Perinatal Mortality in Lambs
Dr Rob Foster
Perinatal mortality can be very high and limit sheep production and viability. Limiting perinatal mortality in lambs is therefore an important part of sheep production. David McFarlane in New Zealand and his seminal paper in 1965 describing an autopsy method for the investigation of perinatal losses, represents a huge study on the changes that occur in lambs in the perinatal period.
Defining perinatal and neonatal is a quagmire. McFarlane (1965) defined perinatal mortality as death during or within seven days of birth. This definition appears to be widely accepted. This is in line with the WHO definition of the perinatal period in humans. Based on this definition, death just before birth (late abortion or stillbirth), death at the time of birth (stillbirth) and in the first week of life is perinatal death. The neonatal period, as definied by the WHO is from birth of a normal infant to 28 days. The early neonatal period is the first week. The late neonatal period is from 7 days on. When assessing papers, it is important to know the definitions used.
Dr Kevin Haughey and Dr Stan Dennis published widely on perinatal mortality also, and wrote many publications on the topic in the 1970s. Despite the ease and high economic advantage of limiting perinatal mortality, it is often overlooked.
The prevalence of perinatal mortality in many sheep raising areas is very high and of the order of 25-80%. Well managed flocks can have less than 5% perinatal mortality.
In general, 71% of cases are related to prenatal events, 13% with postnatal events and 16% are undiagnosed
Perinatal mortality in lambs should be approached from a production or herd basis. Most causes can be corrected by adjusting flock management, so a focus on identifying those changes in management that will result in a lower mortality is preferred, and is the approach that is used here. The major management changes that can be implemented include:
- Ewe nutrition
- Monitoring of newborn lambs
- Minimising mismothering
- Hygeine and infection control
Holmøy IH, Waage S. Time trends and epidemiological patterns of perinatal lamb mortality in Norway. Acta Vet Scand. 2015; 57: 65
The perinatal period is one where the lamb goes from an aquatic a terrestrial environment. In between is passage of the lamb through the pelvis of the mother - a very tight squeeze. The events around lambing and independence require a very finely tuned series of events that must be done is a set sequence. Physiologically, the processes are very complicated and it is miraculous that any neonate survives. Control of the processes and their complexity means that perinatal mortality is inevitable - minimizing the loss is the aim.
The major physiological steps that influence perinatal survival are
- late term development
- udder development
- Ewe-lamb bonding
The major factors that prevent perinatal survival are
- placental insufficiency
- maternal underfeeding
- intrapartum hypoxemia and dystocia
The first steps are diagnosis, diagnosis, diagnosis. Identify if there is a problem, and then identify the problem. In a well managed flock, the maximum of 10% perinatal mortality will have lambs that die in each of the general categories - late term abortion, stilbirth and postnatal mortality. Routine post mortem evaluation of perinatal lambs will identify the potential causes and provide a guide to future lamb health. The procedure is simple and yet has the potential to provide incredibly valuable information. It is also very rewarding.
Examination of a dead lamb is one of the easier and simpler post mortem procedures. As with all necropsies, the procedure should be done in a routine manner and relevant details should be recorded.
- As the prospector, you and anyone else involved with the handling of newborn lambs and fetal membranes should wear appropriate personal protective equipment. Placentas and birth fluids can contain zoonotic agents of which Coxiella burnetti is the one of particular concern as it is highly infectious and the infectious particles are present in aerosols. Protective clothing, gloves, eye wear, and an appropriately fitted mask with a biological filter is a minimum. A method for disinfection and disposal of the area and materials should also be in place.
- Record the body weight of each lamb
- External examination should include careful evaluation of
- external surface for meconium staining,
- the umbilicus,
- hooves for eponychia and plaques,
- tongue, lips, rump and distal limbs for edema
- Internal examination by the standard protocol of removing the upper (and left) forelimb, hindlimb, skin and body walls of the abdomen and thoraxparticularly making note of
- size of thyroid
- aeration of lungs
- perirenal, pericardial and epicardial fat
- abomasal content
- intestinal content and intestinal lymphatics
- internal aspects of the umbilicus
- any other abnormalities
- Examination of brain
The birthweight of lambs is critical for overall lamb survivability. It is one of the most important overall management factors contributing to perinatal lamb mortality. It is estimated that about 70% of perinatal deaths are related to prenatal factors, 13 % to postnatal factors and 16% are unknown. The normal birthweight of a lamb is between 3 and 5 kg regardless of the number of siblings. A large lamb is much more prone to birth trauma and a small lamb will be weaker, have less reserves and tolerance for low temperatures, is more likely to suffer postpartum trauma, more likely to be predated, is less likely to receive adequate colostrum or milk and therefore suffer from infections or starve.
A low birth weight is from inadequate ewe nutrition, ewe disease, reduced functional placental reserve (for example from placentitis), and less commonly, congenital viral infection.
A high birthweight is usually from over nutrition in the pre-partum period.
There are 3 parts to death during the periparturient time period: late term abortion, stillbirth, and postpartum mortality. These equate to the terminal part of pregnancy, death during the birth process and up to 3 hours after birth, and death following initial survival of the birth process (from 3 hours to 7 days postpartum).
Aborted lambs dead en utero before the normal time of birth have one or more of the following characteristics: they
- are not fully developed
- are covered in viscous amniotic fluid
- are meconium stained
- have indicators of fetal autolysis including the presence of bloody subcutaneous and cavity fluids were dead in utero for between 36 and 72 hours.
- have an intact umbilical cord and often have an accompanying placenta
- have no indicators of having survived the birth process such as no evidence of aeration of lungs
- amniotic fluid in their stomachs
Stillborn lambs are those that died during the birth process or soon after. They have one or more of the following:
- fully formed/developed
- no evidence of aeration of lungs or partial aeration of lungs
- amniotic fluid in their stomachs
- meconium staining
- blunt ending, flacid umbilical cord without a thrombus
- swelling of the head or rump
- intracranial hemorrhage
Neonatal lambs. There are several indicators of whether a lamb has survived the birth process. These are
- aeration of lungs: fully aerated lungs can only be present if the lamb survived the birth process. Lambs with no air in their lungs were born dead. those lambs with partial aeration died in the immediate postpartum period.
- umbilical cord: those lambs with an intact umbilical cord died before or during the birth process. An umbilical cord that ends in a taper, is pointed or has a "V" shape, and has a thrombus is from a lamb that was live at birth.
- eponychium: lambs that stand quickly remove the eponychium from their feet. Those on soft bedding may retain them even after walking normally.
- milk in stomach. Lambs that drink have a milk clot in their stomach. The exception is when lambs are hand (tube) fed - they dont need to suckle for this!
Lambs that are late term abortions or stillbirths are treated as aborted fetuses as far as laboratory procedures. They should be handled as abortions, be investigated as a failure of pregnancy and be treated as potentially infectious with personal protective equipment suitable to prevent zoonotic transmission of Coxiella burnetti.
Most laboratories have a protocol (and therefore a long list of samples to collect) for dealing with lambs that are aborted or suffered a stillbirth. Laboratory evaluation aims to determine whether the event was infectious or not. The general and common infectious causes for failure of pregnancy of sheep are well-known, and include infection with Chlamydia abortus, Coxiella burnetti, Campylobacter fetus and Toxoplasma gondii. The first three of these cause placentitis and this is usually readily identifiable in the affected placentas. Carefully examination of the cotyledons is required to identify the characteristic focal necrosis of Toxoplasma gondii infection. Certain regions of the world have specific 'other' infectious agents that can result in late term abortion or stillbirth.
We will look specifically at the failure of pregnancy side of investigations elsewhere (go to Failure of Pregnancy).
It is possible, with careful observation of lambs to determine at what stage of the postpartum period death occurred. The time period equates to one of the following:
- ability to stand. When lambs stand up after birth their eponychia become dry and are sloughed. Those that stand must be strong enough and coordinated enough to do so. Small weak lambs (body weight less than 3 kg) are those that tend not to stand. Lambs that are large and overweight ( body weight more than 5 kg) usually have a reason such as rib fractures or haemorrhage of the brain that indicate birth trauma. Some also have indications of dystocia including swelling of the lips, tongue, and or head.
- ability to suckle. Lambs with sufficient strength and coordination, and whose mothers are available and are lactating, will have milk in their stomach. Within a short period of time this milk should enter the small intestine and lymphatics should contain chyle. Those who do not consume milk will starve and their brown fat will be metabolised.
One should then investigate and categorise lambs that have suckled according to specific causes of death.
The transition from an aquatic to terrestrial environment requires a change of acquisition of oxygen and release of carbon dioxide from the placenta to the lungs. Complete (fetal) atelectasis therefore occurs in aborted foetuses and those that died during the birth process before air could be inhaled. Partial atelectasis indicates an attempt to inhale air but with incomplete results or could indicate aspiration of amniotic fluid and thus preventing complete aeration of the lungs. The pattern of aspiration of amniotic fluid is a generalised mosaic of atelectasis and aerated lungs with some lobules containing air and others not in a patchwork appearance.
Amount and catabolism of brown fat
Lambs are able to use their stores of brown fat as an energy source and for thermogenesis. In the research performed by Haughey (1973), lambs born at 1°C regardless of access to milk had slight catabolism of their fat beginning at 3 to 5 hours after birth. Marked catabolism occurred 24 hours after birth in conditions of 1°C. Catabolism was more prominent in those that had not suckled yet was present in all lambs born at either 1°C or 18°C. Even at 35°C, lambs that did not suckle had slight or moderate catabolism from 26 to 47 hours after birth.
The amount of fat is also germaine, and lambs with a lower body weight often have less fat and therefore less reserves. Comparison between lambs in a group, and between lambs with different body weights is the best way to judge overall amount of fat.
A clear or yellow fluid in the subcutaneous tissues (edema) of the distal limbs, ears, and tail occurs with increasing prevalence in lambs exposed to cold conditions beginning approximately 4.5 hours after birth. In the experiments performed by Haughey (1973) at temperatures of 1°C, 18°C and 35°C the prevalence of edema was 80% at 1°C, 50% at 18°C and 12.5% at 35°C. in the 1°C and 18°C groups, the prevalence of edema was similar between groups of lambs that had suckled or not suckled. edema was particularly identified in the distal hindlimbs, then tail and then often one forelimb. Edema of the ears and muzzle was uncommon and only in those that were cold and starved. It was surmised that the front limbs were less likely to develop edema because cold lambs preferred to rest in sternal recumbency during which time their front limbs are tucked under their bodies. The tail and hindlimbs remain exposed.
Hemorrhage of the central nervous system
Haemorrhage in the central nervous system, most readily identified in the meninges of the brain, is widely believed to be the result of birth trauma and or hypoxia. The prevalence of haemorrhage varies widely. When Haughey (1973a) reported on vascular abnormalities in the central nervous system he found 70% of all lambs that died in the parturient (during birth or within three hours after birth) and postparturient (more than three hours after birth) periods had some evidence of haemorrhage in the meninges that varied from bloodstained cerebrospinal fluid through to definite subdural haematomas. 93.5% of lambs dying in the postpartum period have evidence of haemorrhage. This prevalence was higher than indicated by others but was the first systematic examination of the nervous system. The type of haemorrhage is reported varied from bloodstained CSF to occasional petechial haemorrhages to outright subdural haematomas.
The lesions of hypoxic/ischemic/metabolic brain injury varies greatly from nothing to subtle edema to congestion of meninges to meningeal haemorrhage and gross brain edema. Likewise the histological lesions can vary in severity and location. When the examination of the brain is done in the perinatal period, the likelihood of underrepresenting this type of injury will be great. If there are no lesions but there is patchy atelectasis (see above) or meconium staining of the coat, this should be suspected. It is likely that many cases will be classified as either starvation, trauma or unknown. One must accept the limitations of autopsy.
It is uncommon to see rib fractures in lambs, whereas they occur relatively commonly in the larger species including calves and foals. when they are present one could consider either an underlying abnormality with bone development (such as osteogenesis imperfecta) or trauma. if the fractures were from birth trauma, one would expect them in large lambs and in particular those above 5 kg in weight. Lambs can also have rib fractures from postnatal trauma such as being crushed or stood on. It is usually only the weak small lambs that are unable to move that are inadvertently crushed by their mothers. Mismothering by one ewe, and injury when a lamb attempts to suckle from a different ewe is possible, as is predation.
Haemorrhage of liver
Because the liver is in the centre of the body, blunt forces are transmitted from either the chest or the abdomen and can result in rupture of the liver capsule. It is possible for this haemorrhage to be birth trauma, but blunt force trauma is also possible. One should always consider the possibility of a combination of trauma and a failure of the coagulation cascade.
There are several different causes of focal hepatitis in lambs. Some are congenital infections and the others are postnatal infections. several greater than 5 mm and often several centimetre circular regions of hepatitis the characteristic findings of Campylobacter and Flexispira infection. these typically are congenital infections. Hundreds of small 1 to 2 mm foci is more typical of Listeria monocytogenes infection.and this is usually a congenital infection also. Postnatal infection from the naval up the umbilical vein into the liver can occur from a wide variety of infectious organisms. This type of spread to the liver may just involve part of the liver and usually the right lobes. Culture of the organ is required for definitive evaluation and is usually only undertaking when there is a flock problem.
There is a large difference in the patterns of autolysis between lambs that are aborted or are stillbirth versus those that are alive and develop gastrointestinal flora. Fetal autolysis has been studied and is covered in the section on examination and control of failure of pregnancy. In summary, however, the presence of bloody fluid in the subcutaneous tissues of the chest and abdomen and the presence of cavity fluid in the chest and abdomen indicates death of a fetus between 36 and 72 hours after death. This should not be confused with anasarca, where in the fluid is clear or slightly straw coloured.autolysis of lamb foetuses after birth and which have an intestinal flora matches autolysis in older animals.
There are three main patterns of pneumonia seen in neonatal lanbs.they include
- cranio ventral fibrinous bronchopneumonia
- diffuse interstitial pneumonia from sepsis
- multifocal or embolic pneumonia, from septicemia
More detail about the lesions and their meanings given below. Mannheimia haemolytic is the common bacteria responsible for fibrinous bronchopneumonia, be be stymie tree loci for multifocal or embolic pneumonia and any agent causing septicaemia or toxaemia will result in a diffuse interstitial pattern.
The official definition of septicemia is a combination of bacteria in the blood (bacteremia) and the systemic reaction and products of bacterial infection (sepsis). Acutely septic lambs may just have a reddening of all their serosal surfaces because of cytokine and other inflammatory products causing widespread vasodilation and increase blood flow through capillaries. There is also often increased permeability of capillaries and venules resulting in oedema with or without an increase in cavity fluid. In particularly severe instances, fibrinogen enters the tissue or the cavity space and results in fibrin deposition. This is most obvious in the lung and on the serosal surfaces of the abdomen and thorax. Joints can also be involved and within the synovial fluid, the presence of flects of fibrin it is a classical and characteristic change.
Colostrum uptake is vital for immunity in lambs. If serum immunoglobilins are lower than normal consider
- ewe mammary disease
- failure of suckling
- diarrhea and small intestinal absorption issues
- iodine excess (over suplimentation of ewe in late gestation) inhibiting uptake.
Anomally is implies incorrect formation of tissues or structures of the body. The word 'congenital' relates to a change present at birth. There are many different processes that can be congenital including infections, metabolic arrangements, nutritional abnormalities as well as anomalies.
A very low number of lambs will develop congenital abnormalities and die at or soon after the time of birth. It is usually only those that are very obvious that are identified; subtle changes or those that do not have a structural basis such as an inability to develop surfactant, mistiming of haemodynamic changes in the birth process and the like will not be identified. these are simply form that group that is known as "idiopathic" or "no diagnosis".
Dennis and Liepold (1968) reported on 21 lambs with congenital hernias. 10 were diaphragmatic, 5 were umbilical, 3 were abdominal, 2 were scrotal, and 2 were perineal. 12 were with other anomalies.
In a large study of lambs with congenital defects (Dennis 1975c), the most common was abnormalities of the jaws. This was followed by atresis ani, arthrogryposis and ventriculus septal defects of the heart. There were 401 malformed lambs representing 10% of those examined
The cause of abnormalities of the jaws or of atresia ani are not known, and are usually regarded as an unfortunate occurrence.
Arthrogryposis, hydranencephaly and cyclopia indicate infection of the lamb early in pregnancy with a neurotrophic virus such as Akabane virus or Cache Valley Fever virus or exposure to a toxin such as cyclopamine, jervine or veratrosine of Veratrum californicum on day 14, are readily recognised
One of the more common congenital abnormalities relate to the formation of the heart. Overriding aorta and septal defects and persistent ductus arteriosus occur.
Myocardial necrosis and mineralisation
Congenital white muscle disease does not occur very frequently, but if the vitamin E and or selenium concentrations in the maternal diet are sufficiently low it is possible for lambs to be born with myocardial necrosis from this. The lesions are typically subendocardial. In those countries where foot and mouth disease virus is found, the lesions of myocarditis are virtually identical to those of myocardial necrosis from vitamin E or selenium deficiency.
Examination of the thyroid gland should be a routine part of any ovine necropsy and this is especially the case with lambs. Photographs of lambs with a thyroid as big as their heads make for high drama but subtle increases in the size of the thyroid gland are only obvious to those who routinely examine and know the size of normal thyroid. lambs with goitre are frequently weak and are unable to thermoregulate, stand and suckle, or avoid trauma.
The diagnosis of anaemia is made when the organs of the body are very pale - much paler than normal. Pallor of the liver is often the most obvious, but once the prospector is experienced, general body pallor becomes easier to identify. Anaemia in lambs is usually from blood loss. This can be from trauma and rupture of a viscus, fractures or other injury. Anaemia also occurs from failure of the coagulation cascade. The lack of a clot in the umbilical vessels, haemorrhage around the umbilical arteries near the bladder, or carcase pallor without an obvious cause all suggest a coagulation problem.
Coagulopathy caused by an environmental toxicosis or of an inherited nature affects groups of lambs. Identifying a cause in a single case is almost impossible. Once a lamb is dead, function tests cannot be done.
Necropsy examination of a lamb should be systematic with a view to examine and identify lesions, and select suitable tissues for further testing. There are areas which may not be routinely examined, but which should have special attention. In particular, the brown fat stores of the pericardial and perirenal areas, the subcutaneous tissues of the distal limbs, the thyroid, and the brain, should be carefully examined.
Starvation is the common term for when lambs use up their fat stores and become increasingly weak and die. Energy balance for a newborn lamb is a highly dynamic situation. The initial energy source is glycogen in the liver, but the exhaustion of this cannot be determined at necropsy. Perirenal and epicardial fat are readily visible and are the main indicators. All lambs must receive nutrients soon after birth, and in the usual circumstance, this is milk from the mother. A lamb of an adequate birthweight with good coordination and a compliant mother that is lactating should receive adequate nutrition to survive and thrive. There are, however, two sides to this energy ledger. On the one side is adequate intake and on the other is energy expenditure.
reasons for an inadequate intake are
- Ewe factors such as
- poor milk production,
- mammary disease,
- mismothering including poor mothering instinct, inexperience, stressful environment, overcrowding,
- presence of predators and
- myriad other factors which influence the behaviour of the ewe and the supply and letdown of milk.
- insect infestation including biting flies, myiasis
- Lamb factors include low birth weight lambs, birth trauma, anaemia, presence of congenital abnormalities and other fetal disease
reasons for increased energy expenditure or loss are
- excessive cold, particularly wet and windy conditions
- excessive movement
The lesions seen in affected lambs are primarily those of metabolism of the brown fat stores of the pericardium, epidcardium and perirenal regions. Those lambs that had no or an inadequate intake have no evidence of abomasal milk and or evidence of uptake of milk with a lack of chyle in the mesenteric lymphatics. There may be other lesions to explain an inadequate intake.
Lambs are either predated or mutilated after death. Most of the ``predators`` are scavengers - animals that will eat dead carcases. They will eat dead lambs or lambs that already have an imminent death from other causes, such as starvation.
An otherwise normal lamb - one without catabolism of fat, and for which no other lesion is found - with evidence of damage from predators is classified as being predated. Post mortem predation is when there is some other cause or indication of preexistent disease.
Predators of neonatal lambs vary in type from locale to locale. Feral pigs, foxes, coyotes, eagles, crows, ravens, ants (Smith 1962, Jordan and Le Feuvre 1989) are implicated. Many of these have a characteristic approach to attacking a lamb. Crows usually peck at the eyes, mouth and tongue, anus and umbilicus. A lamb rendered blind by ants will have keratoconjunctivitis. Foxes kill by crushing the chest from below and then attack the tongue, tail, thighs, lower jaw. Eagles and hawks attack the chest cavity. Domestic dogs are indiscriminate.
Ants swarm over the lamb, but blindness is particulary problematic in lamb survival.
Foxes and other canids
Congenital infection of a lamb is when the lamb is infected en utero and subsequently affected after birth. lens are normally affected before birth, occasionally at the time of birth or in the immediate postpartum period. This is an uncommon event. laboratory investigation of such infections is not routinely performed unless it is obvious from post-mortem examination that many lambs are dying in the preparturient, parturient or immediately perinatal period. Lambs with unexplained causes of death or have lesions implicating a particular infectious agent are those that are usually evaluated.
Classical ovine pathogens that cause failure of pregnancy are usually responsible, and include Coxiella burnetti, Chlamydia abortus, Campylobacter fetus, Toxoplasma gondii, Brucella ovis, Listeria monocytogenies, Border disease virus, and arboviruses such as Cache Valley Virus and Akabane Virus
There are all manner of infectious disease that occurs in the first week of life. They tend to be related to septicemia from umbilical infection, pneumonia and wound infections. The overall prevalence is usually very low unless there is a breakdown in 'hygeine' such as the use of a contaminated multiuse injectable. Additionally, any agent causing failure of pregnancy can cause lamb mortality.
Neonatal diarrhoea is less commonly seen, especially in extensive sheep raising areas. Any lamb with sepsis can also have diarrhoea as part of a systemic response. Diarrhoea causing agents are similar in lambs as they are for other species and includes intestinal colibacillosis and rotaviral infections.
Umbilical infection occurs when the umbilicus is contaminated and bacteria gain access to the vascular system. Many enter the venous system via the umbilical vein, but there is often involvement of the umbilical arteries too. Rarely does infection of the urachus cause problems. Organisms involved are of the environmental types - Escherishia coli, Trueperella (Arcanobacterium) pyogenes, and Staphylococcus aureus. Clostridia can be added to this group too.
The lesions seen are edema and reddening of the soft tissues around the umbilicus. The lesions can be minimal - especially in Clostridium related diseases. There may be a typical umphalophlebitis, pus within the umbilical veins and focal hepatitis. The lesions may just be those of septicemia (above).
The lesions of pneumonia are usually very dramatic. The classical cranioventral distribution with affected lung being solid, having failed to collapse, a red 10 discolouration of the tissue and a coating of fibrin on the pleural surface are the typical changes of Mannheimia haemolytica infection of the lungs. There is usually indications of systemic sepsis with reddening of all serosal windings and occasionally with petechial haemorrhages in the thorax and abdomen. There is often fibrin within fluid in the pleural space.
A diffuse pneumonia caused by Bibersteinia trehalosi has a different appearance. This bacterium is a cause of septicemiaand as such there are systemic lesions including a reddening of all serosal surfaces, increased fluid often with fibrin in body cavities, and in particular particular haemorrhage in multiple organs including the lungs. The lungs may also fail to collapse at have either a multifocal consolidation or, overall, the lungs are heavy, fail to collapse and have abundant oedema. They may be diffusely dark red in colour.
The lesions of septicemia are often subtle. The bacteria involved are those involved in naval ill and wound infection - an entry point is needed. The suspicion of septicemia is made when the dead lamb has no readily identifiable lesions of starvation, dystocia or trauma, or pneumonia. Affected lambs have a diffuse reddening of the carcase and particularly of serosal surfaces and lungs. There may also be a subtle strands of fibrin on serosal surfaces, within joints or on the meninges. The presence of petechial hemorrhages in many organs and expecially the lungs, focal hepatitis and increased cavity fluids may also be present. If the number of lambs affected by sepsis is sufficient, culture of filtering organs and of affected joints, serosal surfaces and meninges should provide the agent. In the majority of cases, identifying the source and changing of management/hygeine will be the aim.
Campylobacter fetus and Campylobacter jejuni cause failure of pregnancy and usually abortion but on occasion can cause perinatal mortality secondary to late term infection of the placenta. The lesions seen include those of sepsis and can include fibrinous polyserositis and hepatitis or focal hepatic necrosis.
Wound/injection site infections
Bacterial infection of wounds ( sites of castration, ear tags, tail docking) does not occur unless the environment is highly contaminated or contaminated instruments are used. The lesions can be very subtle and similar to the lesions seen around the umbilicus. While the range of bacteria is similar to those of naval ill, Clostridial wound infections is the bane of sheep production everywhere. The Clostridium often found is C septicum.Wounds are contaminate with spores of this environmental contaminant and the toxins produced by the bacteria are responsible for death - often the local wound and the systemic lesions are minimal. A slight excess in cavity fluid with some flects of fibrin, a redding of serosal surfaces and prominence of vessels throughout the body are some of the changes. Culture and the appropriate histological lesions of the sites is required for confirmation.
Iatrogenic means human interventionis either completely or partially responsible for the disease and/or death. Over vigourous obstetrical manipulation will result in trauma including fractures and cerebral haemorrhage. Incorrect techniques in tail docking, castration and ear tagging are less obvious than a fracture but are still lethal. Poor injection technique can be missed diagnosed as clostridial wound infection. The injection of contaminated biologicals (often with endotoxin) or overdosing with selenium will produce sufficient endothelial damage to mimic toxaemia and/or septicaemia. If there is a very highly percentage of neonatal mortality with systemic signs of sepsis, investigation of injection dosage and material is warranted.
Rift Valley fever phlebovirus (RVFV)
Rift Valley Fever Phlebovirus (Kingdom: Orthornavirae; Phylum Negarvaviricota; Order Bunyavirales; Family Phenuiviridae; Genus Phlebovirus) is commonly called Rift Valley fever virus, and is the cause of Rift Valley fever in southern Africa, especially the Rift Valley of Kenya but elsewhere in Africa. It is transmitted by mosquitoes, and causes hemorrhagic fever in humans and death of sheep primarily. Adults, lambs and sheep fetuses are affected. In perinatal lambs and neonates, it causes hepatic necrosis - multifocal to panlobular single cell to regional necrosis of hepatocytes. Virus is present in hepatocytes, leading to hepatocyte cell death. It affects the spleen also with necrosis of the red pulp. Petechae and edema of many organs occurs. Lymphocytolysis is prominent, but whether this is the direct effect of virus or due to stress is not clear.
Odendaal L, Davis AS, Fosgate GT, Clift SJ. Lesions and Cellular Tropism of Natural Rift Valley Fever Virus Infection in Young Lambs. Vet Pathol. 2020; 57: 66-81.
Dennis SM (1969) Predators and perinatal mortality of lambs in Western Australia. Aust Vet J 1969, 45: 6-9
Dennis SM (1974) Perinatal lamb mortality in Western Australia. 1. General procedures and result. Aust Vet J 1974, 50: 443-449
Dennis SM (1974) Perinatal lamb mortality in Western Australia. 2. Noninfectious conditions. Aust Vet J 1974, 50: 450-453
Dennis SM (1974) Perinatal lamb mortality in Western Australia. 3. Congenital infections. Aust Vet J 1974, 50: 507-510
Dennis SM (1974) Perinatal lamb mortality in Western Australia. 4. Neonatal infections. Aust Vet J 1974, 50: 450-453
Dennis SM (1975) Perinatal lamb mortality in Western Australia. 5. Vibrionic infection. Aust Vet J 1975, 51: 11-13
Dennis SM (1975) Perinatal lamb mortality in Western Australia. 6. Listeric infection. Aust Vet J 1975, 51: 75-79
Dennis SM (1975) Perinatal lamb mortality in Western Australia. 5. Congenital defects. Aust Vet J 1975, 51: 80-82
Dennis SM, Leipold HW. Congenital hernias in sheep. J Am Vet Med Assoc. 1968 Apr 1;152(7):999-1003.Dutra F, Quintans G, Banchero G (2007) Lesions in the central nervous system associated with perinatal lamb mortality. Aust Vet J 2007, 85: 405-413
MacFarlane D (1965) Perinatal Lamb losses. NZ Vet J 1965, 13: 116-135.
Haughey KG (1973) Vascular abnormalities in the central nervous system associated with perinatal lamb mortality. 1. Pathology. Aust Vet J 1973, 49: 1-8
Haughey KG (1973) Vascular abnormalities in the central nervous system associated with perinatal lamb mortality. 2. Association of the abnormalities with recognised lesions. Aust Vet J 1973, 49: 9-15
Haughey KG (1973) Cold Injury in newborn lambs. Aust Vet J 1973, 49: 555-562
Haughey KG, Hughes KL, Hartley WJ (1967) The occurrence of congenital infections associated with perinatal lamb mortality. Aust Vet J 1967; 43: 413-420
Johnson JS, Laegreid WS, Basaraba RJ, Baker DC (2006) Truncated Gamma-Glutamyl Carboxylase in Rambouillet Sheep Vet Pathol 2006; 43: 430-437.
Johnson JS, Soute BA, Olver CS, Baker DC (2006) Defective gamma glutamyl carboxylase activity and bleeding in Rambouillet Sheep. Vet Pathol 2006; 43: 726-732
Jordan DJ, Le Feuvre AS. (1989) The extent and cause of perinatal lamb mortality in 3 flocks of Merino sheep. Aust Vet J 1989, 66: 198-201
Mellor DJ (1988) Integration of perinatal events, pathophysiological changes and consequences for the newborn lamb. Br Vet J 1988, 144: 552-569
Moule GR (1950) Some problems of sheep breeding in semiarid tropical Queensland. Aust Vet J 1950, : 29-37
Moule GR (1954) Observations on mortality amongst lambs in Queensland. Aust Vet J 1954, : 153-171
Richardson C (1977) Morphological parameters of intra-uterine growth retardation in the newborn lamb. Vet Rec 1977, 101: 151-152
Rook JS, Scholman G, Wing-proctor S, Shea M-E (1990) Diagnosis and control of neonatal losses in sheep. Vet Clinics of Neth America: Food Anim Pract. Advances in Sheep and Goat Medicine 1990, 6: 531-562
Smith ID (1962) Reproductive wastage in a merino flock in central western Queensland. Aust Vet J 1962, : 500-507
|Whole body||Low birth weight (<3kg)||poor ewe nutrition, placentitis|
|High birth weight (>5 kg)||High/excessive ewe nutrition|
|Various anomalies||teratogenic plants, infections, hereditary, etc|
|Chewed on, eyes missing, with hemorrhage||predation|
|Swelling of head||Edema||Dystocia, fetomaternal disproportion.|
|Feet||Eponychium present||too weak to stand|
|anemia, hemorrhage||exposure to anticoagulants|
|Perineum||diarrhea||Infectious disease - viral, bacterial|
Edema of head and or limbs, meconium staining
|Dystocia, high birth weight|
|Edema and haemorrhage of distal limbs||frostbite|
|Edema and hemorrhage||Trauma|
|High birth weight|
|Umbilical hyperemia and edema||umbilical infection|
|Skeletal muscle||White colour with white streaks||White muscle disease|
|Bones and joints||Anomalies||anomalies|
|Tongue, esophagus||ulcers||Bibersteinia trehalosi|
|hemorrhage, infarcts||Bibersteinia trehalosi|
|Heart||Mineralization||White muscle disease, foot and mouth disease.|
|Many including over-riding aorta and septal defects||Anomalies|
|Multifocal necrosis or abscesses||
Many bacteria, including Staphlococcus, Listeria, Campylobacter.
|Fat stores||reduced stores||Ewe nutrition, placental abnormality (see low birth weight)|
|catabolised||starvation, extreme weather|
|Brain||hemorrhage, especially medulla oblongata and cervical spinal cord.||Birth trauma, high birth weight|
|anomalies||viral infections, toxicosis, heritable trait etc|
|oedema, periventricular leukomalacia, or lamina necrosis||Birth hypoxia, high birth weight|
|Abomasum||empty||starvation, ewe milk production, mismothering|
|Legs||subcutaneous edema and hemorrhage||frostbite!|