DEFINITION
Reversible vacuolar change in hepatocytes in dogs, associated with glucocorticoid treatment, hyperadrenocorticism (iatrogenic or spontaneous), or chronic illnesses in other organ systems; typified by high ALP activity without signs of hepatic insufficiency
PATHOPHYSIOLOGY
Glucocorticoids—cause reversible glycogen accumulation in hepatocytes within 2–3 days after administration; injectable and reposital forms usually induce more severe changes than do oral forms; topical, ocular, cutaneous, and aural administration may also produce an effect
Cell swelling—leads to parenchymal enlargement and hepatomegaly
Response (dogs)—marked individual variation related to the type, route, dosage, duration of treatment, and individual sensitivity; may develop even with low-dose, short-term oral medication
May develop with systemic diseases not related to glucocorticoid exposure or hyperadrenocorticism
Association with significant nonhepatobiliary health problems that involve inflammation—suggests a relationship with stress (endogenous glucocorticoid release) or acute phase reactants
Thursday, March 31, 2011
Squamous Cell Carcinoma, Tonsil
OVERVIEW
Rapid and progressive local invasion by cords of neoplastic squamous epithelium arising from the tonsillar fossa into tonsillar lymphoid tissue
Local extension common
Quick to metastasize to lymph nodes (> 98%), lungs (> 63%), and other distant organs (>20)
Composes 20%–25% of all oral tumors and 50% of all intraoral tumors in dogs and cats
Commonly unilateral, affecting the right more than the left tonsil
SIGNALMENT
Middle-aged or old (range, 2.5–17 years) dogs and cats
No known breed or sex predilection
Rapid and progressive local invasion by cords of neoplastic squamous epithelium arising from the tonsillar fossa into tonsillar lymphoid tissue
Local extension common
Quick to metastasize to lymph nodes (> 98%), lungs (> 63%), and other distant organs (>20)
Composes 20%–25% of all oral tumors and 50% of all intraoral tumors in dogs and cats
Commonly unilateral, affecting the right more than the left tonsil
SIGNALMENT
Middle-aged or old (range, 2.5–17 years) dogs and cats
No known breed or sex predilection
Splenomegaly
DEFINITION
Enlargement of the spleen; characterized as either diffuse or nodular
PATHOPHYSIOLOGY
Spleen—removal of senescent and abnormal erythrocytes; filtration and phagocytosis of antigenic particles; production of lymphocytes and plasma cells; reservoir for erythrocytes and platelets; hematopoiesis, as required
Many disorders are related to and reflect splenic functions.
Diffuse
Four general pathologic mechanisms
Inflammatory (splenitis)—associated with infectious agents; classified according to cell type (e.g., suppurative, necrotizing, eosinophilic, lymphoplasmacytic, and granulomatous-pyogranulomatous)
Lymphoreticular hyperplasia—hyperplasia of mononuclear phagocytes and lymphoid elements (in response to antigens); accelerated erythrocyte destruction
Congestion—associated with impaired venous drainage
Infiltration—involves cellular invasion of the spleen or deposition of abnormal substances
Enlargement of the spleen; characterized as either diffuse or nodular
PATHOPHYSIOLOGY
Spleen—removal of senescent and abnormal erythrocytes; filtration and phagocytosis of antigenic particles; production of lymphocytes and plasma cells; reservoir for erythrocytes and platelets; hematopoiesis, as required
Many disorders are related to and reflect splenic functions.
Diffuse
Four general pathologic mechanisms
Inflammatory (splenitis)—associated with infectious agents; classified according to cell type (e.g., suppurative, necrotizing, eosinophilic, lymphoplasmacytic, and granulomatous-pyogranulomatous)
Lymphoreticular hyperplasia—hyperplasia of mononuclear phagocytes and lymphoid elements (in response to antigens); accelerated erythrocyte destruction
Congestion—associated with impaired venous drainage
Infiltration—involves cellular invasion of the spleen or deposition of abnormal substances
Sinus Bradycardia
DEFINITION
Sinus rhythm in which impulses arise from the sinoatrial node at a slower than normal rate
ECG Features
Dogs—sinus rate < 70 bpm (< 60 bpm in giant breeds)
Cars—sinus rate < 120 bpm at home or < 150 bpm at the clinic
Rhythm regular, often with a slight variation in R-R interval; may be irregular if bradycardia due to high vagal tone
Normal P wave for each QRS complex
P-R interval constant
Sinus rhythm in which impulses arise from the sinoatrial node at a slower than normal rate
ECG Features
Dogs—sinus rate < 70 bpm (< 60 bpm in giant breeds)
Cars—sinus rate < 120 bpm at home or < 150 bpm at the clinic
Rhythm regular, often with a slight variation in R-R interval; may be irregular if bradycardia due to high vagal tone
Normal P wave for each QRS complex
P-R interval constant
Shock, Septic
DEFINITION
Develops as a complication of overwhelming systemic infection. Sepsis is defined as a systemic inflammatory response to infection. Occurs in severe sepsis and is associated with hypoperfusion or hypotension that may or may not respond to fluids or pharmacologic cardiovascular support to maintain arterial pressure.
PATHOPHYSIOLOGY
Results from cardiovascular and/or vasomotor failure caused by circulating endotoxin and inflammatory mediator release. Gram-positive or Gram-negative, aerobic or anaerobic, systemic bacterial infection is the most common underlying cause. The primary event is hypovolemia caused by pyrexia, dehydration, and vascular fluid leakage (because of increased microvascular permeability). Differential vasoconstriction and vasodilation of microvascular beds causes pooling of blood and differential tissue perfusion. Vasculitis and thromboembolic events further compromise tissue perfusion. The ultimate result is tissue hypoxemia and metabolic acidosis, leading to multiple organ failure. In Gram-negative bacterial sepsis, endotoxin (a lipopolysaccharide component of the outer bacterial membrane) plays a key role in the activation of the complement and fibrinolytic pathways. Endotoxin also stimulates macrophages to release cytokines, including tumor necrosis factor and interleukin-1, which in turn amplify the systemic response to endotoxin by stimulating neutrophils, endothelial cells, and platelets, and the release of other cellular mediators that are ultimately responsible for the cardiorespiratory and systemic manifestations of septic shock. Gram-positive bacteria produce other bacterial products capable of activating the same mediator responses.
SYSTEMS AFFECTED
Develops as a complication of overwhelming systemic infection. Sepsis is defined as a systemic inflammatory response to infection. Occurs in severe sepsis and is associated with hypoperfusion or hypotension that may or may not respond to fluids or pharmacologic cardiovascular support to maintain arterial pressure.
PATHOPHYSIOLOGY
Results from cardiovascular and/or vasomotor failure caused by circulating endotoxin and inflammatory mediator release. Gram-positive or Gram-negative, aerobic or anaerobic, systemic bacterial infection is the most common underlying cause. The primary event is hypovolemia caused by pyrexia, dehydration, and vascular fluid leakage (because of increased microvascular permeability). Differential vasoconstriction and vasodilation of microvascular beds causes pooling of blood and differential tissue perfusion. Vasculitis and thromboembolic events further compromise tissue perfusion. The ultimate result is tissue hypoxemia and metabolic acidosis, leading to multiple organ failure. In Gram-negative bacterial sepsis, endotoxin (a lipopolysaccharide component of the outer bacterial membrane) plays a key role in the activation of the complement and fibrinolytic pathways. Endotoxin also stimulates macrophages to release cytokines, including tumor necrosis factor and interleukin-1, which in turn amplify the systemic response to endotoxin by stimulating neutrophils, endothelial cells, and platelets, and the release of other cellular mediators that are ultimately responsible for the cardiorespiratory and systemic manifestations of septic shock. Gram-positive bacteria produce other bacterial products capable of activating the same mediator responses.
SYSTEMS AFFECTED
Shock, Cardiogenic
DEFINITION
Results from profound impairment of cardiac function leading to a decrease in stroke volume and cardiac output, venous congestion, and peripheral vasoconstriction.
Cardiac dysfunction may be caused by hypertrophic or dilated cardiomyopathies, pericardial tamponade, outflow obstructions, thrombosis, severe endocardiosis, heartworm disease, or severe arrhythmias.
Cardiac “pump” failure may also be secondary to systemic diseases causing myocardial dysfunction such as sepsis.
Results in hypotension and compromised tissue perfusion, with reduced tissue oxygen delivery
Results from profound impairment of cardiac function leading to a decrease in stroke volume and cardiac output, venous congestion, and peripheral vasoconstriction.
Cardiac dysfunction may be caused by hypertrophic or dilated cardiomyopathies, pericardial tamponade, outflow obstructions, thrombosis, severe endocardiosis, heartworm disease, or severe arrhythmias.
Cardiac “pump” failure may also be secondary to systemic diseases causing myocardial dysfunction such as sepsis.
Results in hypotension and compromised tissue perfusion, with reduced tissue oxygen delivery
Sepsis and Bacteremia
DEFINITION
Bacteremia—defined as the presence of bacterial organisms in the bloodstream
Sepsis—systemic response to bacterial infection (e.g., fever, hypotension)
Terms are not synonymous, although often used interchangeably
PATHOPHYSIOLOGY
Shedding of bacterial organisms into the bloodstream—may occur transiently, intermittently, or continually
The most critical host response for elimination of bacteremia—provided by mononuclear phagocyte system of the spleen and liver; activation leads to release of numerous cellular mediators (cytokines), some of which are beneficial and others detrimental; may lead to death of the host
Neutrophils—relatively more important for defense against extravascular infection
Bacteremia—transient, subclinical event or may escalate to overt sepsis when the immune system is overwhelmed; generally of more pathologic significance when the bloodstream is invaded from venous or lymphatic drainage sites
Bacteremia—defined as the presence of bacterial organisms in the bloodstream
Sepsis—systemic response to bacterial infection (e.g., fever, hypotension)
Terms are not synonymous, although often used interchangeably
PATHOPHYSIOLOGY
Shedding of bacterial organisms into the bloodstream—may occur transiently, intermittently, or continually
The most critical host response for elimination of bacteremia—provided by mononuclear phagocyte system of the spleen and liver; activation leads to release of numerous cellular mediators (cytokines), some of which are beneficial and others detrimental; may lead to death of the host
Neutrophils—relatively more important for defense against extravascular infection
Bacteremia—transient, subclinical event or may escalate to overt sepsis when the immune system is overwhelmed; generally of more pathologic significance when the bloodstream is invaded from venous or lymphatic drainage sites
Salmonellosis
DEFINITION
A bacterial disease that causes enteritis, septicemia, and abortions and is caused by many different serotypes of Salmonella
PATHOPHYSIOLOGY
Salmonella—a gram-negative bacterium; colonizes the small intestine (ileum); adheres to and invades the enterocytes; eventually enters and multiplies in the lamina propria and local mesenteric lymph nodes; cytotoxin (cell death) and enterotoxin (increases cAMP) are produced; inflammation occurs; and prostaglandin synthesis ensues; results in secretory diarrhea and mucosal sloughing
Uncomplicated gastroenteritis—organisms are stopped at the mesenteric lymph node stage; patient has only diarrhea, vomiting, and dehydration
Bacteremia and septicemia following gastroenteritis—more serious disease; focal extraintestinal infections (abortion, joint disease) or endotoxemia may result; may lead to organ infarction, generalized thrombosis, DIC, and death
Some patients recover from the septicemic form but suffer prolonged recovery as a result of their debilitated state.
A bacterial disease that causes enteritis, septicemia, and abortions and is caused by many different serotypes of Salmonella
PATHOPHYSIOLOGY
Salmonella—a gram-negative bacterium; colonizes the small intestine (ileum); adheres to and invades the enterocytes; eventually enters and multiplies in the lamina propria and local mesenteric lymph nodes; cytotoxin (cell death) and enterotoxin (increases cAMP) are produced; inflammation occurs; and prostaglandin synthesis ensues; results in secretory diarrhea and mucosal sloughing
Uncomplicated gastroenteritis—organisms are stopped at the mesenteric lymph node stage; patient has only diarrhea, vomiting, and dehydration
Bacteremia and septicemia following gastroenteritis—more serious disease; focal extraintestinal infections (abortion, joint disease) or endotoxemia may result; may lead to organ infarction, generalized thrombosis, DIC, and death
Some patients recover from the septicemic form but suffer prolonged recovery as a result of their debilitated state.
Rotavirus Infections
OVERVIEW
Nonenveloped, double-stranded RNA virus; rota (Latin; “wheel”) for shape of the capsid; genus within the family Reoviridae; relatively resistant to environmental destruction (acid and lipid solvents); unique double-capsid protects virus from inactivation in the upper gastrointestinal tract.
Wide host range, identified in almost every species investigated
Most significant cause of severe gastro-enteritis in young children (< 2 years) and animals throughout the world
Transmission—fecal–oral contamination
Infection—affects mature epithelial cells on luminal tips of the intestinal villi; causes swelling, degeneration, and desquamation; denuded villi contract; results in villous atrophy with loss of absorptive capability and loss of brush border enzymes (e.g., disaccharidases); leads to osmotic diarrhea
Nonenveloped, double-stranded RNA virus; rota (Latin; “wheel”) for shape of the capsid; genus within the family Reoviridae; relatively resistant to environmental destruction (acid and lipid solvents); unique double-capsid protects virus from inactivation in the upper gastrointestinal tract.
Wide host range, identified in almost every species investigated
Most significant cause of severe gastro-enteritis in young children (< 2 years) and animals throughout the world
Transmission—fecal–oral contamination
Infection—affects mature epithelial cells on luminal tips of the intestinal villi; causes swelling, degeneration, and desquamation; denuded villi contract; results in villous atrophy with loss of absorptive capability and loss of brush border enzymes (e.g., disaccharidases); leads to osmotic diarrhea
Rhinitis and Sinusitis
DEFINITION
Rhinitis—inflammation of the mucous membrane of the nose
Sinusitis—inflammation of the associated paranasal sinuses
Rhinosinusitis—coined term, because one rarely occurs without the other
PATHOPHYSIOLOGY
May be acute or chronic, noninfectious or infectious
Patients seen in clinics usually have chronic disease.
All causes are often complicated by opportunistic secondary microbial invasion.
Associated mucosal vascular congestion and friability, excessive mucus gland secretion, neutrophil chemotaxis, and nasolacrimal duct obstruction—lead to congestion, obstructed airflow, sneezing, epistaxis, nasal discharge (mucopurulent), and epiphora
Turbinate and facial bone destruction—may develop with neoplastic or fungal disease
Rhinitis—inflammation of the mucous membrane of the nose
Sinusitis—inflammation of the associated paranasal sinuses
Rhinosinusitis—coined term, because one rarely occurs without the other
PATHOPHYSIOLOGY
May be acute or chronic, noninfectious or infectious
Patients seen in clinics usually have chronic disease.
All causes are often complicated by opportunistic secondary microbial invasion.
Associated mucosal vascular congestion and friability, excessive mucus gland secretion, neutrophil chemotaxis, and nasolacrimal duct obstruction—lead to congestion, obstructed airflow, sneezing, epistaxis, nasal discharge (mucopurulent), and epiphora
Turbinate and facial bone destruction—may develop with neoplastic or fungal disease
Tuesday, March 29, 2011
Reovirus Infections
OVERVIEW
Respiratory enteric orphan virus (reovirus)—genus in the family Reovirus; nonenveloped, double-stranded RNA virus; isolated from respiratory and enteric tracts; not associated with any known disease (hence orphan)
Ubiquitous in geographic distribution and host range, virtually every species of mammal, including humans
Virus—infects mature epithelial cells on luminal tips of the intestinal villi; causes cellular destruction, resulting in villous atrophy (similar to rotavirus and coronavirus)
Loss of absorptive capability and loss of brush border enzymes (e.g., disaccharidases) leads to osmotic diarrhea.
Respiratory enteric orphan virus (reovirus)—genus in the family Reovirus; nonenveloped, double-stranded RNA virus; isolated from respiratory and enteric tracts; not associated with any known disease (hence orphan)
Ubiquitous in geographic distribution and host range, virtually every species of mammal, including humans
Virus—infects mature epithelial cells on luminal tips of the intestinal villi; causes cellular destruction, resulting in villous atrophy (similar to rotavirus and coronavirus)
Loss of absorptive capability and loss of brush border enzymes (e.g., disaccharidases) leads to osmotic diarrhea.
Q Fever
OVERVIEW
Caused by the zoonotic rickettsia Coxiella burnetii
Infection—most commonly by inhalation or ingestion of organisms while feeding on infected body fluids (urine, feces, milk, or parturient discharges), tissues (especially placenta), or carcasses of infected animal reservoir hosts (cattle, sheep, goats); can occur after tick exposure (many species of ticks implicated)
Lungs—thought to be main portal of entry to systemic circulation
Organism replicates in vascular endothelium; causes widespread vasculitis; severity depends on the pathogenicity of the strain of organism; vasculitis results in necrosis and hemorrhage in lungs, liver, and CNS
An extended latent period exists after recovery until chronic immune-complex phenomena develop; organism reactivated out of the latent state during parturition, resulting in large numbers entering the placenta, parturient fluids, urine, feces, and milk
Endemic worldwide
Caused by the zoonotic rickettsia Coxiella burnetii
Infection—most commonly by inhalation or ingestion of organisms while feeding on infected body fluids (urine, feces, milk, or parturient discharges), tissues (especially placenta), or carcasses of infected animal reservoir hosts (cattle, sheep, goats); can occur after tick exposure (many species of ticks implicated)
Lungs—thought to be main portal of entry to systemic circulation
Organism replicates in vascular endothelium; causes widespread vasculitis; severity depends on the pathogenicity of the strain of organism; vasculitis results in necrosis and hemorrhage in lungs, liver, and CNS
An extended latent period exists after recovery until chronic immune-complex phenomena develop; organism reactivated out of the latent state during parturition, resulting in large numbers entering the placenta, parturient fluids, urine, feces, and milk
Endemic worldwide
Pulmonary Mineralizations
OVERVIEW
Both calcification and ossification and may be generalized or localized
Discrete—if individual mineral deposits can be identified
Diffuse—preclude identification of individual deposits
Calcification—dystrophic or metastatic; dystrophic: occurs secondary to tissue degeneration or inflammation; metastatic: occurs secondary to metabolic disease; may be normal (e.g., the pleura in old dogs or premature calcification of the tracheal and bronchial cartilages in chondrodystrophic breeds); often a sign of inactivity of a lesion, thus most focal calcifications are functionally unimportant
Ossification—also called heterotopic bone formation; calcification of a bony matrix; pulmonary ossification in the form of small, multiple nodules (osteomas) common in normal dogs
Generalized pulmonary mineralizations of unknown cause—reported in dogs and cats under descriptive terms: pulmonary alveolar microlithiasis or pumice stone lung, bronchiolar microlithiasis, idiopathic pulmonary calcification or ossification
Both calcification and ossification and may be generalized or localized
Discrete—if individual mineral deposits can be identified
Diffuse—preclude identification of individual deposits
Calcification—dystrophic or metastatic; dystrophic: occurs secondary to tissue degeneration or inflammation; metastatic: occurs secondary to metabolic disease; may be normal (e.g., the pleura in old dogs or premature calcification of the tracheal and bronchial cartilages in chondrodystrophic breeds); often a sign of inactivity of a lesion, thus most focal calcifications are functionally unimportant
Ossification—also called heterotopic bone formation; calcification of a bony matrix; pulmonary ossification in the form of small, multiple nodules (osteomas) common in normal dogs
Generalized pulmonary mineralizations of unknown cause—reported in dogs and cats under descriptive terms: pulmonary alveolar microlithiasis or pumice stone lung, bronchiolar microlithiasis, idiopathic pulmonary calcification or ossification
Proteinuria
DEFINITION
A subjective increase in urinary protein detected by dipstick analysis; objectively, a urinary protein:creatinine ratio > 1 or a 24-h urinary protein content > 20 mg/kg
PATHOPHYSIOLOGY
Greater than normal delivery of low-molecular-weight plasma proteins to the glomerulus
Excessive leakage of proteins across the glomerular basement membrane secondary to altered permselectivity of the glomerulus
Reduced tubular reabsorptive capacity for proteins, or exudation of blood or serum into the lower urinary tract
A subjective increase in urinary protein detected by dipstick analysis; objectively, a urinary protein:creatinine ratio > 1 or a 24-h urinary protein content > 20 mg/kg
PATHOPHYSIOLOGY
Greater than normal delivery of low-molecular-weight plasma proteins to the glomerulus
Excessive leakage of proteins across the glomerular basement membrane secondary to altered permselectivity of the glomerulus
Reduced tubular reabsorptive capacity for proteins, or exudation of blood or serum into the lower urinary tract
Potassium, Hypokalemia
DEFINITION
Serum potassium concentration < 3.5 mEq/L
PATHOPHYSIOLOGY
Potassium is the major intracellular cation and thereby largely responsible for maintenance of intracellular volume.
The ratio of intracellular to extracellular potassium concentration is important in determining the cellular membrane potential. Rapid alterations in extracellular potassium concentration alter this ratio and predispose an animal to arrhythmias and conduction disturbances in excitable tissues (e.g., heart, nerve, and muscle)
Hypokalemia can be caused by excessive potassium loss via the gastrointestinal tract or kidneys or movement of potassium from the extracellular fluid compartment into cells (i.e., translocation).
Serum potassium concentration < 3.5 mEq/L
PATHOPHYSIOLOGY
Potassium is the major intracellular cation and thereby largely responsible for maintenance of intracellular volume.
The ratio of intracellular to extracellular potassium concentration is important in determining the cellular membrane potential. Rapid alterations in extracellular potassium concentration alter this ratio and predispose an animal to arrhythmias and conduction disturbances in excitable tissues (e.g., heart, nerve, and muscle)
Hypokalemia can be caused by excessive potassium loss via the gastrointestinal tract or kidneys or movement of potassium from the extracellular fluid compartment into cells (i.e., translocation).
Polyphagia
DEFINITION
Increased food intake
PATHOPHYSIOLOGY
Failure to assimilate or loss of nutrients (e.g., maldigestion/malabsorption syndromes such as EPI)
Inability to use nutrients (e.g., diabetes mellitus, poor quality diets, GI parasites)
Hypoglycemia (e.g., insulinoma, insulin overdose)
Increased metabolic rate or demand (e.g., hyperthyroidism, cold environments, pregnancy, lactation)
Psychologic or learned behaviors (e.g., palatable diets, competition, drugs such as anticonvulsants or glucocorticoids)
Increased food intake
PATHOPHYSIOLOGY
Failure to assimilate or loss of nutrients (e.g., maldigestion/malabsorption syndromes such as EPI)
Inability to use nutrients (e.g., diabetes mellitus, poor quality diets, GI parasites)
Hypoglycemia (e.g., insulinoma, insulin overdose)
Increased metabolic rate or demand (e.g., hyperthyroidism, cold environments, pregnancy, lactation)
Psychologic or learned behaviors (e.g., palatable diets, competition, drugs such as anticonvulsants or glucocorticoids)
Poisoning (Intoxication)
DEFINITION
Acutely ill patients are often diagnosed as poisoned when no other diagnosis is obvious.
Direct efforts toward stabilizing the patient.
Make the diagnosis after determining preexisting conditions and initially controlling clinical signs.
Goals of treatment—providing emergency intervention; preventing further exposure; preventing further absorption; applying specific antidotes; hastening elimination; providing supportive measures; offering client education
Suspected intoxication—suspected toxic materials and specimens may be valuable from a medicolegal aspect; maintain a proper chain of physical evidence; keep good medical records.
Valuable time can be saved by applying the appropriate treatment for a suspected or known intoxicant.
Acutely ill patients are often diagnosed as poisoned when no other diagnosis is obvious.
Direct efforts toward stabilizing the patient.
Make the diagnosis after determining preexisting conditions and initially controlling clinical signs.
Goals of treatment—providing emergency intervention; preventing further exposure; preventing further absorption; applying specific antidotes; hastening elimination; providing supportive measures; offering client education
Suspected intoxication—suspected toxic materials and specimens may be valuable from a medicolegal aspect; maintain a proper chain of physical evidence; keep good medical records.
Valuable time can be saved by applying the appropriate treatment for a suspected or known intoxicant.
Pneumonia, Bacterial
DEFINITION
The fully developed inflammatory response to virulent bacteria in lung parenchyma characterized by exudation of cells and fluid into conduction airways and alveolar spaces
PATHOPHYSIOLOGY
Bacteria—enter the lower respiratory tract primarily by the inhalation or aspiration routes; enter less commonly by the hematogenous route; infections incite an overt inflammatory reaction.
Tracheobronchial tree and lungs—normally not continuously sterile
Oropharyngeal bacteria—frequently aspirated; may be present for an unknown interval in the normal tracheobronchial tree and lung; have the potential to cause or complicate respiratory infection; cloud interpretation of airway and lung cultures
Respiratory infection—development depends on the complex interplay of many factors: size, inoculation site, number of organisms and their virulence, and resistance of the host
Viral infections—alter bacterial colonization patterns; increase bacterial adherence to respiratory epithelium; reduce mucociliary clearance and phagocytosis; thus may allow resident bacteria to invade the lower respiratory tract
Exudative phase—inflammatory hyperemia; serous exudation of high protein fluid into interstitial and alveolar spaces
Leukocytic emigration phase—leukocytes infiltrate the airways and alveoli; consolidation, ischemia, tissue necrosis, and atelectasis owing to bronchial occlusion, obstructive bronchiolitis, and impaired collateral ventilation
Mortality—associated with severe hypoxemia (low arterial oxygen concentration) and sepsis
The fully developed inflammatory response to virulent bacteria in lung parenchyma characterized by exudation of cells and fluid into conduction airways and alveolar spaces
PATHOPHYSIOLOGY
Bacteria—enter the lower respiratory tract primarily by the inhalation or aspiration routes; enter less commonly by the hematogenous route; infections incite an overt inflammatory reaction.
Tracheobronchial tree and lungs—normally not continuously sterile
Oropharyngeal bacteria—frequently aspirated; may be present for an unknown interval in the normal tracheobronchial tree and lung; have the potential to cause or complicate respiratory infection; cloud interpretation of airway and lung cultures
Respiratory infection—development depends on the complex interplay of many factors: size, inoculation site, number of organisms and their virulence, and resistance of the host
Viral infections—alter bacterial colonization patterns; increase bacterial adherence to respiratory epithelium; reduce mucociliary clearance and phagocytosis; thus may allow resident bacteria to invade the lower respiratory tract
Exudative phase—inflammatory hyperemia; serous exudation of high protein fluid into interstitial and alveolar spaces
Leukocytic emigration phase—leukocytes infiltrate the airways and alveoli; consolidation, ischemia, tissue necrosis, and atelectasis owing to bronchial occlusion, obstructive bronchiolitis, and impaired collateral ventilation
Mortality—associated with severe hypoxemia (low arterial oxygen concentration) and sepsis
Pneumocystosis
OVERVIEW
Pneumocystis carinii—saprophyte of the mammalian respiratory tract is whose life cycle completed in the alveolar spaces; classified as an atypical fungal organism based on analysis of nucleic acids
Infections—dogs, clinical; cats, subclinical; usually confined to the respiratory tract; a reported case of disseminated disease in a dog
Transmission—infected to susceptible animal within a species; strain differences may account for the lack of interspecies transmission.
Pneumocystis carinii—saprophyte of the mammalian respiratory tract is whose life cycle completed in the alveolar spaces; classified as an atypical fungal organism based on analysis of nucleic acids
Infections—dogs, clinical; cats, subclinical; usually confined to the respiratory tract; a reported case of disseminated disease in a dog
Transmission—infected to susceptible animal within a species; strain differences may account for the lack of interspecies transmission.
Plague (Yersinia pestis)
OVERVIEW
Yersinia pestis—gram-negative, bipolar staining rod; an Enterobacteriaceae; reservoir includes wild rodents (sylvatic), ground squirrels, prairie dogs, rabbits, bobcats, coyotes
Occurs worldwide
U.S.—reported cases from New Mexico, Arizona, California, Colorado, Idaho, Nevada, Oregon, Texas, Utah, Washington, Wyoming, and Hawaii
Common from May to October
Infected vectors (fleas) transmit the bacterium in bite.
Bacteria—rapidly migrate from skin lymphatics to regional lymph nodes; survive phagocytosis (because of capsule protection) and multiply in lymph nodes; phagocytic cells rupture and organism is resistant to further phagocytosis.
Infection—fever and painful lymphadenopathy (bubo); intense local inflammation results in bubonic plague; intermittent bacteremia; lymph nodes may rupture; may become septicemic with or without lymph node involvement
Cats—highly susceptible to infection; severe fatal disease
Dogs—naturally resistant to infection
Yersinia pestis—gram-negative, bipolar staining rod; an Enterobacteriaceae; reservoir includes wild rodents (sylvatic), ground squirrels, prairie dogs, rabbits, bobcats, coyotes
Occurs worldwide
U.S.—reported cases from New Mexico, Arizona, California, Colorado, Idaho, Nevada, Oregon, Texas, Utah, Washington, Wyoming, and Hawaii
Common from May to October
Infected vectors (fleas) transmit the bacterium in bite.
Bacteria—rapidly migrate from skin lymphatics to regional lymph nodes; survive phagocytosis (because of capsule protection) and multiply in lymph nodes; phagocytic cells rupture and organism is resistant to further phagocytosis.
Infection—fever and painful lymphadenopathy (bubo); intense local inflammation results in bubonic plague; intermittent bacteremia; lymph nodes may rupture; may become septicemic with or without lymph node involvement
Cats—highly susceptible to infection; severe fatal disease
Dogs—naturally resistant to infection
Perineal Hernia
OVERVIEW
Results from a defect in the musculature of the pelvic diaphragm
Allows herniation of retroperitoneal fat or pelvic viscera through the pelvic diaphragm
Organ systems potentially involved—GI, musculoskeletal, urologic, reproductive
SIGNALMENT
Much more common in dogs than cats
Almost exclusively (95%) male dogs
Usually older than 5 years of age
Boston terriers, collies, boxers, Pekingese, and mongrels overrepresented
Results from a defect in the musculature of the pelvic diaphragm
Allows herniation of retroperitoneal fat or pelvic viscera through the pelvic diaphragm
Organ systems potentially involved—GI, musculoskeletal, urologic, reproductive
SIGNALMENT
Much more common in dogs than cats
Almost exclusively (95%) male dogs
Usually older than 5 years of age
Boston terriers, collies, boxers, Pekingese, and mongrels overrepresented
Pericarditis
OVERVIEW
Inflammatory condition of the parietal (pericardial sac) and/or visceral (epicardium) pericardium; clinical syndromes caused by pericardial effusion, constrictive pericarditis, inflammatory extension to surrounding tissues (pleural, myocardium), or the underlying cause of the pericarditis
In dogs—most commonly seen as idiopathic hemorrhagic pericarditis, is a mild inflammatory condition that can lead to life-threatening pericardial effusion and tamponade
SIGNALMENT
Dogs and cats
Idiopathic hemorrhagic pericarditis more common in young to middle-aged, medium to large-breed dogs (e.g., great Pyrenees, Great Dane, Saint Bernard, golden retriever); males predisposed
Others depend on the underlying disease.
Inflammatory condition of the parietal (pericardial sac) and/or visceral (epicardium) pericardium; clinical syndromes caused by pericardial effusion, constrictive pericarditis, inflammatory extension to surrounding tissues (pleural, myocardium), or the underlying cause of the pericarditis
In dogs—most commonly seen as idiopathic hemorrhagic pericarditis, is a mild inflammatory condition that can lead to life-threatening pericardial effusion and tamponade
SIGNALMENT
Dogs and cats
Idiopathic hemorrhagic pericarditis more common in young to middle-aged, medium to large-breed dogs (e.g., great Pyrenees, Great Dane, Saint Bernard, golden retriever); males predisposed
Others depend on the underlying disease.
Pelvic Bladder
OVERVIEW
Describes a condition in which the neck of the bladder is located extremely caudally in the pelvic canal and the urethra is shortened or displaced; most often associated with incontinence in young intact female dogs, but some dogs with pelvic bladder do not exhibit urinary incontinence
SIGNALMENT
Dogs and rarely cats; the difference in prevalence between species is presumably because the cat has a longer urethra than a dog of similar size.
May occur in dogs of both sexes, either intact or neutered, but primarily affects young intact female dogs (< 1 year of age); usually detected in male dogs after neutering
Describes a condition in which the neck of the bladder is located extremely caudally in the pelvic canal and the urethra is shortened or displaced; most often associated with incontinence in young intact female dogs, but some dogs with pelvic bladder do not exhibit urinary incontinence
SIGNALMENT
Dogs and rarely cats; the difference in prevalence between species is presumably because the cat has a longer urethra than a dog of similar size.
May occur in dogs of both sexes, either intact or neutered, but primarily affects young intact female dogs (< 1 year of age); usually detected in male dogs after neutering
Parvoviral Infection - Dogs
DEFINITION
CPV-2 infection is an acute systemic illness characterized by hemorrhagic enteritis.
Often fatal in pups, who may collapse in a “shock-like” state and die suddenly without enteric signs, after only a brief period of malaise.
The myocardial form, observed in pups during the early outbreaks when the dog population was fully susceptible, is now rare.
Most pups are now protected against neonatal infection by maternal antibodies.
Monoclonal antibodies have revealed antigenic changes in CPV-2 since its emergence in 1978.
The original virus is now virtually extinct in the domestic dog population.
The viruses currently circulating in dogs, designated CPV-2a and CPV-2b, have been genetically stable since 1984.
These viruses are more virulent than the original isolates, and case mortality rates appear to be higher than in the earliest outbreaks.
Most of the clinical literature is based on the response of dogs to CPV-2 and should be reevaluated in light of the emergence and dominance of the newer types in dogs.
As with rabies variants, the antigenic changes in CPV-2 do not affect the ability of various vaccines to protect dogs.
CPV-2 infection is an acute systemic illness characterized by hemorrhagic enteritis.
Often fatal in pups, who may collapse in a “shock-like” state and die suddenly without enteric signs, after only a brief period of malaise.
The myocardial form, observed in pups during the early outbreaks when the dog population was fully susceptible, is now rare.
Most pups are now protected against neonatal infection by maternal antibodies.
Monoclonal antibodies have revealed antigenic changes in CPV-2 since its emergence in 1978.
The original virus is now virtually extinct in the domestic dog population.
The viruses currently circulating in dogs, designated CPV-2a and CPV-2b, have been genetically stable since 1984.
These viruses are more virulent than the original isolates, and case mortality rates appear to be higher than in the earliest outbreaks.
Most of the clinical literature is based on the response of dogs to CPV-2 and should be reevaluated in light of the emergence and dominance of the newer types in dogs.
As with rabies variants, the antigenic changes in CPV-2 do not affect the ability of various vaccines to protect dogs.
paralysis
DEFINITION
Paresis—weakness of voluntary movement
Paralysis—lack of voluntary movement
Quadriparesis (tetraparesis)—weakness of voluntary movements in all limbs
Quadriplegia (tetraplegia)—absence of all voluntary limb movement
Paraparesis—weakness of voluntary movements in pelvic limbs
Paraplegia—absence of all voluntary pelvic limb movement
PATHOPHYSIOLOGY
Weakness—may be caused by lesions in the upper or lower motor neuron system
Cell bodies or nuclei for the upper motor neuron system—located within the brain; responsible for initiating voluntary movement
Axons from these cell bodies—form tracts (rubrospinal, corticospinal, vestibulospinal, reticulospinal) that descend from the brain to synapse on interneurons in the spinal cord
Interneuronal axons—then synapse on large (a) motor neurons in the ventral gray matter of the spinal cord
Large motor neurons—cell bodies of origin for the lower motor neuron system, which is responsible for spinal reflexes
Collections of lower motor neurons in the cervical and lumbar intumescences—give rise to axons that form the ventral nerve roots, the spinal nerves, and (ultimately) the peripheral nerves that innervate limb muscles
Evaluation of limb reflexes—determine which system (upper or lower motor neuron) is involved
Upper motor neurons and their axons—inhibitory influence on the large motor neurons of the lower motor neuron system; maintain normal muscle tone and normal spinal reflexes; if injured, spinal reflexes are no longer inhibited or controlled and reflexes become exaggerated or hyperreflexic.
Large a motor neurons or their processes (peripheral nerves)—if injured, spinal reflexes cannot be elicited (areflexic) or are reduced (hyporeflexic).
Paresis—weakness of voluntary movement
Paralysis—lack of voluntary movement
Quadriparesis (tetraparesis)—weakness of voluntary movements in all limbs
Quadriplegia (tetraplegia)—absence of all voluntary limb movement
Paraparesis—weakness of voluntary movements in pelvic limbs
Paraplegia—absence of all voluntary pelvic limb movement
PATHOPHYSIOLOGY
Weakness—may be caused by lesions in the upper or lower motor neuron system
Cell bodies or nuclei for the upper motor neuron system—located within the brain; responsible for initiating voluntary movement
Axons from these cell bodies—form tracts (rubrospinal, corticospinal, vestibulospinal, reticulospinal) that descend from the brain to synapse on interneurons in the spinal cord
Interneuronal axons—then synapse on large (a) motor neurons in the ventral gray matter of the spinal cord
Large motor neurons—cell bodies of origin for the lower motor neuron system, which is responsible for spinal reflexes
Collections of lower motor neurons in the cervical and lumbar intumescences—give rise to axons that form the ventral nerve roots, the spinal nerves, and (ultimately) the peripheral nerves that innervate limb muscles
Evaluation of limb reflexes—determine which system (upper or lower motor neuron) is involved
Upper motor neurons and their axons—inhibitory influence on the large motor neurons of the lower motor neuron system; maintain normal muscle tone and normal spinal reflexes; if injured, spinal reflexes are no longer inhibited or controlled and reflexes become exaggerated or hyperreflexic.
Large a motor neurons or their processes (peripheral nerves)—if injured, spinal reflexes cannot be elicited (areflexic) or are reduced (hyporeflexic).
Papillomatosis
OVERVIEW
Papillomaviruses (PVs)—group of nonenveloped, double-stranded DNA viruses that induce proliferative cutaneous tumors in cats and dogs and mucosal tumors in dogs; each is host and fairly site-specific, with characteristic clinical and microscopic changes in infected tissues.
Tumors—papillomas, warts, or verrucae; generally benign; spontaneously regress; rarely may undergo conversion to SCC
Lesions—often multiple, well demarcated, and exophytic; sometimes hyperkeratotic plaques or with papules; may be deeply pigmented (black or brown), pink, tan, or white
Infection—inoculation through breaks in the epidermis or mucosal epithelium; iatrogenic transmission through use of contaminated instruments possible
Papillomaviruses (PVs)—group of nonenveloped, double-stranded DNA viruses that induce proliferative cutaneous tumors in cats and dogs and mucosal tumors in dogs; each is host and fairly site-specific, with characteristic clinical and microscopic changes in infected tissues.
Tumors—papillomas, warts, or verrucae; generally benign; spontaneously regress; rarely may undergo conversion to SCC
Lesions—often multiple, well demarcated, and exophytic; sometimes hyperkeratotic plaques or with papules; may be deeply pigmented (black or brown), pink, tan, or white
Infection—inoculation through breaks in the epidermis or mucosal epithelium; iatrogenic transmission through use of contaminated instruments possible
Pancreatitis
DEFINITION
Inflammation of the pancreas
Acute pancreatitis—inflammation of the pancreas that occurs abruptly with little or no permanent pathologic change
Chronic pancreatitis—continuing inflammatory disease that is often accompanied by irreversible morphologic change
PATHOPHYSIOLOGY
Most defense mechanisms prevent pancreatic autodigestion by the enzymes it secretes.
Under select circumstances, these natural defenses fail; autodigestion occurs when these digestive enzymes are activated within acinar cells.
Local and systemic tissue injury is due to the activity of released pancreatic enzymes and a variety of inflammatory mediators such as kinins, free radicals, and complement factors.
Inflammation of the pancreas
Acute pancreatitis—inflammation of the pancreas that occurs abruptly with little or no permanent pathologic change
Chronic pancreatitis—continuing inflammatory disease that is often accompanied by irreversible morphologic change
PATHOPHYSIOLOGY
Most defense mechanisms prevent pancreatic autodigestion by the enzymes it secretes.
Under select circumstances, these natural defenses fail; autodigestion occurs when these digestive enzymes are activated within acinar cells.
Local and systemic tissue injury is due to the activity of released pancreatic enzymes and a variety of inflammatory mediators such as kinins, free radicals, and complement factors.
Monday, March 28, 2011
Ovarian Tumors
OVERVIEW
Epithelial (carcinoma), germ cell (dysgerminoma and teratoma), and sex-cord stromal (granulosa cell tumor, Sertoli-Leydig cell tumor, thecoma, and luteoma) tumors
Dogs—rare (0.5%–1.2% of tumors); 40% carcinomas, 10% germ cell, and 50% sex-cord
Cats—extremely rare (0.7%–3.6% of tumors); 15% germ cell and 85% sex-cord
Metastasis common
Some tumors produce hormones.
Epithelial (carcinoma), germ cell (dysgerminoma and teratoma), and sex-cord stromal (granulosa cell tumor, Sertoli-Leydig cell tumor, thecoma, and luteoma) tumors
Dogs—rare (0.5%–1.2% of tumors); 40% carcinomas, 10% germ cell, and 50% sex-cord
Cats—extremely rare (0.7%–3.6% of tumors); 15% germ cell and 85% sex-cord
Metastasis common
Some tumors produce hormones.
Oral Ulceration
DEFINITION
Destruction of the oral epithelium, exposing underlying connective tissue
PATHOPHYSIOLOGY
Cell—cell and cell—matrix adhesion proteins are responsible for maintaining the integrity of the mucosal lining of the oral cavity.
Disease processes that destroy keratinocytes or adversely affect their adhesion to one another or to the subjacent basement membrane result in erosions, ulcerations, and desquamation.
Immunologic processes that have a deleterious effect on the integrity of the epithelial—basement membrane submucosa complex may be involved in causing ulcers to form.
Destruction of the oral epithelium, exposing underlying connective tissue
PATHOPHYSIOLOGY
Cell—cell and cell—matrix adhesion proteins are responsible for maintaining the integrity of the mucosal lining of the oral cavity.
Disease processes that destroy keratinocytes or adversely affect their adhesion to one another or to the subjacent basement membrane result in erosions, ulcerations, and desquamation.
Immunologic processes that have a deleterious effect on the integrity of the epithelial—basement membrane submucosa complex may be involved in causing ulcers to form.
Obesity
DEFINITION
The presence of body fat in sufficient excess to compromise normal physiologic function or predispose to metabolic, surgical, and/or mechanical problems
PATHOPHYSIOLOGY
Animal factors—although breed predispositions have been reported, any animal may become obese; inactivity is an important risk factor in both dogs and cats, as are increasing age and neutering.
Dietary factors—no specific diet other than a surfeit of “table scraps” and “treats” has been shown to increase risk in dogs; in cats, consumption of “high-fat” diets reportedly increases risk.
Feeding management—many animals are overfed; reasons for excessive food consumption include ignorance of proper feeding practices, inappropriately generous feeding recommendations by manufacturers, emphasis on food palatability both by owners and manufacturers, and inadequate explanation by veterinarians of appropriate body condition for the pet and how to maintain it.
Owner factors—many owners of overweight pets are overweight themselves and engage in feeding as a social activity; clients also may consider their pet to be “one of the family” and be unwilling to deprive a loved one of food; these factors may undermine simple-minded “eat less and exercise more!” approaches to management of obesity; they must be identified and acknowledged by both client and therapist for long-term resolution of obesity.
The presence of body fat in sufficient excess to compromise normal physiologic function or predispose to metabolic, surgical, and/or mechanical problems
PATHOPHYSIOLOGY
Animal factors—although breed predispositions have been reported, any animal may become obese; inactivity is an important risk factor in both dogs and cats, as are increasing age and neutering.
Dietary factors—no specific diet other than a surfeit of “table scraps” and “treats” has been shown to increase risk in dogs; in cats, consumption of “high-fat” diets reportedly increases risk.
Feeding management—many animals are overfed; reasons for excessive food consumption include ignorance of proper feeding practices, inappropriately generous feeding recommendations by manufacturers, emphasis on food palatability both by owners and manufacturers, and inadequate explanation by veterinarians of appropriate body condition for the pet and how to maintain it.
Owner factors—many owners of overweight pets are overweight themselves and engage in feeding as a social activity; clients also may consider their pet to be “one of the family” and be unwilling to deprive a loved one of food; these factors may undermine simple-minded “eat less and exercise more!” approaches to management of obesity; they must be identified and acknowledged by both client and therapist for long-term resolution of obesity.
Neutropenia
DEFINITION
Neutrophil count < 2900 neutrophils/mL in dogs and < 2500 neutrophils/mL in cats Can develop alone or as a component of pancytopenia Often accompanied by a left shift and toxic change (e.g., cytoplasmic basophilia, cytoplasmic vacuolation, Döhle bodies, and toxic granulation)
PATHOPHYSIOLOGY
Results from one of three mechanisms—(1) deficient neutrophil production in the bone marrow, (2) cells shifting from the circulating neutrophil pool to the marginal neutrophil pool in the blood, and (3) reduced neutrophil survival because of excessive tissue demand or immune-mediated destruction of cells
Most commonly associated with infection, because emigration of neutrophils from the blood into the tissues exceeds the rate at which the bone marrow can replace them.
Neutrophil count < 2900 neutrophils/mL in dogs and < 2500 neutrophils/mL in cats Can develop alone or as a component of pancytopenia Often accompanied by a left shift and toxic change (e.g., cytoplasmic basophilia, cytoplasmic vacuolation, Döhle bodies, and toxic granulation)
PATHOPHYSIOLOGY
Results from one of three mechanisms—(1) deficient neutrophil production in the bone marrow, (2) cells shifting from the circulating neutrophil pool to the marginal neutrophil pool in the blood, and (3) reduced neutrophil survival because of excessive tissue demand or immune-mediated destruction of cells
Most commonly associated with infection, because emigration of neutrophils from the blood into the tissues exceeds the rate at which the bone marrow can replace them.
Nephrolithiasis
DEFINITION
Nephroliths—uroliths (i.e., polycrystalline concretions or calculi) located in the renal pelvis or collecting diverticula of the kidney
Nephroliths or nephrolith fragments may pass into the ureters (ureteroliths).
Nephroliths that are not infected, not causing obstruction or clinical signs, and not progressively enlarging are termed inactive.
PATHOPHYSIOLOGY
Nephroliths can obstruct the renal pelvis or ureter, predispose to pyelonephritis, and result in compressive injury of the renal parenchyma leading to renal failure; see chapters on the different urolith types for pathophysiology of urolithiasis; in cats, nephroliths composed of blood clots mineralized with calcium phosphate can form secondarily to chronic renal hematuria.
Nephroliths—uroliths (i.e., polycrystalline concretions or calculi) located in the renal pelvis or collecting diverticula of the kidney
Nephroliths or nephrolith fragments may pass into the ureters (ureteroliths).
Nephroliths that are not infected, not causing obstruction or clinical signs, and not progressively enlarging are termed inactive.
PATHOPHYSIOLOGY
Nephroliths can obstruct the renal pelvis or ureter, predispose to pyelonephritis, and result in compressive injury of the renal parenchyma leading to renal failure; see chapters on the different urolith types for pathophysiology of urolithiasis; in cats, nephroliths composed of blood clots mineralized with calcium phosphate can form secondarily to chronic renal hematuria.
Nasal and Nasopharyngeal Polyps
OVERVIEW
Protruding, pink, polypoid growths (benign) arising from the mucous membranes
Nasal—originate from the nasal mucosa in dogs and cats
Nasopharyngeal—originate from the base of the eustachian tube in cats; may extend into the external ear canal, middle, pharynx, and nasal cavity
Protruding, pink, polypoid growths (benign) arising from the mucous membranes
Nasal—originate from the nasal mucosa in dogs and cats
Nasopharyngeal—originate from the base of the eustachian tube in cats; may extend into the external ear canal, middle, pharynx, and nasal cavity
Myocarditis
DEFINITION
Inflammation of the heart muscle, often caused by infectious agents affecting the myocytes, interstitium, vascular elements, or pericardium.
Viral, bacterial, rickettsial, fungal, and protozoal diseases are all associated with myocardial inflammation (i.e., myocarditis).
Pharmacologic agents (e.g., doxorubicin) can also be causative.
PATHOPHYSIOLOGY
Mechanisms—toxin production, direct invasion of myocardial tissue, and immune-mediated myocardial damage; vasculitis associated with systemic disease; allergic reactions and direct myocyte damage caused by pharmacologic agents. Protozoa (e.g., Trypanosoma cruzi) lead to granulomatous myocarditis; viral myocarditis is associated with cell-mediated immunologic reactions.
Myocardial involvement may be focal or diffuse. Clinical manifestations depend on the extent of the lesions. Diffuse, severe involvement may lead to global myocardial damage and CHF; discrete lesions involving the conduction system may cause profound arrhythmias.
Inflammation of the heart muscle, often caused by infectious agents affecting the myocytes, interstitium, vascular elements, or pericardium.
Viral, bacterial, rickettsial, fungal, and protozoal diseases are all associated with myocardial inflammation (i.e., myocarditis).
Pharmacologic agents (e.g., doxorubicin) can also be causative.
PATHOPHYSIOLOGY
Mechanisms—toxin production, direct invasion of myocardial tissue, and immune-mediated myocardial damage; vasculitis associated with systemic disease; allergic reactions and direct myocyte damage caused by pharmacologic agents. Protozoa (e.g., Trypanosoma cruzi) lead to granulomatous myocarditis; viral myocarditis is associated with cell-mediated immunologic reactions.
Myocardial involvement may be focal or diffuse. Clinical manifestations depend on the extent of the lesions. Diffuse, severe involvement may lead to global myocardial damage and CHF; discrete lesions involving the conduction system may cause profound arrhythmias.
Mycoplasma
DEFINITION
Class Mollicutes (Latin, mollis, “soft”; cutis, “skin”); > 80 genera; three families: mycoplasmas, T-mycoplasmas or ureaplasmas, and acholeplasmas
Smallest (0.2–0.3 mm) and simplest procaryotic cells capable of self-replication
Fastidious, facultative anaerobic, gramnegative rods
Lack a cell wall; thus plastic, highly pleomorphic, and sensitive to lysis by osmotic shock, detergents, alcohols, and specific antibody plus complement; enclosed by a trilayered cell membrane built of amphipathic lipids (phospholipids, glycolipids, lipoglycans, sterols) and proteins; most require sterols for growth.
Different from wall-defective or wall-less L-form bacteria, which can revert to the normal cell wall strain
Reproduce by binary fission; genome replication not necessarily synchronized with cell division, resulting in budding forms and chains of beads
Ubiquitous in nature as parasites, commensals, or saprophytes in animals, plants, and insects; many are pathogens of humans, animals, plants, and insects.
Class Mollicutes (Latin, mollis, “soft”; cutis, “skin”); > 80 genera; three families: mycoplasmas, T-mycoplasmas or ureaplasmas, and acholeplasmas
Smallest (0.2–0.3 mm) and simplest procaryotic cells capable of self-replication
Fastidious, facultative anaerobic, gramnegative rods
Lack a cell wall; thus plastic, highly pleomorphic, and sensitive to lysis by osmotic shock, detergents, alcohols, and specific antibody plus complement; enclosed by a trilayered cell membrane built of amphipathic lipids (phospholipids, glycolipids, lipoglycans, sterols) and proteins; most require sterols for growth.
Different from wall-defective or wall-less L-form bacteria, which can revert to the normal cell wall strain
Reproduce by binary fission; genome replication not necessarily synchronized with cell division, resulting in budding forms and chains of beads
Ubiquitous in nature as parasites, commensals, or saprophytes in animals, plants, and insects; many are pathogens of humans, animals, plants, and insects.
Metritis
OVERVIEW
Bacterial uterine infection that develops in the immediate postpartum period (usually within the first week); occasionally develops after an abortion or non-sterile artificial insemination—rarely after breeding
Bacteria—ascend through the open cervix to the uterus; a large, flaccid, postpartum uterus provides an ideal environment for growth; gram-negative (e.g., Escherichia coli) commonly isolated
Potentially life-threatening infection; may lead to septic shock
Directly affects uterus; systemic involvement as sepsis develops
Can become chronic and lead to infertility
Bacterial uterine infection that develops in the immediate postpartum period (usually within the first week); occasionally develops after an abortion or non-sterile artificial insemination—rarely after breeding
Bacteria—ascend through the open cervix to the uterus; a large, flaccid, postpartum uterus provides an ideal environment for growth; gram-negative (e.g., Escherichia coli) commonly isolated
Potentially life-threatening infection; may lead to septic shock
Directly affects uterus; systemic involvement as sepsis develops
Can become chronic and lead to infertility
Meningioma
OVERVIEW
Tumors of the meninges most commonly found intracranially over the cerebrum
Usually solitary masses; occasionally multiple
May occur as plaque-like masses on the floor of the calvaria, paranasally, or (rarely) in a retrobulbar location in dogs more than cats; also develop along the spinal cord but less frequently and with an intradural, extramedullary predilection site
Compress the adjacent tissue, causing vasogenic edema
Dogs—tends to be more invasive into brain parenchyma or surrounding vasculature
Tumors of the meninges most commonly found intracranially over the cerebrum
Usually solitary masses; occasionally multiple
May occur as plaque-like masses on the floor of the calvaria, paranasally, or (rarely) in a retrobulbar location in dogs more than cats; also develop along the spinal cord but less frequently and with an intradural, extramedullary predilection site
Compress the adjacent tissue, causing vasogenic edema
Dogs—tends to be more invasive into brain parenchyma or surrounding vasculature
Mastitis
OVERVIEW
Bacterial infection of one or more lactating glands
Result of ascending infection, trauma to the gland, or hematogenous spread
Escherichia coli, Staphylococci, and B-hemolytic Streptococci—most commonly involved
Potentially life-threatening infection; may lead to septic shock
Sepsis—direct effect on mammary glands with systemic involvement
Bacterial infection of one or more lactating glands
Result of ascending infection, trauma to the gland, or hematogenous spread
Escherichia coli, Staphylococci, and B-hemolytic Streptococci—most commonly involved
Potentially life-threatening infection; may lead to septic shock
Sepsis—direct effect on mammary glands with systemic involvement
Malassezia Dermatitis
OVERVIEW
Malassezia pachydermatis (syn. Pityrosporumcanis)—yeast; normal commensal of the skin, ears, and mucocutaneous areas; can overgrow and cause dermatitis, cheilitis, and otitis in dogs
Yeast numbers in diseased areas are usually excessive, although this is a variable finding.
The causes of the transformation from harmless commensal to pathogen are poorly understood but seem related to allergy, seborrheic conditions, and possibly congenital and hormonal factors.
Malassezia dermatitis and Malassezia-associated seborrheic dermatitis—common in all geographic regions of the world
Cats-similar disease, but rare
Malassezia pachydermatis (syn. Pityrosporumcanis)—yeast; normal commensal of the skin, ears, and mucocutaneous areas; can overgrow and cause dermatitis, cheilitis, and otitis in dogs
Yeast numbers in diseased areas are usually excessive, although this is a variable finding.
The causes of the transformation from harmless commensal to pathogen are poorly understood but seem related to allergy, seborrheic conditions, and possibly congenital and hormonal factors.
Malassezia dermatitis and Malassezia-associated seborrheic dermatitis—common in all geographic regions of the world
Cats-similar disease, but rare
Saturday, March 26, 2011
Magnesium, Hypermagnesemia
DEFINITION
Dogs—serum magnesium >2.51 mg/dL
Cats—serum magnesium >2.3 mg/dL
PATHOPHYSIOLOGY
Magnesium—second only to potassium as the most abundant intracellular cation; most is found in bone and muscle; required for many metabolic functions
Magnesium is an important cofactor in the sodium-potassium ATPase pump that maintains an electrical gradient across membranes and thus plays an important role in the activity of electrically excitable tissues.
Interference with the electrical gradient can change resting membrane potentials; repolarization disturbances result in neuromuscular and cardiac abnormalities.
Magnesium homeostasis is largely controlled by renal elimination; any condition that severely lowers the glomerular filtration rate can elicit hypermagnesemia.
High magnesium concentration impairs transmission of nerve impulses and decreases the postsynaptic response at the neuromuscular junction.
Magnesium has been called nature's calcium blocker; the most serious complications of hypermagnesemia result from calcium antagonism in the cardiac conduction system.
Dogs—serum magnesium >2.51 mg/dL
Cats—serum magnesium >2.3 mg/dL
PATHOPHYSIOLOGY
Magnesium—second only to potassium as the most abundant intracellular cation; most is found in bone and muscle; required for many metabolic functions
Magnesium is an important cofactor in the sodium-potassium ATPase pump that maintains an electrical gradient across membranes and thus plays an important role in the activity of electrically excitable tissues.
Interference with the electrical gradient can change resting membrane potentials; repolarization disturbances result in neuromuscular and cardiac abnormalities.
Magnesium homeostasis is largely controlled by renal elimination; any condition that severely lowers the glomerular filtration rate can elicit hypermagnesemia.
High magnesium concentration impairs transmission of nerve impulses and decreases the postsynaptic response at the neuromuscular junction.
Magnesium has been called nature's calcium blocker; the most serious complications of hypermagnesemia result from calcium antagonism in the cardiac conduction system.
Hypertension, Systemic
DEFINITION
Sustained elevation in systolic or diastolic (or both) arterial blood pressure
PATHOPHYSIOLOGY
Blood pressure is determined by cardiac output and systemic vascular resistance; cardiac output determined by heart rate and stroke volume; systemic arterial blood pressure regulation depends on integration of complex mechanisms within the central and peripheral nervous systems, renal and cardiac tissues, and humoral factors, which synergistically affect cardiac output and peripheral vascular resistance.
Baroreceptors in the carotid sinus and aortic arch respond to changes in blood pressure; a fall in blood pressure increases sympathetic discharge, causing vasoconstriction and increased cardiac contractility and heart rate to return blood pressure to normal, humoral substances that modulate blood pressure include catecholamines, vasopressin, kinins, renin, angiotensin, aldosterone, prostaglandins, and atrial natriuretic peptide; the renin-angiotensin-aldosterone system is probably the most important component.
Hypertension—primary (e.g., essential or idiopathic) or secondary to an underlying disease process; secondary hypertension is more common in veterinary medicine; cause of primary hypertension is not fully understood but some have a hereditary component.
Sustained elevation in systolic or diastolic (or both) arterial blood pressure
PATHOPHYSIOLOGY
Blood pressure is determined by cardiac output and systemic vascular resistance; cardiac output determined by heart rate and stroke volume; systemic arterial blood pressure regulation depends on integration of complex mechanisms within the central and peripheral nervous systems, renal and cardiac tissues, and humoral factors, which synergistically affect cardiac output and peripheral vascular resistance.
Baroreceptors in the carotid sinus and aortic arch respond to changes in blood pressure; a fall in blood pressure increases sympathetic discharge, causing vasoconstriction and increased cardiac contractility and heart rate to return blood pressure to normal, humoral substances that modulate blood pressure include catecholamines, vasopressin, kinins, renin, angiotensin, aldosterone, prostaglandins, and atrial natriuretic peptide; the renin-angiotensin-aldosterone system is probably the most important component.
Hypertension—primary (e.g., essential or idiopathic) or secondary to an underlying disease process; secondary hypertension is more common in veterinary medicine; cause of primary hypertension is not fully understood but some have a hereditary component.
Histoplasmosis
DEFINITION
A systemic fungal infection cause by Histoplasma capsulatum
PATHOPHYSIOLOGY
Mycelial form grows in bird manure or organically enriched soil.
Mycelium—produces infectious spores (microconidia); inhaled into the terminal airways
Spores—germinate in the lungs; develop into yeasts, which are phagocytized by macrophages
Macrophages—distribute the organisms throughout the body
Ingested organisms may directly infect the intestinal tract.
Immune response—determines whether disease develops; affected animals often develop transient, asymptomatic infection.
A systemic fungal infection cause by Histoplasma capsulatum
PATHOPHYSIOLOGY
Mycelial form grows in bird manure or organically enriched soil.
Mycelium—produces infectious spores (microconidia); inhaled into the terminal airways
Spores—germinate in the lungs; develop into yeasts, which are phagocytized by macrophages
Macrophages—distribute the organisms throughout the body
Ingested organisms may directly infect the intestinal tract.
Immune response—determines whether disease develops; affected animals often develop transient, asymptomatic infection.
Hepatitis, Infectious Canine
OVERVIEW
Viral disease of dogs and other Canidae caused by canine adenovirus 1 (CAV-1), which is serologically homogeneous and antigenically distinct from CAV-2, the respiratory virus
Infection—targets parenchymal organs (especially liver), eyes, and endothelium
Oronasal exposure—leads to tonsillar localization and viremia within 4–8 days; saliva and feces infectious during initial viremia
Virus—initially localizes in Kupffer cells and endothelium; replicates in Kupffer cells; release and damage of adjacent hepatocytes and massive viremia; with adequate antibody response, cleared from most organs within 10–14 days; persists in the renal tubules where it may be excreted in urine for 6–9 months
Chronic hepatitis—may develop with only a partial neutralizing antibody response
Cytotoxic ocular injury—leads to anterior uveitis and the classic hepatitis blue eye
Viral disease of dogs and other Canidae caused by canine adenovirus 1 (CAV-1), which is serologically homogeneous and antigenically distinct from CAV-2, the respiratory virus
Infection—targets parenchymal organs (especially liver), eyes, and endothelium
Oronasal exposure—leads to tonsillar localization and viremia within 4–8 days; saliva and feces infectious during initial viremia
Virus—initially localizes in Kupffer cells and endothelium; replicates in Kupffer cells; release and damage of adjacent hepatocytes and massive viremia; with adequate antibody response, cleared from most organs within 10–14 days; persists in the renal tubules where it may be excreted in urine for 6–9 months
Chronic hepatitis—may develop with only a partial neutralizing antibody response
Cytotoxic ocular injury—leads to anterior uveitis and the classic hepatitis blue eye
Hepatic Amyloid
OVERVIEW
Amyloidoses—disorders that share the common feature of pathologic deposition of an extracellular insoluble fibrillar proteinaceous matrix
Amyloid—accumulates secondary to inflammatory or lymphoproliferative disorders or as a familial tendency
Dogs and cats—usually reactive or secondary amyloidosis; underlying primary inflammatory disorder common
Associated familial disorders—certain kindreds of dogs and cats
Multiple organs commonly involved; clinical signs usually owing to renal or liver involvement
Liver involvement—may be insidious; may lead to high liver enzymes, severe hepatomegaly, coagulopathy, liver rupture leading to hemoabdomen, and/or liver failure
Amyloidoses—disorders that share the common feature of pathologic deposition of an extracellular insoluble fibrillar proteinaceous matrix
Amyloid—accumulates secondary to inflammatory or lymphoproliferative disorders or as a familial tendency
Dogs and cats—usually reactive or secondary amyloidosis; underlying primary inflammatory disorder common
Associated familial disorders—certain kindreds of dogs and cats
Multiple organs commonly involved; clinical signs usually owing to renal or liver involvement
Liver involvement—may be insidious; may lead to high liver enzymes, severe hepatomegaly, coagulopathy, liver rupture leading to hemoabdomen, and/or liver failure
Globulin
DEFINITION
Heterogenous group of proteins; includes immunoglobulins, clotting factors, acute-phase proteins, and complement proteins
Hyperglobulinemia—high serum globulin concentration
Hypoglobulinemia—low serum globulin concentration
Gammopathy—any abnormality in the concentration of immunoglobulins
PATHOPHYSIOLOGY
Hyperglobulinemia—from increased production of immunoglobulins and hepatic synthesis of acute-phase proteins; falsely increased by dehydration; classified as either polyclonal or monoclonal; may result in hyperviscosity syndrome and impaired immune function
Polyclonal gammopathies—from production of immunoglobulins by several different cell lines; usually in response to persistent antigenic stimulation
Monoclonal gammopathies—from synthesis of one type of immunoglobulin by a single clone of cells; proliferation may be associated with lymphoid hyperplasia or neoplasia.
Hypoglobulinemia—from either impaired synthesis or extracorporeal globulin loss
Impaired synthesis—results in immunodeficiency syndromes; characterized by chronic infection and unthrifty appearance
Extracorporeal loss—commonly from gastrointestinal disease; also secondary to blood loss; rarely from hepatic insufficiency and renal losses
Heterogenous group of proteins; includes immunoglobulins, clotting factors, acute-phase proteins, and complement proteins
Hyperglobulinemia—high serum globulin concentration
Hypoglobulinemia—low serum globulin concentration
Gammopathy—any abnormality in the concentration of immunoglobulins
PATHOPHYSIOLOGY
Hyperglobulinemia—from increased production of immunoglobulins and hepatic synthesis of acute-phase proteins; falsely increased by dehydration; classified as either polyclonal or monoclonal; may result in hyperviscosity syndrome and impaired immune function
Polyclonal gammopathies—from production of immunoglobulins by several different cell lines; usually in response to persistent antigenic stimulation
Monoclonal gammopathies—from synthesis of one type of immunoglobulin by a single clone of cells; proliferation may be associated with lymphoid hyperplasia or neoplasia.
Hypoglobulinemia—from either impaired synthesis or extracorporeal globulin loss
Impaired synthesis—results in immunodeficiency syndromes; characterized by chronic infection and unthrifty appearance
Extracorporeal loss—commonly from gastrointestinal disease; also secondary to blood loss; rarely from hepatic insufficiency and renal losses
Gastroduodenal Ulcer Disease
DEFINITION
Erosive lesions that extend through the mucosa and into the muscularis mucosa
PATHOPHYSIOLOGY
Gastroduodenal ulcers result from single or multiple factors altering, damaging, or over-whelming the normal defense and repair mechanisms of the “gastric mucosal barrier.”
Factors that make up the “gastric mucosal barrier” and protect the stomach from ulcer formation include the mucus-bicarbonate layer over the epithelial cells, the gastric epithelial cells, gastric mucosal blood flow, epithelial cell restitution and repair, and prostaglandins produced by the gastrointestinal tract.
Factors that cause mucosal barrier damage and predispose to gastroduodenal ulcer formation include inhibiting the epithelial cell's ability to repair, decreasing the mucosal blood supply, and/or increasing gastric acid secretion.
The risk of gastroduodenal ulcer formation increases with the number of insults to the “gastric mucosal barrier.”
Erosive lesions that extend through the mucosa and into the muscularis mucosa
PATHOPHYSIOLOGY
Gastroduodenal ulcers result from single or multiple factors altering, damaging, or over-whelming the normal defense and repair mechanisms of the “gastric mucosal barrier.”
Factors that make up the “gastric mucosal barrier” and protect the stomach from ulcer formation include the mucus-bicarbonate layer over the epithelial cells, the gastric epithelial cells, gastric mucosal blood flow, epithelial cell restitution and repair, and prostaglandins produced by the gastrointestinal tract.
Factors that cause mucosal barrier damage and predispose to gastroduodenal ulcer formation include inhibiting the epithelial cell's ability to repair, decreasing the mucosal blood supply, and/or increasing gastric acid secretion.
The risk of gastroduodenal ulcer formation increases with the number of insults to the “gastric mucosal barrier.”
Fever
DEFINITION
Higher than normal body temperature because of a changed thermoregulatory set point in the hypothalamus; normal body temperature in dogs and cats is 100.2–102.8°F (37.8–39.3°C) Fever of unknown origin (FUO)—at least 103.5°F (39.7°C) on at least four occasions over a 14-day period and illness of 14 days' duration without an obvious cause
PATHOPHYSIOLOGY
Exogenous or endogenous pyrogens cause release of endogenous substances (e.g., interleukin-1 and prostaglandins) that reset the hypothalamic thermoregulatory center to a higher temperature, activating appropriate physiologic responses to raise the body temperature to this new set point. Physiologic consequences include increased metabolic demands, muscle catabolism, bone marrow suppression, heightened fluid and caloric requirements, and possibly disseminated intravascular coagulation (DIC) and shock.
Higher than normal body temperature because of a changed thermoregulatory set point in the hypothalamus; normal body temperature in dogs and cats is 100.2–102.8°F (37.8–39.3°C) Fever of unknown origin (FUO)—at least 103.5°F (39.7°C) on at least four occasions over a 14-day period and illness of 14 days' duration without an obvious cause
PATHOPHYSIOLOGY
Exogenous or endogenous pyrogens cause release of endogenous substances (e.g., interleukin-1 and prostaglandins) that reset the hypothalamic thermoregulatory center to a higher temperature, activating appropriate physiologic responses to raise the body temperature to this new set point. Physiologic consequences include increased metabolic demands, muscle catabolism, bone marrow suppression, heightened fluid and caloric requirements, and possibly disseminated intravascular coagulation (DIC) and shock.
Esophageal Diverticula Basics
OVERVIEW
An abnormal, circumscribed enlargement or dilatation of the esophagus producing a region for accumulation of ingesta
Two types of esophageal diverticula exist.
Pulsion (true) diverticula are associated with high intraluminal pressure leading to mucosal herniation through the muscularis; histologically, the cellular remnants are epithelium and connective tissue.
Traction (false) diverticula are caused by the outward pull of connective tissue on the esophagus; all four cell layers (mucosa, submucosa,muscularis, and adventitia) remain intact.
Approximately 50–70% of diverticula (especially epiphrenic pulsion types) are associated with other lesions of the esophagus ordiaphragm.
Organ systems affected include the gastrointestinal (regurgitation), musculoskeletal (weight loss), and respiratory (aspiration pneumonia).
An abnormal, circumscribed enlargement or dilatation of the esophagus producing a region for accumulation of ingesta
Two types of esophageal diverticula exist.
Pulsion (true) diverticula are associated with high intraluminal pressure leading to mucosal herniation through the muscularis; histologically, the cellular remnants are epithelium and connective tissue.
Traction (false) diverticula are caused by the outward pull of connective tissue on the esophagus; all four cell layers (mucosa, submucosa,muscularis, and adventitia) remain intact.
Approximately 50–70% of diverticula (especially epiphrenic pulsion types) are associated with other lesions of the esophagus ordiaphragm.
Organ systems affected include the gastrointestinal (regurgitation), musculoskeletal (weight loss), and respiratory (aspiration pneumonia).
Thursday, March 24, 2011
Dysphagia
DEFINITION
Difficulty swallowing, resulting from the inability to prehend, form, and move a bolus of food through the oropharynx into the esophagus
Esophageal dysphagia is discussed under the topics Megaesophagus and Regurgitation.
PATHOPHYSIOLOGY
Swallowing difficulties can be caused by mechanical obstruction of the oral cavity or pharynx, neuromuscular dysfunction resulting in weak or uncoordinated swallowing movements, or pain associated with prehension, mastication, or swallowing.
Oral dysphagia refers to difficulty with the voluntary components of swallowing—prehending and forming a bolus of food at the base of the tongue
Pharyngeal dysphagia occurs when there is a malfunction of the involuntary movement of the food bolus through the oropharynx.
Cricopharyngeal dysphagia refers to abnormal movement of the food bolus from the pharynx through the cricopharyngeus muscle, caused by either failure of the cricopharyngeus to relax (cricopharyngeal achalasia) or asynchrony between pharyngeal contractions and cricopharyngeus opening (cricopharyngeal asynchrony).
Deglutition is coordinated by the swallowing center in the brainstem; sensory afferents are transmitted to the swallowing center by CNs V and IX.
Motor efferents responsible for swallowing are carried by CN V, VII, XII (prehension and mastication) and IX and X (pharyngeal contraction); disorders in any of these areas may result in dysphagia.
Difficulty swallowing, resulting from the inability to prehend, form, and move a bolus of food through the oropharynx into the esophagus
Esophageal dysphagia is discussed under the topics Megaesophagus and Regurgitation.
PATHOPHYSIOLOGY
Swallowing difficulties can be caused by mechanical obstruction of the oral cavity or pharynx, neuromuscular dysfunction resulting in weak or uncoordinated swallowing movements, or pain associated with prehension, mastication, or swallowing.
Oral dysphagia refers to difficulty with the voluntary components of swallowing—prehending and forming a bolus of food at the base of the tongue
Pharyngeal dysphagia occurs when there is a malfunction of the involuntary movement of the food bolus through the oropharynx.
Cricopharyngeal dysphagia refers to abnormal movement of the food bolus from the pharynx through the cricopharyngeus muscle, caused by either failure of the cricopharyngeus to relax (cricopharyngeal achalasia) or asynchrony between pharyngeal contractions and cricopharyngeus opening (cricopharyngeal asynchrony).
Deglutition is coordinated by the swallowing center in the brainstem; sensory afferents are transmitted to the swallowing center by CNs V and IX.
Motor efferents responsible for swallowing are carried by CN V, VII, XII (prehension and mastication) and IX and X (pharyngeal contraction); disorders in any of these areas may result in dysphagia.
Distemper - Dogs
DEFINITION
An acute to subacute contagious febrile and often fatal disease with respiratory, gastrointestinal, and CNS manifestations
Caused by CDV, a morbillivirus in the Paramyxoviridae family
Affects many different species of the order Carnivora; mortality rate varies greatly among species.
PATHOPHYSIOLOGY
Natural route of infection—airborne and droplet exposure; from the nasal cavity, pharynx, and lungs, macrophages carry the virus to local lymph nodes, where virus replication occurs; within 1 week, virtually all lymphatic tissues become infected; spreads via viremia to the surface epithelium of respiratory, gastrointestinal, and urogenital tracts and to the CNS
Fever for 1–2 days and lymphopenia may be the only findings during initial period; further development depends on the virus strain and the immune response.
Strong cellular and humoral immune response—may remain subclinical
Weak immune response—subacute infection; may survive longer
Failure of immune response—acute death within 2–4 weeks after infection; convulsions and other CNS disturbances frequent causes of death
An acute to subacute contagious febrile and often fatal disease with respiratory, gastrointestinal, and CNS manifestations
Caused by CDV, a morbillivirus in the Paramyxoviridae family
Affects many different species of the order Carnivora; mortality rate varies greatly among species.
PATHOPHYSIOLOGY
Natural route of infection—airborne and droplet exposure; from the nasal cavity, pharynx, and lungs, macrophages carry the virus to local lymph nodes, where virus replication occurs; within 1 week, virtually all lymphatic tissues become infected; spreads via viremia to the surface epithelium of respiratory, gastrointestinal, and urogenital tracts and to the CNS
Fever for 1–2 days and lymphopenia may be the only findings during initial period; further development depends on the virus strain and the immune response.
Strong cellular and humoral immune response—may remain subclinical
Weak immune response—subacute infection; may survive longer
Failure of immune response—acute death within 2–4 weeks after infection; convulsions and other CNS disturbances frequent causes of death
Capillariasis
Capillaria plica is a parasite that invades the mucosa or submucosa of the bladder or (rarely) the renal pelvis and ureter, causing a mild inflammatory response.
C. plica in dogs and cats and C. feliscati in cats have been uncommonly associated with signs of lower urinary tract disease.
First stage in life cycle of C. plica is passage of bipolar ova in urine. After earthworms ingest embryonated ova, the parasite develops into the infective stage. Ingestion of infective earthworm results in a patent infection in dogs in 58–88 days.
Details of life cycle of C. feliscati are poorly understood.
C. plica in dogs and cats and C. feliscati in cats have been uncommonly associated with signs of lower urinary tract disease.
First stage in life cycle of C. plica is passage of bipolar ova in urine. After earthworms ingest embryonated ova, the parasite develops into the infective stage. Ingestion of infective earthworm results in a patent infection in dogs in 58–88 days.
Details of life cycle of C. feliscati are poorly understood.
Babesiosis
RBC destruction and anemia caused by Babesia spp. of intracellular protozoa
B. cani—a large (4–7 mm-long), pear-shaped parasite of canine RBCs; in the U.S., strains generally cause mild or inapparent disease in adults (unless immunosuppressed), but severe disease in pups; South African strains cause severe disease and death in some adult dogs.
B. gibsoni—a small (2.5 mm), ring-shaped organism that causes severe disease in most infected adult dogs; rare in the U.S. but common in Africa and Asia; organisms can be difficult to see in stained blood films.
B. felis—a very small (1 mm), ring-shaped organism that occurs in cats in Africa and southern Asia; of similar size and morphology to Cytauxzoon felis, which occurs in cats in the U.S.
B. cani—a large (4–7 mm-long), pear-shaped parasite of canine RBCs; in the U.S., strains generally cause mild or inapparent disease in adults (unless immunosuppressed), but severe disease in pups; South African strains cause severe disease and death in some adult dogs.
B. gibsoni—a small (2.5 mm), ring-shaped organism that causes severe disease in most infected adult dogs; rare in the U.S. but common in Africa and Asia; organisms can be difficult to see in stained blood films.
B. felis—a very small (1 mm), ring-shaped organism that occurs in cats in Africa and southern Asia; of similar size and morphology to Cytauxzoon felis, which occurs in cats in the U.S.
Alopecia
DEFINITION
Common disorder
Characterized by a complete or partial lack of hair in areas where it is normally present
May be associated with a multifactorial cause
May be the primary problem or only a secondary phenomenon
Common disorder
Characterized by a complete or partial lack of hair in areas where it is normally present
May be associated with a multifactorial cause
May be the primary problem or only a secondary phenomenon
Actinomycosis
OVERVIEW
An infectious disease caused by gram-positive, branching, pleomorphic, rod-shaped bacteria of the genus Actinomyces
A. viscosus—most commonly identified; survives in microaerophilic or anaerobic conditions
Rarely found as the single bacterial agent in a lesion; more commonly, it is a component of a polymicrobial infection.
There may be synergism between Actinomyces and other organisms.
SIGNALMENT
Dogs and cats
Especially common in young male dogs of sporting breeds
SIGNS
Infections—usually localized; may be disseminated; cervicofacial area commonly involved
Cutaneous swellings or abscesses with draining tracts—yellow granules (“sulfur granules”) may be seen in associated exudates.
Pain and fever
Exudative pleural or peritoneal effusions
Retroperitonitis—in one study, Actinomyces was identified in 3 of 34 affected dogs
Osteomyelitis of vertebrae or long bones—probably secondary to extension of cutaneous infection; lameness or a swollen extremity may develop
Motor and sensory deficits—reported with spinal cord compression by granulomas
An infectious disease caused by gram-positive, branching, pleomorphic, rod-shaped bacteria of the genus Actinomyces
A. viscosus—most commonly identified; survives in microaerophilic or anaerobic conditions
Rarely found as the single bacterial agent in a lesion; more commonly, it is a component of a polymicrobial infection.
There may be synergism between Actinomyces and other organisms.
SIGNALMENT
Dogs and cats
Especially common in young male dogs of sporting breeds
SIGNS
Infections—usually localized; may be disseminated; cervicofacial area commonly involved
Cutaneous swellings or abscesses with draining tracts—yellow granules (“sulfur granules”) may be seen in associated exudates.
Pain and fever
Exudative pleural or peritoneal effusions
Retroperitonitis—in one study, Actinomyces was identified in 3 of 34 affected dogs
Osteomyelitis of vertebrae or long bones—probably secondary to extension of cutaneous infection; lameness or a swollen extremity may develop
Motor and sensory deficits—reported with spinal cord compression by granulomas
Tuesday, March 22, 2011
Actinomycosis
OVERVIEW
An infectious disease caused by gram-positive, branching, pleomorphic, rod-shaped bacteria of the genus Actinomyces
A. viscosus—most commonly identified; survives in microaerophilic or anaerobic conditions
Rarely found as the single bacterial agent in a lesion; more commonly, it is a component of a polymicrobial infection.
There may be synergism between Actinomyces and other organisms.
An infectious disease caused by gram-positive, branching, pleomorphic, rod-shaped bacteria of the genus Actinomyces
A. viscosus—most commonly identified; survives in microaerophilic or anaerobic conditions
Rarely found as the single bacterial agent in a lesion; more commonly, it is a component of a polymicrobial infection.
There may be synergism between Actinomyces and other organisms.
Acidosis, Metabolic
Definition
Primary decrease in plasma bicarbonate concentration ([HCO3-]; dogs, <18 mEq/L; cats, <16 mEq/L) with high hydrogen ion concentration ([H+]), low pH, and a compensatory decrease in carbon dioxide tension (Pco2)
Primary decrease in plasma bicarbonate concentration ([HCO3-]; dogs, <18 mEq/L; cats, <16 mEq/L) with high hydrogen ion concentration ([H+]), low pH, and a compensatory decrease in carbon dioxide tension (Pco2)
Abscessation
DEFINITION
An abscess is a localized collection of purulent exudate contained within a cavity.
PATHOPHYSIOLOGY
Bacteria are often inoculated under the skin via a puncture wound; the wound surface then seals.
When bacteria and/or foreign objects persist in the tissue, purulent exudate forms and collects.
Accumulation of purulent exudate—if not quickly resorbed or discharged to an external surface, stimulates formation of a fibrous capsule; may eventually lead to abscess rupture
Prolonged delay of evacuation—formation of a fibrous abscess wall; to heal, the cavity must be filled with granulation tissue from which the causative agent may not be totally eliminated; may lead to chronic or intermittent discharge of exudate from a draining sinus tract
An abscess is a localized collection of purulent exudate contained within a cavity.
PATHOPHYSIOLOGY
Bacteria are often inoculated under the skin via a puncture wound; the wound surface then seals.
When bacteria and/or foreign objects persist in the tissue, purulent exudate forms and collects.
Accumulation of purulent exudate—if not quickly resorbed or discharged to an external surface, stimulates formation of a fibrous capsule; may eventually lead to abscess rupture
Prolonged delay of evacuation—formation of a fibrous abscess wall; to heal, the cavity must be filled with granulation tissue from which the causative agent may not be totally eliminated; may lead to chronic or intermittent discharge of exudate from a draining sinus tract
Abortion
DEFINITION
- Abortion—expulsion of one or more live or dead fetuses that cannot sustain extrauterine life
- Pregnancy loss—all pregnancy wastage, including embryonic death, reabsorption of early fetal losses, mummification, abortion, and dystocia
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