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Related Concept Videos

Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the exudate's...

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Bovine Mammary Gland Biopsy Techniques
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Published on: December 23, 2018

Malignant edema in postpartum dairy cattle.

Jenee S Odani1, Patricia C Blanchard, John M Adaska

  • 1California Animal Health and Food Safety Laboratory System, University of California Davis, San Bernardino, CA 92408, USA.

Journal of Veterinary Diagnostic Investigation : Official Publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
|November 11, 2009
PubMed
Summary

Clostridium septicum caused malignant edema in five postparturient Holstein cattle. Diagnosis involved bacterial culture and fluorescent antibody testing, revealing severe tissue damage and edema post-calving.

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Area of Science:

  • Veterinary Medicine
  • Bacteriology
  • Animal Pathology

Background:

  • Postparturient vulvovaginitis and metritis can occur in cattle.
  • Clostridium septicum is a known cause of malignant edema.

Purpose of the Study:

  • To describe five cases of vulvovaginitis and metritis in cattle caused by Clostridium septicum.
  • To detail the clinical signs, gross and microscopic findings, and diagnostic methods used.

Main Methods:

  • Case report describing five Holstein cattle with postparturient infections.
  • Diagnosis confirmed by bacterial culture and fluorescent antibody testing for Clostridium septicum.
  • Gross and microscopic examination of affected tissues.

Main Results:

  • All five cases were attributed to Clostridium septicum infection.
  • Clinical signs included perineal/perivulvar swelling, fever, and depression within 1-3 days postpartum.
  • Gross findings revealed extensive gelatinous, hemorrhagic edema and longitudinal tears in the reproductive tract.
  • Microscopic examination showed necrotic and ulcerated mucosae with Gram-positive rods consistent with C. septicum.

Conclusions:

  • Clostridium septicum is a causative agent of malignant edema in postparturient cattle.
  • Parturition trauma appears to predispose cattle to this condition.
  • Prompt diagnosis and identification of C. septicum are crucial for understanding and managing these cases.