History
A 1-day-old female Quarter Horse was retrieved still alive from a flash-flooded area in a farm in north Georgia during the summer of 2008. Physical examination of the foal revealed weakness and marked hypothermia. Supportive treatment consisting of plasma transfusion and IV fluid therapy was quickly initiated, but the foal died 5 hours after being rescued. The carcass was submitted for necropsy.
Clinical and Gross Findings
Grossly, the abdominal cavity contained moderate amounts of serous, cloudy, yellow fluid. The kidneys were bilaterally swollen and diffusely dark red and contained multiple, pale, 1- to 2-mm, slightly depressed foci distributed throughout the capsular and cut surfaces (Figure 1). In addition, there was diffuse bilateral adrenocortical hemorrhage as well as multiple areas of hemorrhage on the epicardium and tracheal mucosa. The lungs were diffusely swollen and dark red, and copious amounts of fluid oozed out from the parenchyma on the cut surface (edema). The stomach contained small amounts of curdled milk. No other gross changes were noted, and fresh samples of kidney tissue were submitted for aerobic bacterial culture.
Photograph of transverse section of a kidney of a 1-day-old female foal that had weakness and hypothermia after retrieval from a flash-flooded area. The foal died 5 hours after rescue. In the renal cortex, there are multifocal to coalescing, well-demarcated, pale, slightly depressed, and soft areas that correspond to foci of necrosis and suppurative inflammation (arrows).
Citation: Journal of the American Veterinary Medical Association 247, 5; 10.2460/javma.247.5.493
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →
Histopathologic and Laboratory Findings
Histologic findings included disseminated, vascular-associated suppurative foci in multiple organs. Renal changes were bilateral and consisted of multifocal accumulations of neutrophils admixed with fibrin and colonies of coccobacilli that could be observed within glomerular or interstitial vessels throughout the cortex and less often the medulla (Figure 2). Multifocally, the lumina of midsized interstitial vessels contained numerous neutrophils and colonies of gram-negative coccobacilli with occasional areas of thrombosis. In addition, coalescing suppurative foci had expanded the interstitial spaces where they were admixed with necrotic tubular debris and extensive areas of edema and hemorrhage. These coalescing foci represented areas of glomerular replacement by inflammatory infiltrates that extended to the adjacent renal tissue. The perivascular spaces and renal capsule of each kidney were markedly expanded by edema and scattered neutrophils. In addition to the renal changes, there was bilateral adrenocortical hemorrhage associated with multiple, well-demarcated necrotic foci (containing moderate numbers of neutrophils and colonies of coccobacilli) and areas of vascular thrombosis with occasional bacterial emboli. Similar changes were observed throughout the hepatic parenchyma and pulmonary alveolar septa. Aerobic bacterial culture of fresh samples of kidney tissue yielded heavy growth of Actinobacillus equuli.
Photomicrograph of a section of kidney tissue obtained from the foal in Figure 1. In the main image, the central area represents a disrupted glomerular tuft that has been effaced by large numbers of neutrophils admixed with hemorrhage and necrotic debris (center), degenerating tubules (arrow), and numerous peripheral colonies of bacteria (arrowheads). H&E stain; bar = 100 μm. Inset—Image of glomerular accumulation of numerous gram-negative coccobacilli (arrow). Gram special stain (Lillie Twort); bar = 100 μm.
Citation: Journal of the American Veterinary Medical Association 247, 5; 10.2460/javma.247.5.493
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: multifocal, embolic, suppurative, and necrotizing glomerulonephritis; interstitial pneumonia; hepatitis; and adrenalitis, with vascular thrombosis and intralesional colonies of gram-negative coccobacilli.
Case summary: A equuli septicemia in a neonatal foal.
Comments
Gross and histologic findings in the foal of the present report were typical of bacterial neonatal septicemia, and the etiologic diagnosis was confirmed when aerobic bacterial culture of fresh samples of kidney tissue yielded A equuli. Actinobacillus equuli are gram-negative bacilli or coccobacilli (generally considered opportunistic bacteria) that rarely cause localized disease in adult horses but that have been frequently associated with equine neonatal septicemia and death.1–7 Clinical signs of localized disease in adult horses may include pleuropneumonia, peritonitis, endocarditis, arthritis, orchitis, septicemia, and abortion.8–11 Actinobacillus equuli may be isolated from the digestive and reproductive tracts of healthy horses, evidence of its low pathogenicity for adult, immunocompetent animals.4,9,11 In contrast, septicemia is a major cause of death in neonatal foals2,12 such as the one of this report. Fatal neonatal infections may be acquired by the transplacental route, during parturition, after postpartum contact with the dam, or following environmental contamination.9
Major risks or predisposing factors associated with neonatal infection and septicemia include partial or complete failure of passive transfer, poor condition of the dam, alterations in gestational duration, perinatal stress, poor sanitary or environmental conditions, improper umbilical care, and presence of coinfections.6,9 Although the primary site of infection may remain undetermined for most foals with neonatal septicemia, the gastrointestinal and respiratory systems are usually considered as the most likely portals of entry for bacterial contamination.2 The umbilicus has been reported as a common primary focus of infection in cases of neonatal septicemia by some authors,13 but the septicemic process can occur as a result of infections originating elsewhere in the body.2 However, the incidence of omphalophlebitis among foals with neonatal septicemia may be underestimated; given that an affected umbilicus may appear normal during clinical or gross examination, there is the possibility that omphalophlebitis may remain undetected as the primary cause for septicemia.3 Other common bacteria involved in cases of neonatal septicemia in foals include Escherichia coli, Klebsiella spp, Enterococcus spp, Streptococcus spp, and Staphylococcus spp.2,6,12 Some authors report a predilection for younger foals (mean age, 1.3 days) to develop septicemia due to A equuli infection, in contrast to foals with septicemia due to other bacterial infections (mean age, 3.2 days).3
Clinically, foals with neonatal septicemia may develop minimal or nonspecific signs that can make a definitive diagnostic determination difficult.12 Affected foals may have signs of depression, anorexia, inability to stand, and recumbency. These signs may be progressive and lead to severe dehydration and hypoglycemia.2,6,9,11 By the time septicemia is established, most foals develop sudden onset of fever, colic, diarrhea, joint swelling, uveitis, and systemic deterioration reflected by tachycardia, weak pulse, cyanosis, and death.2,6,7
Necropsy findings are also variable in foals with neonatal septicemia. Foals that die suddenly usually have developed no gross lesions. However, those that survive for a few days may have multifocal pale areas that represent foci of embolic suppurative inflammation in several organs, including the kidneys, lungs, and liver as well as fibrinosuppurative meningitis, pleuritis, peritonitis, osteomyelitis, polyarthritis, or pneumonia and multifocal areas of hemorrhages throughout the body cavities.2,4 Suppurative embolic glomerulonephritis such as observed in the foal of this report is one of the most common gross findings in septicemic foals infected with A equuli.4 Similar to what was observed in this foal, histologic findings are characterized by disseminated foci of necrosis and suppurative inflammation associated with bacterial emboli and vascular thrombosis within several organs, most notably in the glomerular capillary tufts.4
Treatment is usually ineffective in cases of neonatal septicemia because many of the affected foals die within a short period following infection.2 Supportive care including broad-spectrum antimicrobial treatment may be effective if the condition is diagnosed at an early stage. Bacteriologic culture of blood samples may be performed to determine the type of bacterial agent and its antimicrobial susceptibility, and treatment can be altered when antimicrobial susceptibility data become available.2,6
The gross and histologic findings in the foal of this report were characteristic of equine neonatal septicemia.1–7 The diagnosis was confirmed by the identification of A equuli in fresh samples of kidney tissue.
References
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