Due to the low calcium content of meat and meat by-products, nutritional secondary hyperparathyroidism and/or low calcium rickets can be a severe problem in domestic carnivores maintained on diets which are not balanced in calcium:phosporous ratio. This type of diet results in poor mineralization of bones in young animals or excess bone resorption in older animals maintained on an improperly balanced diet

Hoskins, Johnny

Kautz, Williams

English

Due to the low calcium content of meat and meat by-products, nutritional secondary hyperparathyroidism and/or low calcium rickets can be a severe problem in domestic carnivores maintained on diets which are not balanced in calcium:phosporous ratio. This type of diet results in poor mineralization of bones in young animals or excess bone resorption in older animals maintained on an improperly balanced diet.</p

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Low Calcium Rickets in Young CatsbyWilliams Kautz*andJohnny HoskinstINTRODUCTIONDue to the low calcium content of meatand meat by-products, nutritionalsecondary hyperparathyroidism and/or lowcalcium rickets can be a severe problem indomestic carnivores maintained on dietswhich are not balanced in calcium:phosphorus ratio. This type of diet resultsin poor mineralization of bones in younganimals or excess bone resorption in olderanimals maintained on an improperlybalanced diet.Calcium, phosphorus, and vitamin Dareall essential to proper bone growth andmaintenance. All three are closely linked intheir metabolism in the animal body. Toprevent metabolic bone diseases it isessential that all three of these nutrientsare maintained in a proper balance in thediet.CASE REPORTClinical Findings-A 3~ month old maledomestic cat was presented to the clinic inJuly, 1975. The cat had a history oflameness, constipation, swollen abdomen,and generalized body pain of ap-proximately three weeks duration. The catwas on a diet consisting of Gerber highprotein cereal, very small amounts ofcommercial cat food, and raw ground beef.Consultation with the owner revealed,however, that the animal refused the cereal* Mr. Kautz is a fourth year student in the Collegeof Veterinary Medicine, Iowa State University.t Dr. Hoskins is an assistant professor in VeterinaryClinical Sciences in the College of VeterinaryMedicine, Iowa State University.Issue No.3) 1975and commercial food and ate almost en-tirely a ground beef diet.On physical exam the animal showedgeneralized body pain on palpation,especially in the limbs and joints. Theabdomen was distended and the animal haddifficulty standing upright on its hindlimbs. When the animal was placed in astanding position both hind limbs splayedout laterally.Radiographic Findings- Lateral andventral-dorsal scout films were taken andthese showed very thin cortices in all thelong bones and poor mineralization ofbones. There was a sharp deviation of thespinal column at T1 0-TIl indicating apossible compression fracture at thislocation. There was a folding fracture onthe distal end of one femur, the sternumwas deformed dorsally, there was ventrallordosis of the lumbar spine, and the ulnarand fibular tarsal bones were curved ab-normally. The pelvic area was very hard todelineate but appeared compressed andsmall for this age animal. In addition thelong bones lacked the normal trabecularpattern which should be seen with propermineralization of bone. 7Blood Paramete'rs - Blood profile wasunremarkable except for an elevated serumphosphorus level of 7.7 mg%. Bloodcalcium was within the normal limits at 9.4mg%.5Based on the case history and the aboveclinical findings a tentative diagnosis ofnutritional secondary hyperparathyroidismwas made. Due to the many fractures seenradiographically and the possibility of asevere fracture of the spinal column, the79owners decided to allow euthanization ofthe animal. The animal was kept in a wardfor approximately two weeks and placed ona commercial canned diet during thisperiod. During this time the animal ex-perienced remission of some clinical signsincluding its pain and inability to walk. Atthe end of two weeks the animal waseuthanized and a post mortem examinationperformed.Pathological Findings - Gross: Majororgans contained no gross lesions. Thethyroids and parathyroids were normal insize and contained no gross lesions. Othersys terns of the body contained no grosslesions with the exception of the skeletalsystem. Examination of the ribs revealedseventeen pathological fractures at variouslocations throughout the rib cage. Thesefractures appeared to have well formedcalluses around them. Pathological frac-tures were also seen in the right distalfemur and the left proximal tibia, and bothof these had well formed calluses. Acompression fracture was found at thoracicvertebrae TIO and TIl. No other grosslesions were observed.Histopathology: Sections through theparathyroids revealed only mild hyper-trophy of the chief cells. This was indicatedby a small increase in the cytoplasmiccontent of these cells. No marked hyper-trophy of the parathyroids was noted.Sections through the fracture sightsshowed well formed cartilaginous callusesand good osteoid formation. However, notmuch evidence was seen to indicate newbone formation and bone remodeling at thefracture sights. In one sight it was notedthat blood ~essels had begun to invade theosteoid matrix in a possible attempt atmineralization. It was hypothesized thatthis beginning of new bone growthprobably occurred after the animal wasplaced on a balanced diet in the clinic.Based on the pathological findings, thefinal diagnosis was low calcium rickets.DISCUSSIONIt is relatively easy for the clinician to seethe radiographic changes indicating poormineralization of bones.! The majorproblem facing the clinician is one of properdiagnosis and subsequent treatment of one80of the many conUluons wnlcn can causethese changes in bone. To do this one needsa good basic knowledge of calcium andphosphorus metabolism in relation to bonegrowth.Ionized calcium is absorbed primarily inthe ileum. This absorption process ismarkedly enhanced by the presence ofvitamin D. Calcium ';absorption is markedlyreduced when high fat levels are present inthe intestine because insoluble calciumsoaps are formed and the calcium is thenlost in the feces. Severe gastroenteritis canalso cause decreaseg. absorption of calciumions. 3The normal excretory pathway of calciumis via the gastrointe~tinal tract in the feces.The kidneys excrete, very little calcium butit is a threshold substance and in chronichypercalcemia the transport maximum canbe exceeded and calcium spills over into theurine in sufficient amounts to cause renalcalculi. 6 Normally all calcium is reab-sorbed by the kidney tubules but in diseaseconditions in which bone is being resorbeddecreased amounts of calcium are returnedto the blood.Serum calcium and phosphorus con-centrations are normally inversely relatedbut in disease conditions both may beelevated or lowered.The two hormones, parathormone andcalcitonin, along with vitamin D, areprimarily responsible for controlling bloodlevels of calcium and phosphorus.Parathormone acts in the kidneys, theskeleton, and the gastrointestinal tract.6 \Itssecretion is controlled primarily by calciumion concentration in the blood.In the kidneys parathormone binds withcells and causes increased tubular reab-sorption of calcium and enhances excretionof potassium, phosphorus, and bicar-bonate. 6 Parathormone also increases thecapacity of the kidney to produce activevitamin D, which aids calcium absorptionfrom the gut and increases calciummobilization from bone.Parathormone acts on the gastroin-tes tinal tract indirectly through vitamin Dto increase calcium absorption through theileal mucosa.Parathormone acts on bone at the cellularlevel to decrease bone binding capacity forcalcium and increase osteoclastic activityIowa State University Veterinarianwhich results in erosion of well calcifiedbone.Calcitonin acts primarily on the bone andsecondarily in the kidney. Calcitonininhibits bone resorption and decreases lossof calcium from bone with a resultinghypocalcemia and hypophosphatemia. Italso accelerates calcium and phosphorusremoval from blood.As previously mentioned, vitamin Denhances calcium absorption from theintestine, but it should also be noted thatexcess vitamin D intake can cause boneresorption of calcium and phosphorus witha resulting overflow of calcium into thekidney causing failure due to formation ofrenal calculi.There are several diseases associatedwith calcium and phosphorus metablolismwhich the clinician must include in hisdifferential diagnosis when poor bonemineralization is diagnosed radio-graphically.Primary hyperparathyroidism due to aparathyroid neoplasm is extremely rare.It has been reported only a few times in thedog and never in the cat. This disease canbe diagnosed by a progressive increase inblood calcium and decrease in bloodphosphorus levels. The only treatment isto surgically remove the affectedpara'thyroid gland. 2 ,8Rickets can be caused by several thingsincluding a low calcium diet, lowphosphorus diet, low vitamin D intake, achronic gastroenteritis preventing adequateabsorption of calcium, or by excess fat inthe diet resulting in the formation of in-soluble calcium salts. 3 •6 Diagnosis ofrickets requires a careful analysis of thediet of the affected animal. In addition,blood profile can be helpful. In lowphosphorus rickets serum phosphoruswill be low and serum calcium is usuallynormal. 2,3 Low calcium rickets is usuallyalways accompanied by nutritionalsecondary hyperparathyroidism becausethe low calcium levels in the blood willstimulate parathormone secretion. Thus,the hypocalcemia and hyperphosphatemiaone would expect with this disease canreadily be compensated by increasedresorption of calcium from bone and byincreased .excretion of phosphorus throughthe kidneys. In this disease blood values forIssue No.3) 1975these two nutrients can be very misleading.Treatment for the condition consists ofdietary correction of the imbalance and/orcorrecting the gastroenteritis or fat intakein the diet.Renal secondary hyperparathyroidism iscaused by a chronic renal insufficiencywhich prevents normal calcium reab-sorption in the tubules and stops excretionof phosphorus.:~·4 The phosphorusbuilds up in the blood and consequentlyblood calcium is lowered and theparathyroids are stimulated. In diagnosisblood values are helpful and the clinicianwill see a high phosphorus which is notcompensated because of the kidneysdecreased ability to excrete phosphorus.-!However, parathormone activi-ty maycompensate the low calcium levels andblood calcium may be normal. Treatment isprimarily aimed at the renal problem first.Nutritional secondary hyper-parathyroidism can be caused by a lowcalcium intake in the diet, a calcium-phosphorus imbalance with excessivephosphorus, or by a low vitamin D3 in-take. 3 Diagnosis of this disease alsorequires a careful analysis of the diet andmonitoring of blood calcium andphosphorus. The clinician must be carefulin relying too much on blood levels in thisdisease because hypocalcemia andhyperphosphatemia are readily com-pensated by increased bone resorption andincreased excretion of phosphates.Treatment consists of putting the animal ona diet with a calcium: phosphorus ratio of1.5 to 1. Use of a good commercial diet isrecommended for young animals and amineral supplemented beef diet for olderanimals who will not accept a commercialdiet.Several precautions should be followedwhen treating metabolic bone diseases. 31. Steroids are contraindicated in all casesdue to their detrimental effects onosteoblasts. They also cause necrosis of<;>steocytes in bone.2. Generalized th~rapy with minerals andvitamins in large doses should beavoided until the specific cause of theproblem is identified.3. Only one analysis of blood for minerallevels is not sufficient for diagnosis ofmetabolic bone diseases. Several81analyses should be done on successivedays to establish a trend in serum levelsof calcium and phosphorus.REFERENCES1. Carlson, William D.: Veterinary Radiology. 2ndedition. Lea and Febiger Co., Philadelphia, Pa.(1967): 434, 440.2. ]ubb, K.V.F. and Kennedy, Peter C.: Pathology ofDomestic Animals. 2nd edition. Volume 1.Academic Press, New York. (1970): 418, 20-25, 38-40.3. Kirk, Robert W.: Current Veterinary Therapy V. W.B. Saunders Co., Philadelphia, Pa. (1974): 105-109,797-805.4. Osborne, Carl A.: Canine and Feline Urology. W.B. Saunders Co., Philadelphia, Pa. (1972): 140-14l.5. Swenson, Melvin].: Duke's Physiology of DomesticAnimals. 8th edition. Cornell University Press.Ithaca, N. Y. (1970): 665-667.6. White, Abraham; Handler, Philip; Smith, Emil L.:Principles of Biochemistry. 5th edition. McGrawHill Co., New York. (1973): 995-1005, 1042-1049.7. Whittick, William G.: Canine Orthopedics. Lea andFebiger Co., Philadelphia, Pa. (1974): 42-47.Eperythrozoonosis In SwinebyMarge Claxton*andDr. J. P. Kunesh, D.V.M., M.S., Ph.D.!Eperythrozoonosis is an "acute febrile,icteroanemic disease of shoats" 2 causedby the rickettsial organism Eperythrozoonspp. There are two species which arecommonly associated with swine, E. suis}which produces a febrile disease, and E.parvum} which is innoxious. Other commonnames for eperythrozoonosis include epy,swine icteroanemia, yellow belly, andanaplasmosis-like disease.E. suis organisms are relatively large,coccoid bodies (average size of o.8u indiameter) found attached to RBC's and alsofree in the plasma. Transmission of theorganism occurs via several methods: 1)bloodsucking ectoparasites especiallymange (Sarcoptes scabei var suis) and lice(Hematopinus suis), 2) mechanical tran-smission (needles, ear notching, taildocking, castration, etc.), and 3) in uterotransmission.In utero transmission was shown to existby an experiment conducted by Dr. A. R.Smith at the University of Illinois. A bredgilt which had been serologically positive(titer 40) for at least 5 months previouslywas purchased and her pigs were delivered* Mrs. Claxton is a fourth year student in theCollege of Veterinary Medicine, Iowa State University.t Dr. Kunesh is a Professor of Veterinary ClinicalSciences at Iowa State University.82via cesarian section (germ free). The pigs,therefore, had no contact with the sow orother infected pigs. Out of a litter of 13pigs, parasites were observe4 in the bloodof all the pigs during the first week.Wright-Giemsa stained blood smears weremade to confirm the infection. Three of the13 died and all dead and moribund pigs hadhemoglobins of 1.9-3.0 g/100 ml. andPC'V's of 10.5-12.5. 4/Most parasites in swine don't change theblood picture much, E. suis being an ex-ception. The total red count may drop aslow as 1-2 million cells/cubic mm. (normalis 7 million cells/cubic mm.), thus creatinga severe anemia and icterus: Hemoglobinlevels decrease to 2-4 gm. (normal is 13gm.) and the bone marrow becomeshyperplastic while total white count in-creases slightly or remains the same.Incubation time for the disease is ap-proximately 6-10 days. Increased tem-perature of 104 0 to 107 0 , anorexia,depression, and severe and rapid blooddestruction with a subsequent decrease inthe numbers of parasites are characteristicclinical signs of epy. Later in the course ofthe disease icterus, polypnea, weakness,and bile stained feces are observed.On posting a diseased animal, icterus,yellow liver and a soft, enlarged spleen areIowa State University Veterinarian

Low Calcium Rickets in Young Cats

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Low Calcium Rickets in Young Cats

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