Etiology

Infectious endometritis is a major cause of infertility and early pregnancy loss^* and is estimated to affect 25% to 40% of broodmares.¹⁰⁹ These infections become established when normal defense mechanisms fail to clear potentially pathogenic organisms after they are introduced into the uterus.²⁸² The most common sources of uterine contamination include coitus, parturition, artificial insemination, and aseptic genital examination and manipulation.^149,381,385 Age, parity, number of barren years, and uterine biopsy grade influence likelihood of persistence of infection.^76,333

The organisms most frequently isolated from mares with endometritis are Streptococcus equi subsp. zooepidemicus, Escherichia coli, Pseudomonas aeruginosa, and Klebsiella pneumoniae.^149,356,385 Infections caused by P. aeruginosa or K. pneumoniae are often considered venereal diseases because the organisms are often introduced during coitus, insemination with infected semen, or genital manipulations. K. pneumoniae capsule types 1, 2, and 5 are highly pathogenic.³⁰⁷

Commensal bacteria such as Actinomyces pyogenes, Proteus spp., and Staphylococcus spp. are occasionally isolated from mares with endometritis. They are considered likely to be the causative organisms of endometritis if the diagnosis is supported by cytologic or histopathologic evidence of concurrent inflammation. Alpha-hemolytic Streptococcus, Enterobacter spp., and Staphylococcus epidermidis are rarely causes of equine endometritis and should be considered simple contaminants.⁷⁹ Corynebacterium spp. and anaerobic bacteria such as Bacteroides fragilis may occasionally cause endometritis in horses.⁶ Anaerobes are most often isolated from postpartum and foal-heat samples.³³⁵ Taylorella equigenitalis is the causative agent of a highly contagious venereal metritis, contagious equine metritis (CEM) (see Chapter 41).

The pathogenicity of bacteria depends on their ability to adhere to the endometrium, preventing their removal by normal uterine clearance mechanisms. Adhesive proprieties of S. equi subsp. zooepidemicus are probably mediated by fibronectin-binding proteins and hyaluronic acid capsule.^{130,199,232,433} Attachment of K. pneumoniae to endometrial cells is facilitated by pili and capsule.¹²⁹ Persistent colonization by P. aeruginosa is assisted by the secretion of an adhesive matrix that forms a biofilm.²⁹¹ These biochemical proprieties also are important in resistance of bacteria to opsonization, phagocytosis, and the action of antimicrobials.^{96,113,284,433} Resistance to phagocytosis is often observed with S. equi subsp. zooepidemicus and K. pneumoniae and is probably mediated by antigenic variation, antiphagocytic M-like proteins, hyaluronic acid capsule, or polysaccharide and Fc receptors.^113,433 Bacterial toxins promote deterioration of complement and exacerbate uterine inflammation.²⁴³

Candida spp. and Aspergillus are the most common fungal organisms isolated from the uterus of mares with endometritis.³⁸⁵ The incidence of fungal infection in mares with endometritis is estimated to vary between 0.1% and 5%.^{99,100,120,318,444} Fungal organisms isolated from the equine uterus include Aspergillus spp., several Candida spp., Cryptococcus neoformans, Fusarium spp., Hansenula anomala, Hansenula polymorpha, several Rhodotorula spp., Scedosporium apiospermum, Saccharomyces cerevisiae, Trichosporon beigelii, and Torulopsis candida.^*

Prolonged antibiotic therapy may be a predisposing factor for yeast overgrowth.⁴⁴⁴ The use of antibiotic-containing semen extenders for artificial insemination may be partially responsible for the apparent increase in the number of mares with fungal endometritis (J. Aurich, personal communication). Transmission of fungal organisms from stallions has not been demonstrated, although fungi have been cultured from the urethra (Mucor spp.), fresh semen (Absidia spp.), and extended semen (Candida spp.) of stallions.²⁵²

Mycoplasma spp. have been isolated from the external genitalia and semen of clinically normal and infertile stallions, but their exact role in uterine infection is not well established.^273,367,448 In vitro, Mycoplasma equigenitalium produces a consistent cytopathic effect on the ciliated epithelium of the oviduct, with variable severity depending on strain.³¹ M. equigenitalium, M. subdolum, and Acholeplasma spp. are associated with infertility, endometritis, vulvitis, and abortion in mares and with reduced fertility and balanoposthitis in stallions.^{167,201,203,273} M. equigenitalium and M. subdolum were isolated from the genital tract of mares (5%-34%) and aborted equine fetuses (7%); however, the presence of mycoplasmas is not always correlated with reduced fertility.^{30,167,201,203,273}

Pathogenesis

Physical Barriers.

The uterine cavity is protected from ascending infection by several anatomic structures.²³⁷ The first line of defense is provided by the seal of the normal vulvar labia. Evaluation of vulvar and perineal conformation should be included in all prebreeding examinations or evaluations for infertility. The vulva should be in a vertical position aligned with the anal opening (Fig. 8-1, A). The labia should be tight, with most of its length below the tuber ischii. The vulvar lips may become parted as a consequence of malformation caused by previous traumatic injuries or lesions (Fig. 8-1, B). In older multiparous mares, there is a tendency for extreme relaxation of the vulvar lips, particularly during estrus, as well as tilting of the dorsal aspect of the vulva caused by relaxation of the perineal body. In this situation the vulva becomes horizontal as it is pulled cranially over the tuber ischii (Fig. 8-1, C). These anatomic changes predispose the mare to pneumovagina (windsucking) and pneumouterus, ultimately causing urine to pool in the cranial vagina and contaminate the uterus when the cervix is open. Contamination with fecal material adds to the increased risk of infection.

Fig. 8-1 A, Normal conformation of vulva in the mare. B, Abnormal conformation with parting of vulvar lips at dorsal commissure. C, Abnormal conformation with tilting of vulvar lips.

The second physical barrier in the prevention of contamination of the vagina and eventually the uterus is the vestibulovaginal sphincter. In a normal mare the vestibulovaginal area remains sealed even when the vulvar labia are parted. Compromised vestibulovaginal sphincter function is suspected when air is sucked into the vagina or if the examiner is able to visualize the vaginal cavity directly after parting the vulvar lips. The vestibulovaginal sphincter may become compromised secondary to rectovaginal tears and other foaling injuries.

The third important anatomic barrier to infection is the cervix. The cervix is open during estrus, late gestation, and in the immediate postpartum period. However, compromised cervical function is observed in some mares, and this entity may remain open during anestrus and even diestrus. The most common cause of cervical incompetence is a cervical lesion consequent to dystocia.

A plan for treatment and prevention of uterine infection should include a plan to reestablish normal barrier function. Surgical procedures such as episioplasty, vestibulovaginoplasty, and rectovaginal tear repair should be considered if indicated.

Diagnosis

Uterine infection may be suspected on the basis of a history of infertility, recurrent endometritis, mucopurulent vaginal discharge, predisposing anatomic features, early embryonic loss, or observation of fluid accumulation on examination of the uterus by ultrasonography. Clinical signs may include vaginal discharge. Confirmation of the diagnosis of uterine infection requires endometrial cytology and uterine culture. Uterine biopsy may be helpful in some cases.

Accumulation of large quantities of fluid during estrus or postbreeding is a good indication of mare susceptibility to endometritis (Fig. 8-2). Resistant mares eliminate mating-induced endometritis within 6 to 12 hours after breeding, whereas susceptible mares may retain variable amounts of fluid for several days. Accumulation of fluid in the uterus is associated with decreased pregnancy rates. All mares should be evaluated 24 hours after breeding and treated if a pocket of fluid remains within the uterine cavity.^{25,255,278,320} Mares with a history of infertility or that are known to be susceptible to endometritis should be evaluated or treated as early as 6 hours after breeding.³⁹²

Fig. 8-2 Persistent mating-induced endometritis (PMIE). A, C, and D, Ultrasonograms of uterus at 6, 12, and 18 hours after insemination, respectively. B, Corpus hemorrhagicum. E and F, Uterus after initiation of oxytocin therapy.

Several methods for collection of uterine cytology samples have been described. These include the use of double-guarded swabs, uterine cytology brushes, and low-volume uterine flushes.⁷⁴ In the authors’ opinion, uterine cytology brushes and small-volume uterine flushes provide the best specimens for endometrial cytology (Fig. 8-3). Swabs are often reliable if there is fluid in the uterus or if the swab is wetted with a sterile saline solution before sampling.

Fig. 8-3 Top, Single-guarded uterine swab with “pop-out” cap that can be used to collect material of endometrial cytology. Middle, Double-guarded swab for endometrial culture and cytology. Bottom, Double-guarded endometrial brush for cytology.

Interpretation of uterine cytology samples may be confusing because of the lack of standardized methodology for evaluation. The most common staining technique for uterine cytologic specimens is a rapid Wright-Giemsa stain (Diff-Quik). Interpretation is based on evaluation of the type of cells and organisms observed^74,75 (Fig. 8-4). Quantitative methods for the interpretation of equine endometrial cytology have been reviewed recently.⁷⁴ Diagnosis of endometritis may be based on the number of neutrophils per number of high-power microscopic fields, as a ratio of neutrophils to epithelial cells, or as a percentage of all cells. Endometrial cytology may provide an important clue to fungal infection. Cytology may be negative if infection is recent.¹⁰⁰

Fig. 8-4 Endometrial cytology stained with Diff-Quik. A, Normal endometrial cells. B, Slight inflammatory reaction. C, Mating-induced inflammation (note sperm cells). D, Severe infectious inflammation.

Endometrial swabs should always be submitted for anaerobic and aerobic bacterial as well as fungal culture. Blood agar plating may be used in the initial fungal culture, but specific culture techniques are required for more precise diagnosis.¹⁰⁰

Endometrial biopsy is an important and highly accurate method for the diagnosis of uterine inflammation. Special staining techniques, such as Gomori’s methamine silver, are particularly helpful for the diagnosis of fungal endometritis.¹⁴⁰

Interpretation of diagnostic results may be challenging at times. Bacteriologic culture and cytology from endometrial biopsy are most accurate (high sensitivity and positive predictive value) for diagnosis of endometritis. The sensitivity of bacteriologic culture from endometrial biopsy is 82%; diagnosis based on cytologic and bacteriologic examination of endometrial swabs has a sensitivity of 77% and 34%, respectively.²⁷⁹

Therapy

Treatment of equine endometritis may include local or systemic antimicrobial therapy, uterine lavage, plasma infusions, and colostrum infusion. Most treatment recommendations are made on the basis of clinical experience, with limited evidence for comparative efficacy within the veterinary literature. The authors most frequently recommend treatment of uterine infections with uterine lavage to remove debris and other products of inflammation that may reduce antimicrobial activity, followed by antimicrobial therapy for 5 to 7 days.

Prevention

Prevention of uterine infection is accomplished by decreasing the likelihood of contamination and by early recognition and treatment of PMIE. Contamination of the uterus can be prevented by correcting vulvar conformation and observing strict hygiene during breeding and genital manipulation. Susceptible mares should be monitored before breeding and bred using minimum-contamination breeding technique.¹⁹⁵ The purpose of this monitoring is to reduce the chance of contamination of the uterus by bacteria and to eliminate the products of the inflammatory reaction caused by semen.

The primary mechanism for prevention of fluid accumulation in the uterus is contraction of the uterine musculature in response to oxytocin. Oxytocin release is observed in mares after mating, teasing, genital manipulation, and infusion of fluid into the uterine cavity.^73,281,369 Oxytocin injection improves uterine defense by promoting uterine fluid evacuation.^{11,218,227,320} Administration of 20 IU of oxytocin intramuscularly (IM) induces uterine contraction for up to 90 minutes.²⁴⁶ Oxytocin administration to mares susceptible to PMIE at 4 hours after breeding aids in the elimination of excess fluid and improves fertility.^25,320,336 The standard dose for an average mare is 10 IU intravenously (IV) or 20 to 25 IU IM. ^{70–72,246,320,392} Large doses may decrease uterine contractions.^72,246 Oxytocin therapy may be repeated every 6 hours for 24 to 48 hours after breeding.^278,392 A 7% increase in pregnancy rate is reported with a single injection of oxytocin (25 IU IM) within 72 hours of breeding.³²⁰ Oxytocin does not interfere with ovulation or gamete transport if administered no earlier than 4 hours after breeding.^55,278

Prebreeding and postbreeding uterine lavage may be indicated in mares that tend to accumulate a substantial amount of fluid during estrus.^57,59,60,407

Prostaglandin F_2α (PGF_2α; 5-10 mg IM) or its analog, cloprostenol (250 μg IM), is recommended for the treatment of mares with PMIE because of their ecbolic proprieties.^{55,220,278,396} Cloprostenol induces weaker but more sustained uterine contractions than oxytocin and is helpful when excessive uterine edema is present.⁹³ Repeated administration of cloprostenol should be avoided because it has been associated with transient reduction of circulating progesterone levels during diestrus.^55,278

Prophylactic in utero administration of antibiotics to PMIE-susceptible mare after breeding has been suggested. A combination of oxytocin treatment and intrauterine infusion of broad-spectrum antibiotics increases pregnancy rates in susceptible mares.^4,320 However, such an approach may pose some risk of development of antimicrobial resistance.

Ascendant Placentitis

Ascending placentitis is the most common type of placentitis in horses.^306,316,445 Bacteria isolated from the placenta are comparable to those isolated from the uterus of mares with endometritis.^175,331,445 Streptococcus equi subsp. zooepidemicus, E. coli, Pseudomonas aeruginosa, Enterobacter spp. and Klebsiella pneumoniae are the most frequent isolates.^{89,175,316,375,431}

In a retrospective study of 954 cases of equine abortion, placentitis was recognized in 24.7% of all submissions.¹⁷⁸ A bacterial or fungal organism was isolated in 68.6% of placentitis cases, and 57.4% of cases yielded bacteria both from the placenta and the fetal organs. The most common microorganisms isolated include S. equi subsp. zooepidemicus, E. coli, Leptospira spp., nocardioform Actinomyces, P. aeruginosa, Streptococcus equisimilis, Enterobacter agglomerans, K. pneumoniae, α–hemolytic streptococci, Staphylococcus aureus, and Actinobacillus spp.^101,134 Other bacteria isolated include Proteus mirabilis, Citrobacter diversus, and fecal and environmental contaminants.¹⁷⁸ Abortions resulting from hematogenous infection with Actinobacillus equuli⁴²⁵ and Corynebacterium pseudotuberculosis have been reported.^145,308

There is a wide geographic variation in the frequency of specific bacterial and fungal isolates associated with equine placentitis and abortion. A high incidence of fungal placentitis is reported in England.⁴³¹ The incidence of mycotic placentitis varies from region to region because of climate and other environmental factors.^306,430 Emphysematous placentitis caused by clostridial infection was one of the top four causes of bacterial abortion in an early study.³¹⁶ There are numerous reports of Enterobacter agglomerans placentitis in horses.^* The importance of anaerobic bacteria, Mycoplasma spp., Chlamydia, and rickettsial organisms in equine placentitis is uncertain.^108,319,335

Except for placentitis caused by Leptospira spp. or the nocardioform actinomycetes, most equine placentitis occurs in two forms: (1) acute diffuse placentitis with infiltration of neutrophils in the intervillous spaces or (2) focal necrosis of the chorionic villi. Placentitis from abortions before midgestation are chronic, focal, or focally extensive at the cervical area and characterized by necrosis of chorionic villi, presence of eosinophilic material on the chorion, and infiltration of mononuclear inflammatory cells in the intervillous spaces, stroma of villi, chorion, allantois, and vascular layer. Lesions may be either acute or chronic.¹⁷⁸

Bacterial placentitis most often induces abortion between 6 and 9 months of gestation. Placentitis resulting from E. coli tends to cause later abortion and more stillbirths. Placentitis from S. equi subsp. zooepidemicus tends to be acute and focal or diffuse. In acute bacterial placentitis the fetus is generally expelled before 8 months of pregnancy. Acute or diffuse placentitis may not be easy to recognize on gross examination of the placenta. Histologic evaluation of the allantochorion may reveal bacterial emboli with necrosis of chorionic villi or infiltration of neutrophils in the intervillous space. Chronic or focal placentitis typically results in birth of premature or weak foals or late-term abortions. Lesions tend to be located at the cervical star, where discoloration and thickening are observed (Fig. 8-6).

Fig. 8-6 Placenta showing severe ascendant placentitis. A, Allantoic surface. B, Chorionic surface.

Escherichia coli placentitis is usually acute in mares that abort before 7 months of gestation but is more likely to be chronic and focally extensive, involving the cervical star, in mares that abort after 9 months of gestation. Placental edema and the presence of a white mucoid exudate on the chorion and fetal surface are common findings after abortion caused by E. coli placentitis (Fig. 8-7).

Fig. 8-7 Escherichia coli abortion. White mucoid exudate on fetal head surface.

Pseudomonas aeruginosa placentitis causes abortion between 6 and 9 months of gestation. It is usually acute and may be either focal or diffuse with a thickened and discolored cervical star. Histologically, the primary abnormality is ulceration of the chorion with infiltration of neutrophils in the villi, chorionic stroma, and vascular layer.

Lesions caused by infection with Streptococcus equisimilis are similar to those of S. equi subsp. zooepidimicus. Abortion occurs between 6 and 8 months of pregnancy.

Gross and histologic features of mycotic placentitis were described in detail by Hong et al.¹⁷⁸ Mycotic placentitis and abortion are most likely to occur in the late gestational period. Fungal organisms associated with equine abortion include Aspergillus spp.,^{121,145,177,303} mucoraceous fungi, Histoplasma caspulatum,^{153,345,373,374,445} Candida spp.,^249,355,445 Mucor spp.,¹⁴⁵ Coccidioides spp.,^215,250,371 and Cryptococcus neoformans.^34,300,341

Focally extensive placentitis is usually observed at the cervical star and adjacent area as a thick, leathery area. Histologically, except for histoplasmosis and candidiasis, the fungi induce a chronic, extensive placentitis characterized by extensive necrosis of the chorionic villi, neovascularization in the chorionic stroma, infiltration of neutrophils, mononuclear cells, or mixed inflammatory cells in the villi and chorionic stroma, and presence of fungal hyphae in the necrotic debris. Adenomatous hyperplasia with or without squamous metaplasia of the chorionic epithelium are frequently observed.¹⁷⁸ Histoplasma capsulatum caused a multifocal granulomatous placentitis and abortion in one mare in the seventh month of gestation and three mares in the tenth month. Four newborn foals died from severe granulomatous pneumonia within a few days of birth, and a weanling Thoroughbred developed granulomatous pneumonia and lymphadenitis at 5 months of age.³³⁰

With Candida spp. infection, placentitis is generally diffuse, necrotizing, and proliferative with extracellular, yeastlike spores in the chorionic epithelium. Chronic, focally extensive placentitis is most common, with expulsion of foals late in gestation.¹⁷⁸

Hematogenous Multifocal or Diffuse Placentitis

Multifocal or diffuse placentitis is less common than acute, focal placentitis and is usually a result of hematogenous spread of microorganisms to the uterus. This occurs with leptospirosis, salmonellosis, histoplasmosis, and candidiasis. A special focal mucoid form of placentitis, nocardioform placentitis, is emerging as common in several U.S. regions.¹⁷⁸

Leptospira spp. Placentitis

Leptospira spp. placentitis is characterized by diffuse lesions secondary to hematogenous spread (see Chapter 34). Leptospirosis as a cause of placentitis seems to be more frequently diagnosed in Kentucky^{115,116,178,445} than in other regions of the world,^411,431 probably because of specific regional characteristics and the difficulty in isolating or detecting the pathogen. An outbreak of leptospiral abortions has been described on a Thoroughbred farm in California after a flood.¹⁹⁸

Most leptospiral abortions occur between 6 and 9 months of gestation. The affected placenta is thick, heavy, edematous, hemorrhagic, and occasionally covered with a brown mucoid material on the chorionic surface. Occasionally the affected placenta lacks detectable gross lesions. Green discoloration or cystic adenomatous hyperplasia of the allantois is observed in some cases. Fetal antibody against Leptospira spp. may be detected in foals by microagglutination test.¹⁷⁸ Spirochetes are present in large number in the placental sections. Several species of leptospire have been isolated from aborted equine fetuses (e.g., L. pomona, L. grippotyphosa, L. interrogans serovars bratislava and pomona type kennewicki, serovar harjo type hardjoprajitno).^* High-titer agglutinating antibody (>1:6400) may be observed in mares, but interpretation of serologic tests remain difficult without confirmation of infection by culture and isolation. Antibiotic treatment for 5 days (penicillin G) has been reported to help prevent abortion during an outbreak.¹⁹⁸

Nocardioform Placentitis

Nocardioform placentitis is a distinct type of equine placentitis first described in the United States in the late 1980s. Over the past 15 years an increasing number of cases of equine nocardioform placentitis have been diagnosed in Kentucky.^{117,153,177,445}

Nocardioform actinomycetes induce a chronic placentitis that results in late-term abortion, stillbirth, or premature birth. The lesion is an extensive and severe exudative, mucopurulent, and necrotizing placentitis centered on the junction of the placental body and horns rather than the cervical pole.¹⁷⁸ Infection of the placenta is generally thought to be a sequela of the hematogenous spread of the microorganisms from a primary port of entry.^117,413 The fetus is often severely underdeveloped, with no remarkable gross or histologic lesions. The placental lesion is focally extensive (15-30 cm) and frequently located at the base of the uterine horns or at the junction between the body and horns of the placenta. The affected area is thickened, and its chorionic surface is covered with brown, necrotic, mucopurulent exudate and dotted with white or yellow granular structures. Underneath this mucoid material, the chorionic surface is reddish white, mottled, and roughened. Villous necrosis and adenomatous hyperplasia of the allantoic epithelium and hyperplasia with or without squamous metaplasia of the chorionic epithelium are frequently observed.^78,178

Various groups of gram-positive, filamentous, branching bacteria have been implicated as etiologic agents in mares with nocardioform placentitis, including Nocardia spp., Rhodococcus rubropertinctus, and Amycolatopsis spp.^{49,124,177,413} However, most severe infections of this type are caused by the actinomycete Crossiella equi.¹¹⁸

A nocardioform isolate from equine placental lesions in the United States was determined by phylogenetic analysis to be closely related to Crossiella cryophila, a member of the genus Crossiella described in 2001.²¹⁷ Subsequent polyphasic identification found that the isolates represent a new species of Crossiella, for which the name C. equi was proposed.¹¹⁸ Polyphasic taxonomic studies on actinomycete strains isolated from equine placentas from horses in Kentucky and southern United States indicate that the isolates are members of the genus Amycolatopsis. It is proposed that these strains be classified as three novel species of the genus Amycolatopsis and named Amycolatopsis kentuckyensis, Amycolatopsis lexingtonensis, and Amycolatopsis pretoriensis.²¹³

During the 2002 and 2003 foaling seasons, Cellulosimicrobium (Cellumonas) cellulans (formerly Oerskovia xanthineolytica) was isolated from fetal tissues or placentas from cases of equine abortion, premature birth, and term pregnancies in Kentucky. Significant pathologic findings included chronic placentitis and pyogranulomatous pneumonia. In addition, microscopic and macroscopic alterations in the allantochorion from four of seven cases of placentitis were similar to those caused by Crossiella equi and other nocardioform bacteria.⁴⁸

Pathogenesis and Diagnosis of Placentitis

Because of the importance of placentitis in the pathogenesis of bacterial abortion, researchers at the University of Florida developed models for study of ascendant placentitis to gain insight into the pathogenesis of disease and provide a method to optimize diagnostic and treatment recommendations.^{225,226,244,262,368} Bacterial infection of the chorioallantois induces an increase in expression of proinflammatory cytokines (IL-6 and IL-8) in placental tissue. Subsequent release of PGE₂ and PGF_2α into the allantoic fluid leads to premature delivery.^223,226,262 The premature delivery of the fetus is most likely caused by acceleration of the fetal maturation process induced by changes in placental function. The resulting endocrine changes lead to increased uterine contractures and intrauterine pressure, causing dilation and induction of labor. A premature increase in maternal plasma progestins may be an indication of accelerated fetal maturation or fetal stress. Foals may survive if they are near term (>305 days).^225,286,287

Clinically, placentitis is suspected in mares with premature udder development or lactation and vaginal discharge. However, most mares with placentitis do not show any outward signs of infection.^225,445

Placentitis may be diagnosed by transrectal and transabdominal ultrasound examination.^66,402,445 Measurement of the combined thickness of the uterus and placenta (CTUP) by transrectal ultrasonography is particularly helpful in the diagnosis and monitoring of ascendant placentitis.^{193, 327–329,390,394,400} The measurements are obtained 2.5 to 5 cm cranial to the cervical-placental junction using a 5- or 7.5-mHz linear transducer. The area measured should be on the ventral aspect of the uterine body just above the middle branch of the uterine artery (Fig. 8-8). Normal CTUP for light horses is less than 8 mm between 271 and 300 days of gestation, less than 10 mm between 301 and 330 days of gestation, and less than 12 mm from 330 days of gestation to term.^{26,193,327,328,394} These measurements are slightly higher in Warmblood and Draft horses and lower in ponies.^26,66,193 Placental malfunction has been associated with CTUP of greater than 15 mm in horses and greater than 12 mm in ponies after 310 days of gestation.^66,225

Fig. 8-8 Ultrasonogram showing area of measurement of combined uteroplacental thickness. A, Normal. B, Slightly thickened.

During ultrasonographic evaluation, other features of infectious placentitis may be identified. These include placental separation and accumulation of purulent hyperechoic heterogenous fluid between the endometrium and the placenta and increased echogenicity of fetal fluid. Increased echogenicity of fetal fluid is caused by meconium, inflammatory debris, and hemorrhage.²²⁵

Endocrinologic evaluation may also help in determining placental pathology and risk for abortion. The most important hormones evaluated are progestins, which are relatively stable during a normal pregnancy. A change in serum progestin concentration (increase or decrease) by more than 50% or a value that is constantly out of reference laboratory range signals placental pathology or fetal stress.^225,288

After abortion or premature birth, most cases of chronic placentitis are easily recognized on gross examination, but microscopic histologic examination is important to determine the presence of acute placentitis³⁵⁹ (Fig. 8-9). In acute placentitis the infection may be contained within the placenta, and the fetus is usually sterile. Some foals may be born alive with neonatal septicemia.³⁵⁹

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