Metabolic Disorder only not yet finished

1. Non-Infectious Diseases
in Animals
Metabolic Disorders and Genetic Diseases
By: Justine Ivan P. Valencia L. Agr.

2. Definition
 Non-infectious diseases are not caused by virulent
pathogens and are not communicable from one animal to
another.
 Maybe cause by hereditary factors or by the environment.
 Metabolic diseases usually results from a disturbance in the
normal balance of the physiological mechanisms that
maintain stability, or homeostasis.

3. Metabolic Disorders
Metabolic diseases may be inherited or
acquired, the latter case being more
common and important. Metabolic diseases
are clinically important because they affect
energy production or damage tissues critical
for survival.

5. 1. Ketosis in Cattle
(Acetonemia)
 Metabolic disease of lactating cows occurring within a few days to a few
weeks after calving.
 Characterized by hypoglycemia, ketonemia, ketonuria, in appetence, either
lethargy or high excitability, weight loss, depressed milk production and
occasionally incoordination.
 Incidence is highest in high producing cows which are being stall-fed.

7. Etiology
 Any factor that causes a reduction in the intake or absorption of dietary
carbohydrate precursors can cause primary ketosis.

8. Clinical Findings
 In appetence, constipation, mucus-covered feces, depression, a staring
expression, a very obvious loss of weight, a drop in milk production and a
humped back posture suggestive of mild abdominal pain.
 Acetone odor on the breath.
 Hypoglycemia, ketonuria and ketonemia are always present.

9. Diagnosis
 In practice, ketosis is diagnosed by the measurement of betahydroxy
butyrate (BHB), one of two major ketones, that becomes elevated in blood,
urine, and milk of fresh cows.
 The mere presence of hypoglycemia, ketonemia, and ketonuria is not
sufficient for a positive diagnosis of ketosis. Such conditions, of course, may
accompany the pure ketotic syndrome.

10. Prophylaxis
 Animals susceptible to ketosis should be maintained on a relatively high-
energy intake before calving and the level should be increased substantially
after parturition .

11. Treatment
 In thin cows that have been obviously undernourished replacement of
carbohydrate is recommended.
 In fat cows, where nutritional imbalance is more likely to be the cause,
glucocorticoids are as effective. The IV injection of glucose is not sufficiently
effective to be recommended as a sole form of treatment. It is commonly
used as an adjunct to either the injection of glucocorticoids or the oral
administration of propylene glycol.

12. 2. Pregnancy Toxemia in Cattle
(Fat Cow Ketosis, Fat Cow Syndrome)
 A sporadic disease occurs mostly in cows that have become fat because of
heavy feeding in early pregnancy, but which suffer a severe nutritional stress
during the 2 months before calving.
 When the disease is observable clinically it is usually far advanced and
treatment at this stage is unrewarding; the mortality is virtually 100%.

13. Etiology and Pathogenesis
 Pregnancy toxemia is precipitated by large or multiple fetuses, feed low in
energy or protein or high in poorly digestible fiber, and health conditions that
increase energy demand or decrease ability to take in nourishment (eg,
lameness, oral diseases).

14. Clinical Signs
 Both thin and well-conditioned cows can be affected by pregnancy toxemia.
 The first clinical sign is loss of body condition over 1–2 weeks.
 Decreased appetite, rumination, fecal production, and nose-licking are
general clinical signs of illness.
 Affected cows become markedly depressed, weak, ataxic, and recumbent.
 Opisthotonos, seizures, or coma may occur terminally.

15. Diagnosis
 History and clinical signs in a cow in late gestation with marginal feed quality
support a presumptive diagnosis of pregnancy toxemia.
 Ketonuria is present from the early stage of disease and is the most specific
finding; even mild ketonuria should not occur in healthy pregnant cows until a
few days before calving.
 Inexpensive glucometers are available to test blood concentrations of beta-
hydroxybutyrate (BHB) and glucose. Hypoglycemia is also common; however,
cows with seizures or signs of excitement may have hyperglycemia.

16. Treatment and Prevention
 Successful treatment requires early intervention and improved dietary
management.
 Affected cows require aggressive treatment with fluids and other supportive
measures.
 Prevention is based on monitoring body condition and diet in late gestation.
 Recumbent cattle may benefit from good nursing care but rarely respond to
treatment.
 To decrease the energy drain in any cow with pregnancy toxemia, induction of
parturition or removal of the fetus by cesarean should be considered.

17. 3. Pregnancy Toxemia in Ewes
(Pregnancy disease, Lambing paralysis,
Twin-lamb disease, Ketosis)
 A disease of preparturient ewes, primarily characterized clinically by
impaired nervous function.

18. Etiology
 Under nutrition in late pregnancy, with over fed ewes carrying twins or
triplets being more susceptible than ewes in poor condition and those carrying
single lambs.

19. Clinical Signs
 Early clinical signs maybe erratic and difficult to detect.
 listlessness, inappetence, aimless walking, “propping” against any kind of
obstruction, twitching of the muscles of the ears, unusual postures, grinding
of the teeth, blindness, ataxia and death.
LESIONS
 Necropsy findings include fatty livers.
 Adrenal glands maybe swollen.
 Often include multiple fetuses in a state of decomposition, indicating fetal
death prior to maternal death.

20. Diagnosis
 Clinical signs of selective anorexia in late gestation
 Definitive diagnosis via laboratory tests
 Acute hypocalcemia before lambing offers the main problem in differential
diagnosis. (death occurs within 24 hours)

21. Treatment and Prevention
 Administration of energy sources and removal of factors causing reduced
energy availability
- can often be treated successfully with propylene glycol
 Increased care of the newborn offspring
 Ewes or does should not enter the last 6 weeks of gestation with a BCS <
2.5/5; this can be prevented by good feeding management, forage analysis,
and ration formulation.

22. KEY POINTS
 Pregnancy toxemia is a common metabolic disease of pregnant sheep and
goats, usually occurring as the result of management errors during the
gestational season.
 Clinical diagnosis of pregnancy toxemia in sheep and goats should be
confirmed by results of laboratory tests.
 Treatment can be effective if initiated early in the course of disease.
 Prevention of pregnancy toxemia in sheep and goats is based in a thorough
nutritional and health management plan from early pregnancy to parturition.

23. 4. Parturient Paresis in Cows
(Milk Fever, Hypocalcemia, Paresis Puerperalis, Parturient Apoplexy)
 Afebrile disease, occurring soon after parturition, manifested by circulatory
collapse, generalized paresis and depression of consciousness.

24. Etiology
 Dairy cows are at considerable risk for hypocalcemia at the onset of lactation,
when daily calcium excretion suddenly increases from about 10 g to 30 g per
day.
 Hypocalcemia initially causes hyperexcitability of the nervous system, which
typically progresses to decreased strength of muscle contractions and paresis.
 Parturient paresis may occur in cows of any age; however, it is most common
in high-producing dairy cows entering their third or later lactations.

25. Clinical Findings
 Recumbency around the time of parturition
 Hyperexcitability that progresses to flaccid paralysis
3 Stages of Parturient Paresis
 In stage 1, cows are standing and ambulatory; however, they show clinical
signs of hypersensitivity and excitability
 Cows with stage 2 parturient paresis are paretic to the point that they cannot
stand.
 Cows in stage 3 parturient paresis lose consciousness progressively to the
point of coma. They are unable to maintain sternal recumbency and lie flat
on their sides.

26. Treatment
For stage 1 (Standing Cows)
Should be treated with an oral calcium supplement.
-A standard oral dose provides 40–55 g of elemental calcium.
For stage 2 and 3 (Recumbent Cows)
Cows with stage 2 or 3 hypocalcemia require immediate correction of their
hypocalcemia by intravenous calcium infusion. (The jugular vein is the preferred
site for intravenous calcium infusion).

27. Prevention of hypocalcemic relapses in
all affected cows
- Oral calcium administration (oral calcium bolus)
- Subcutaneous calcium (may not be adequately absorbed because of poor
peripheral perfusion during the initial hypocalcemia, thus not be the sole
route of treatment)

28. Prevention
 The most practical and proven method for preventing hypocalcemia is by
feeding an acidogenic diet for ~3 weeks before calving. This approach creates
a compensated metabolic acidosis, increases gastrointestinal calcium
absorption, improves PTH receptor responsiveness, and mobilizes more
calcium from bone.

29. 5. Parturient Paresis in Sheep and Goats
(Milk Fever, Hypocalcemia, Lambing Sickness)
 Parturient paresis in pregnant and lactating ewes and does is a disturbance of
metabolism characterized by acute-onset hypocalcemia and rapid
development of hyperexcitability and ataxia, progressing to depression,
recumbency, coma, and death. Unlike parturient paresis in dairy cattle, which
primarily occurs within a few days of calving, the condition in ewes and does
usually occurs before and less commonly after parturition. This condition may
be underdiagnosed in some situations.

30. Etiology
 Parturient paresis can occur at any time from 6 weeks before to 10 weeks
after parturition; however, the greatest demand for calcium because of
mineralization of the fetal skeleton occurs 1–3 weeks prepartum, particularly
when multiple fetuses are present in utero.
 Whenever an abrupt decrease in calcium intake occurs, the body requires 24–
72 hours to activate the metabolic mechanisms necessary to mobilize stored
calcium.
 Mobilization of stored calcium can be inadequate to meet an animal’s needs
in older ewes and does, in animals with chronic calcium deficiency, and when
diets are calcium deficient.

31. Clinical Findings
 Characteristically occur in outbreaks.
 Earliest signs are slightly hyper excitability, muscle tremors and a stilted gait.
 Parturient paresis occurs more often around parturition and can be
aggravated by stressful situations
 Under field conditions, a response to calcium administration would support
diagnosis of parturient paresis
 A definitive diagnosis can be made only by assessment of calcium
concentration in blood (<2 mmol/L)

32. Prophylaxis and Treatment
 Treatment consists of IV or calcium therapy, preferably with some added
magnesium.
 Affected sheep should be handled with care lest sudden death occur from
heart failure.
 Prevention is largely a matter of avoiding the predisposing causes.

33. 6. Bovine Secondary Recumbency
(Downer Cow Syndrome)
 Bovine secondary recumbency is defined as the inability of cattle to rise
and stand for a period of at least 12–24 hours, resulting from the delayed
or unsuccessful treatment of a different primary cause of recumbency.

34. Etiology
 Hypocalcemia, dystocia, and musculoskeletal injuries resulting from slipping
and falling are considered the most common predisposing factors that may
result in downer cow syndrome.
 Regardless of the initial cause of recumbency, all affected cattle develop
pressure-induced secondary damage to muscles and nerves of the pelvic
limbs, especially when lying on a hard surface.

35. Diagnosis
 Physical examination
Diagnosis of fractures, joint lesions, and nerve injuries is based primarily on the
findings of the physical examination.
 Serum biochemical analysis, urinalysis
Downer cows commonly have increased serum CK, AST, and LDH activity to a
varying extent, which may indicate the presence and severity of muscle trauma.

36. Lesions
 Ischemic necrosis and rupture of muscles of the thigh region are common
necropsy findings in downer cows

37. Treatment
 Treatment is guided by the cause.
- Correction of primary disease including hypocalcemia, other electrolyte
abnormalities.
 Supportive care is of major importance to improving the prognosis.
- Animal welfare considerations are paramount in guiding the overall
management of affected cows.
- Excellent nursing care, pain management, hydration
- Daily assisted attempts to rise; use of a flotation tank as indicated
- Attention to animal welfare concerns

38. Key points
 Pressure damage on muscle and nerve tissue is considered the most important
causative factor.
 A thorough physical examination of the recumbent cow to identify all relevant
primary and secondary causes contributing to recumbency is the basis for
successful treatment
 State-of-the-art nursing and supportive care greatly increase the chances for
a positive outcome.

39. 7. Lactation Tetany of Mares
(Transit tetany, Eclampsia)
 Condition associated with hypocalcemia occurring most often in lactating
mares, either at about 10 days after foaling or 1 to 2 days after weaning.
 Mares have a heavy flow of milk.
 Pregnant mares subjected to hardwork. (stress of work)
 Ocassionally in nonlactating horses, usually following stress such as prolonged
transport. (stress of transport)

40. Clinical Signs
 Body temperature remains close to normal, and the appetite appears
unimpaired but during an attack the animal is unable to eat, urinate, or
defecate.
 Characterized by incoordination, tetany, sweating, muscle tremors, rapid,
violent respiration, and a thumping sound from within the chest, considered
by many to be a spasmodic contraction of the diaphragm.
 Stiffness of the gait and a high carriage of the tail are apparent.

41.  Mildly affected animals may recover spontaneously; severely affected ones go
down in about 24 hours.
 Develop tetanic convulsions and usually die within the next day.

42. Treatment
 Responsive to IV injections of calcium solutions given very slowly is generally
good.
 If associated with transport, it may be advisable to incorporate magnesium in
the solution.

43. 8. Transport Tetany of Ruminants
(Railroad Disease, Railroad Sickness, Staggers)
 A condition affecting well-fed cows and ewes in the advanced stages of
pregnancy during or immediately after long-continued transportation and
stress.
 A form of acute hypocalcemia brought on by adverse conditions during
shipping.

44. Clinical Findings
Commonly observed at destination.
 Early signs of restlessness and uncoordinated movements are followed by
partial paralysis of the hind legs and a staggering gait.
 Pulse rate 100 to 120, while respiration is rapid and labored.
 Extreme thirst may develop.
 Anorexia is regularly observed with a reduction or complete cessation of
peristaltic and rumen activity.
 Abortion may occur as a complication.

45. Prophylaxis and Treatment
 Animals in advanced pregnancy should be given only dry feed for a day or 2
preceding shipment.
 For treatment, IV injections of calcium borogluconate, or calcium
borogluconate with magnesium sulfate given very slowly, preferably with 250
to 500 ml of 50% dextrose solution, followed by stimulants such as
amphetamine are recommended.

46. 9. Puerperal Tetany
(Hypocalcemic tetany, Lactation tetany, Eclampsia)
 A disease occurring in bitches, particularly toy breeds nursing a full, active
litter, and rarely in queens.
 Mostly common in the first 3 weeks of post partum but may occur prepartum,
during parturition or as late as weaning.

47. Etiology
 The demand for calcium during pregnancy and lactation results in exhaustion
of calcium stores and hypocalcemia without accompanying parathyroid
disease.

48. Clinical Findings
 Early signs include panting, restlessness, anxiety and whining, dooling and
champing of the jaws.
 The gait becomes stiff, the animal staggers, collapses and is unable to rise,
the head and the neck are extended and twitching of local muscle groups or
generalized clonic movements occur.
 Pupils are dilated, mucosae are congested and the temperature is elevated
(41.5 degrees C).
 Animal is conscious, Untreated bitches usually die.

49. Diagnosis
 A history of impending or recent parturition in a nursing bitch or queen
coupled with myoclonus or generalized convulsions is diagnostic.
 Serum calcium levels fall below 7 to 8 mg%

50. Treatment
 Elevation of the serum calcium following the IV administration of calcium
gluconate causes immediate remission of signs.
 An additional half dose of a buffered calcium solution can be given by IM
injection to avoid reoccurrence of signs.
 Following parenteranal therapy, oral calcium gluconate and vitamin D and
adequate nutrition are supplied.
 Oral or IV corticosteroids may prevent the occurrence of the disease by
decreasing the incorporation of endogenous calcium into the bone.

51. 10. Hypomagnesemic Tetany in Cattle and Sheep
(Grass tetany, Grass staggers)
 A metabolic disturbance, characterized by hypomagnesemia, occurring most
commonly in adult cows and ewes, especially those that are lactating heavily
and are grazing on lush grass pastures.
 Occurs in cattle of any age or condition, particularly beef cattle.
 Manifested by irritability, tetany and convulsions.

52. Clinical Findings
2 Stages:
1. Development of hypomagnesemia
 In less severe cases, the cow is obviously ill at ease, walks with a stiff gait, is
hypersensitive to touch and sound, urinates frequently and may progress to
the acute , convulsive stage after a period as long as 2 to 3 days.
2. Triggering of the clinical conditions
 In the most acute form of the disease, affected cows, which may be grazing
in an apparently normal manner, suddenly throw up their heads, bellow,
gallop in a blind and frenzied manner, fall and undergo severe paddling
convulsions.

53. Prophylaxis
 Prevention is largely a combination of increasing the intake of magnesium in
danger periods and of management.

54. Treatment
 Usually treatment includes administration of magnesium and calcium
compounds, and sometimes sedatives if the convulsion and tetany are severe.
 An IV injection containing both calcium and magnesium is used, but it must be
given slowly and the effect on the heart beat watched carefully.
 A less risky alternative is to give the calcium IV and magnesium sulfate
subcut.

55. 10. A. Hypomagnesemic Tetany of Calves
 Characterized by hypomagnesemia, and commonly hypocalcemia.
 Clinically identical with grass tetany in adult cattle.
Occurrence:
2- to 4-month-old calves on sole milk diet, or in younger calves on milk replacer
or with chronic scours.
Treatment:
• 10% solution of magnesium sulfate (100 ml subcut.)
• Followed by oral administration of 10 to 15 gm magnesium oxide daily.

56. 11. Hypoglycemia of Piglets
(Baby pig disease, Fading pig disease)
 An important primary cause of death in piglets under one week of age,
accounting for 15 to 25% of total piglet mortality and a final common pathway
to death in other piglet diseases.

57. Etiology
Piglets have effective metabolic response to cold and fully functional peripheral
vasoconstriction but their lack of insulating subcut. fat (until 1 to 2 weeks old)
allows marked heat loss demands rapid glucose utilization depleting glycogen
reserves; if then milk intake is impaired, hypoglycemia and death impend.
 Predisposition of piglet hypoglycemia occurs from any disease of the sow
which decreases or inhibits milk production or let down, farrowing hysteria or
puerpural disease, agalctia from ergot poisoning or nipple necrosis.
 Also large litter of size with an in adequate number of teats precludes proper
nursing.

58. Clinical Findings
 Behavior changes from normal vigorous sucking and play alternating with
sleep to solitary lassitude.
 Individual pigs aimlessly wander with faltering gait , crying weakly.
 Piglets area gaunt with pale cold clammy skin, hypothermia, poor muscle tone
and are unresponsive to external stimuli.
 Terminally, piglets exhibit convulsions with jaw champing, salivation, milk
opisthotonus, nystagmus, forelimb, hind limb contraction, coma and death.

59. Diagnosis
Generally diagnosed through:
 Examination of the sow and environment for predisposing factors.
 Piglet response to glucose treatment.
Lesions
 Inadequate milk intake with minimal ingesta in the alimentary tract,
 Dehydration,
 Small hard liver and,
 Frequently, a white precipitate in the renal pelvis and ureters.

60. Treatment and Prophylaxis
 Treatment is 15 ml of 5% glucose given IP.
 Treated pigs should be place under a heat lamp or in an equivalent warm
environment.
 Sustained energy intake must be provided to avoid relapse.

61. 12. Obesity

62. 13. High-Mountain Disease
 Bovine high-mountain disease is a condition that occurs in cattle pastured
at high altitude. Low oxygen saturation in the air leads to pulmonary
hypertension, with subsequent edema in ventral tissues of the chest and
abdomen. Treatment typically requires movement to lower elevation, and
prevention through selective breeding for resistant stock is often
preferred.

63. Etiology
 The disease is related to the chronic hypoxic condition that results from high
altitude, which causes pulmonary vasoconstriction and hence pulmonary
hypertension.
 Other stresses, such as pneumonia, lungworm infection, subzero weather,
chronic pulmonary lesions, or raptured diaphragm, are often superimposed
upon the already partially compromised pulmonary circulation and disguise
the etiology.

64. Clinical Findings
 Subacute brisket edema, that extends cranially and caudally
 Pleural effusion and ascites
 Distension and pulsation of jugular veins

65. Treatment
 It is essential that animals be moved to a lower altitude with minimal
restraint, stress and excitement.
 General supportive therapy, including antibiotics to combat pneumonia,should
be administered.
 Recovered animals should not be returned to high altitudes, since the disease
may recur.
 Inherited susceptibility is likely, affected cattle should not be retained for
breeding.

66. 14. Postparturient Hemoglobinuria
 A disease of high-producing dairy cows that occurs 2 to 4 weeks after
parturition.
 Characterized by intravascular hemolysis, hemoglobinuria and anemia.

67. Etiology
 Caused is unknown.
 Incidence generally low but upto 50 %of affected animals may die.
 Diets high in cruciferous plants, or beep pulp, and prolonged feeding on
phosphorus-deficient diets are said to be predisposing factors.

68. Clinical Findings
 Rapid IV hemolysis leads to hemoglobinuria, extreme pallor and a markedly
increased cardiac impulse.
 Dehydration, weakness and a marked drop in milk yield are prominent signs.

69. Treatment
 Transfusion of large quantities of whole blood may be the only effective
treatment of severely affected animals.
 In less severe cases, 6 gm of sodium acid phosphate in 300 ml of distilled
water may be administered IV followed by subcut. Injections at 12 – hour
intervals or by daily oral doses of the same amount of phosphate.
 Bone meal should be added to the ration.

70. 15. Porcine Stress Syndrome
 Acute, shocklike syndrome, often fatal, which may occur following stress
including that due to such routine management procedures as handling or
moving.

71. Etiology
 Results from a heritable defect in ability to maintain homeostasis, so that
stress causes excessive stimulation of β-adrenergic receptors, with the rapid
depletion of ATP , rapid muscle glycogenolysis and excessive production of
muscle lactate.
 Occurs most often in extremely muscular pigs.
 Greatest incidence in Pietren, Poland China, and certain lines of Landrace
pigs.
 Frequently in pigs kept in partial or total confinement.

72. Clinical Findings
 Impending PSS may be signaled by a rapid tail tremor.
 Alternating areas of blanching and erythema may be noted in white or light-
skinned pigs, followed by cyanosis.
 Dyspnea is common with open-mouthed breathing and elevated body
temperature.
 Muscle becomes rigid, the pig is reluctant to move and it may collapse and
quickly die.
 Rigor mortis develops within a few minutes.

73. Postmortem Examination
May reveal:
 PSE pork –pale, soft, exudative
In other cases:
 DFD pork – dark, firm, dry

74. Diagnosis
 The similarity between PSS and the malignant hyperthermia syndrome (MHS)
led to development of the halothane test for susceptibility to PSS.
 CPK (creatine phosphokinase) and halothane test are best administered to 15
to 25 kg pigs.

75. Treatment and Control
 Pigs showing signs of stress should be allowed to rest, and it may be desirable
to tranquilize pigs in advance of possible stress if they are known to be PSS-
susceptible.
 In its early stages, IV administrations of tranquilizers, fast-acting
hydrocortisone, and bicarbonate to help reduce lactate acidosis, but in
advanced cases in which the pig iss unstable to stand, PSS is irreversible.f
 Since susceptibility of PSS is inherited, appropriate breeding methods can
rapidly reduce its incidence.

76. 16. Photosensitization
 Presence of photodynamic agent renders an animal hypersensitivity to light.
 The active rays are those absorbed by the photosensitizing agent.
 Often extend into the visual spectrum and usually are quite harmless to the
unsensitized animal.
 Lesions develop rapidly unlike sunburn.
 Condition is best shown in sheep and cattle, but may occur in any animal.

77. Etiology
 Photosensitizing substances may be introduced into the body by ingestion or
by injection, or become operative through faulty liver function or aberrant
pigment metabolism.

78. 3 Mechanisms of Photosensitization
1. Primary Photosensitization
2. Hepatogenous Photosensitization
3. Facial Eczema

79. 16. A. Primary Photosensitivity
 Primary photosensitivity caused by the ingestion of photosensitizing agents
not normally present in diet.
Long known sources of such compounds:
 Plants of the genus Hypericum (St. John’s wort or Klamath weed)
 Fagopyrum esculentum (buck wheat)
 Families of plants Umbelliferae
 and Rutaceae

80. 16. B. Hepatogenous Photosensitivity
 A condition caused by the accumulation of a photodynamic agent in the skin
that sensitizes it to ultraviolet radiation.
 Exposure of nonpigmented skin to UV radiation results in dermatonecrosis.

81. 16. C. Facial Eczema
(Pithomycotoxicosis)
 A photosensitization of sheep and cattle arising from liver damage caused by
the ingestion of toxic spores of the saprophytic mold Pithomycotoxicosis

82. Clinical Findings
 The lesions and signs of photosensitivity are the same regardless of its cause.
 Photosensitized animals show photophobia immediately when they are
exposed to sunlight.
 Erythema develops rapidly and is followed by edema.
In sheep, commonly affected parts are the face and ear. (“Big head”)
In cattle, any unpigmented area including the tongue but the teats and udder
appear to be more sensitive.

83. Prophylaxis and Treatment
 Symptomatic treatment is being imposed.
 Control can be done by preventing access to the offending plants.
 Grazing on plants known to be safe and confining stock to small areas and
feeding them hay.
 Animals should be given adequate shade or, preferably, housed and allowed
out to graze only during darkness.

84. 16. D. Congenital Photosensitivity in
Southdown Sheep

85. 17. Congenital Porphyria Erythropoietica

86. References
 The Merck Veterinary Manual. RAHWAY, N.J., U.S.A. MERCK & CO.,INC. 1979
 Bagheri and Rico. June. 2022. Ketosis in the dairy cow: Friend or Foe?. Sept.
2023.<extension.umd.edu/resource/ketosis-dairy-cow-friend-or-foe>
 Fthenakis. Oct. 2022. Pregnancy Toxemia in Sheep and Goats. Sept. 2023.
<https://www.msdvetmanual.com/metabolic-disorders/hepatic-
lipidosis/pregnancy-toxemia-in-sheep-and-goats>
 Oetzel. Oct. 2022. Parturient paresis in cows. Sept. 2023.
<https://www.msdvetmanual.com/metabolic-disorders/disorders-of-calcium-
metabolism/parturient-paresis-in-cows>
 Grünberg. Oct. 2022. Bovine Secondary Recumbency. Sept. 2023.
<https://www.msdvetmanual.com/musculoskeletal-system/bovine-
secondary-recumbency/bovine-secondary-
recumbency?query=the%20downer%20cow>