| inflammation of arterioles, venules, and capilaies is ‘often secondary to immune- ‘complex disease Laboratory Profiles of Diseases —— a Immune-Mediated Vasculitis Soluble antigen-antibody complexes adhering to vessel walls disrupt the endothelium causing platelet adhesion and inflammatory infiltration. Secondary ischemic lesions occur in peripheral nerves, joints, kidneys, intestine, coronary arteries, CNS, eyes, and skin. Infectious, parasitic, and immune-mediated diseases that produce soluble immune complexes cause these vascular lesions. Interpretation A high serum globulin indicates chronic inflammation. Proteinuria and low serum albumin suggest glomerular lesions. The low platelet count could be the result of, hemorrhage or intravascular coagulation. High serum ALT indicates liver necrosis. Neutrophilia with lymphopenia and eosinopenia indicates systemic stress. Special tests, such as the Coombs’ test or heartworm antigen test, may disclose the underlying antigen source. A high serum triglyceride level indicates a defect in endothelial lipoprotein lipase from vascular lesions Differential Diagnoses + Infectious vasculitis: positive serologic tests for rickettsiae + Lupus erythematosus: positive antinuclear (ANA) test + Heartworm infection: microfilariae found or positive heartworm antigen test + Disseminated intravascular coagulation: fibrin degradation products, increased clot lysis + Primary thrombocytopenia: bone marrow examination, positive platelet factor III test, positive platelet antibody test589} Bua o syns eWLON» -wonesiyut sytudouneu peyesoueBapuou 10 ‘seejanuouoW! ‘pny owas ‘ys0281A paseazoop smoys UoneUIWExD PIU OT» ‘sudeuojuowoy6 seyeqpu cones yojoud:ouuRea!S aU + “amazon snoys enssa paseye jo Asdorg ‘sys9) jeroeds { ‘anor ca | aseauy aseyeydsoyd aurexy AgN Mad “Tat | sized 2uap sorpoq Zu nity ssloonuad —E| O38 somnPaPeEEN 2 psy 1OW sye> PME (ida) open: et Su igo oust i igh say aL PT] 3] poo(qn230 sppeatia ‘SOUO}aY srydoseg, sopuiadd3u | soon) see | jou2Isajou) umumqy 1 ior uigra Ayuves8 g100¢ fl eee | ie sqydohneu pueg SAMI | sasourkypoa puv enypajad snooueynoqns pur snoauein3 Ssatnqeam © SsoUaUITr] « eungfod « eisdipsod + eIRaIOUY «| Spa POO ABrexpe 6 susig | 9% sunnasoy popoayy-aunaausesvosiq) Soc,in the United States heart ‘worm disease has been detected in every state ‘adult heartworms. and their microfaria ccause pulmonary hypertension, right heart failure, and immune-complex disease Laboratory Profiles of Diseases Li ae Heartworm Disease (Dirofilariasis) Heartworms cause valvular heart disease, hepatic congestion, poor renal perfusion, and immune-complex disease. Signs of heart failure are related to the number of adult worms in the heart and great vessels. Antibody-antigen reactions cause kidney disease and arteritis. Emboli can cause lesions in the lungs, kidneys, or brain. Interpretation Allergic reaction to the parasite produces eosinophilia and basophilia. Mechanical destruction of RBCs causes anemia, hemoglobinemia, and hemoglobinuria. High serum ALT and AST activities indicate liver necrosis from increased portal pressure Decreased renal blood flow increases the BUN. This azotemie is classified as prerenal azotemia, Proteinuria and hypoalbuminemia suggest concurrent glomerulonephritis. Heartworm disease is diagnosed by finding circulating microfilariae or a positive heartworm antigen test. Differential Diagnoses + Mitral valve disease: no eosinophilia or basophilia * Chronic renal disease: low urine specific gravity, no marked albuminuria + Cholangiohepatitis: elevated serum bilirubin level| “poo|q jo uojeuEX® | pidoosoxoqw uo oeyeyoroqui 10 188} ueB que UOINUEDL anqSOg + ! “fydonsedty sgjnoyjuen Gupeoiput ‘yuauiBas SHO pabre|Ue Ue MOUS DOS + “wayed Gun] yenysiewu sup pue ‘souaue Azevowind ‘ye0y pabvejua ue Moys SydesBoIpeY + 5383} 2)90d 901i lwngoi uiumgy asedr| ase aseyeydsoyd aufeny dN 199) Mad Add Sve (ids) DIV] euapeg a] sarpog 208 (1058) 15¥| sjeysis) | | fot dD os) SAPP sye> eeu en al et Sam | ‘uigopiouray gaat SRL | [N24 a spe at PaO sudoseg sopuan(Su a syydousoa fl rang | ssioatoh anes goods sevbouduur] FE dan ugeap a sudonnay, asi sydonnau pueg ‘urueary SDAMIeOL Nng| ssorneiom © spumos | Aoyendsay « Taupe | vyan03 « snusinu eof « | su8ig_ ——— 69F (orsoumyfouiy as0esiq] uuomys0epy:saseosig) SoqLaboratory Profiles of Diseases Acute Babesiosis Babesia causes regenerative ‘anemi ‘organisms may bbe observed on RBCs of capillary blood Babesia is a tick-borne parasite that infects red blood cells, causing hemolytic anemia, thrombocytopenia, and fever. Animals that survive the acute disease become clinically normal carriers. These carriers usually cannot be distinguished from normal animals. Interpretation The primary abnormality is regenerative hemolytic anemia High serum AST and ALT activities indicate liver necrosis. Increased hemolysis and secondary liver damage from hypoxia cause bilirubinemia and bilirubinuria. Microvascular stasis results in renal lesions and disseminated intravascular coagulation. Babesia-specific antibody coating of parasitized red blood cells produces a positive Coombs’ test Despite the reticulocytosis, the MCV is low because of the spherocytosis induced by the globulin coating the red cells. The blood smear shows marked anisocytosis. This is indicated by a high red cell distribution width (RDW). Differential Diagnoses + Other causes of regenerative anemia: no Babesia organisms on RBCs « Bxtravascular hemolysis ([gG immune-mediated anemia) no bilirubinemia + Intravascular hemolysis (IgM immune-mediated anemia, Heinz-body anemia, leptospirosis, microangiopathy): no Babesia organisms on RBCs(au) apy uonnausip yo pas oes “seu | aos u wonepatBop uuay ansod pur Lay La"L1d paseaout» -syou 956020) Bupsiied pu oq 0yesyseu ¢ Busy sn ua Op< S949 SOUS 80 le e610 Biseqeg padeys-s2e ay soyensuoUep Yeu9 0 wBrEU ‘euutd a Jo Seyeydeo wos poo yo uoneUnEXe 2160101K9 + “fyeGawouaids moys hew sydesBo1pey + ise} e190ds im se) so ee SOmt SOgM. grat oo1g.im29 | ‘soupy | soon) ‘ung L yues8 ogpadg Hd aSeysi0woy ‘Howidysoa pur jenpaaiag « Aypedouapeydushy « Ayeouroredayy © ‘AqeBauouayds « eumuigo,owayy » gonad e | uworssaidaq « PIUIOUY « | epaiouy + ur ‘eu use sults a —= sioupax_| Aa Mat sid saspoq Zuo soot Soma PaIeepAN, roN (op anoyetion, qo(BowoHt syudoseg 1 syydoussog sevouopy sovboyduky syudonnay, syydonnox pueg SOaM AL, sqsoysaqog amy $i? sasnesiq 80g) Te URON] uynqor ft wml deed asedwry | aseyeydsoyd aureyyy |} 199 dD 1299) LV (L05s).1Sv ® sppeatia| oie 18152)01D Cf peor ‘mgr pan ‘uignatig 2s00n19 aurumeet, Nn von nun Axyspurayp pootd PooEmrichia canis replicates in mononuclear cells, causing lymphade- nopathy, splenomegaly, ‘and hepato- megaly thrombocytopenia is due to peripheral destruction of platelets Ehrlichiosis Laboratory Profiles of Diseases Ehrlichia canis is transmitted by the brown dog tick, Rhipicephalus sanguineus. The rickettsia replicates within mononuclear cells in the blood, spleen, liver, and lymph nodes, causing organ enlargement from lymphoreticular hyperplasia. Infected monocytes attach to small vessels, causing vasculitis and hemorrhage. Immunocompetent dogs usually eliminate the organism after clinical illness. In other dogs, such as some German Shepherds, a chronic phase causes bone marrow depression, Interpretation Platelet consumption and destruction by antiplatelet antibody cause thrombocytopenia. High total plasma protein and globulin levels suggest immunoglobulin excess. Protein in the Urine and a high urine protein:creatinine ratio indicate glomerulonephritis. High serum alkaline phosphatase, GGT, and bilirubin values indicate cholestasis from lymphoreticular hyperplasia. A high serum ALT activity indicates hepatic necrosis. Altered coagulation tests and low platelets cause hemorrhage Differential Diagnoses + Rocky Mountain spotted fever: leukocytosis with thrombocytopenia, positive antigen or antibody test + Lymphosarcoma: many immature cells in lymph node aspirates + Systemic lupus erythematosus: usually no bone marrow depression, positive ANA test « Immune-mediated thrombocytopenia: usually bone marrow depression oe een ee | ew