h, increases by 72 h, and then declines; B-cell proliferation and significant GCHT and hyperplasia (GCHTH) and bronchial smooth muscle hypertrophy recur more prominently. After three challenges, there is significantly increased induced bronchus-associated lymphoid tissue (iBALT) formation, GCHTH, and smooth muscle hypertrophy. Elevated levels of Th2 cytokines, IL-4, IL-5, and IL-13, are present in bronchial lavage fluids. Sensitized mice have precipitating antibody and positive Arthus skin reactions but also develop significant levels of IgE antibody to OVA but only 1 week after challenge. We conclude that the asthma like lung lesions induced in these models is preceded by immune complex-mediated eosinophilic vasculitis and iBALT formation. There are elevations of Th2 cytokines that most likely produce bronchial lesions that resemble human asthma.
    [Show full text]
  • Farmer's Lung: a Study of an Early Acute Fatal Case
    Thorax (1968), 23, 490. Farmer's lung: a study of an early acute fatal case D. F. BARROWCLIFF AND P. G. ARBLASTER From the Group Laboratory, Warwick, and the Royal Hampshire Counity Hospital, Winchester The clinical and pathological findings in a fatal case of farmer's lung in a 17-year-old youth are described. His lungs were uncomplicated by chronic disease, and his first exposure to mouldy hay probably occurred only weeks before his death. As this was an acute attack, whose duration could be measured in days, the changes seen are probably the earliest to be recorded, and the probable nature of the sensitivity reaction can be deduced. The pathological process is seen to be an acute centrilobular bronchopneumonia of a special type and is associated with an obstructive bronchio- litis. There is a focal interstitial pneumonia with much proliferation of alveolar epithelium, and there is a necrotic exudate in which neutrophils and eosinophils are seen along with mononuclears, some lymphocytes, and plasma cells. The alveolar spaces are in many cases obscured, but others contain a haemorrhagic fluid. Alveolar capillaries show an acute vasculitis, with platelet and fibrin deposition, and with acute neutrophil infiltration. Serological and mycological data are included. Precipitins to mouldy hay and to Thermopolyspora polyspora were found in the serum. In dusts collected from his habitat T. polyspora was found. We think the bronchiolitis explains the severe dyspnoea, and the vasculitis accounts for the malaise, fever, and haemoptysis. The histological findings are compared with accounts of experimentally produced Arthus reactions and tuberculin reactions, and we give our reasons for believing the fundamental lesion to be an Arthus reaction.
    [Show full text]