Bacterial CV Infections Flashcards
What are the body’s immune defenses that help prevent CV infections?
Innate Defenses
1. Phagocytic cells (macrophages, PMNs), especially in the spleen and liver -> remove potential pathogens from vascular system
Adaptive Defenses
1. Macrophages (APCs)
2. Neutrophils and Macrophages (phagocytosis)
3. Lymphoid Tissue (Bcells = Ab prduction, Tcells = Thelper and cytotoxicity)
Transient Bacteremia
Bacteria that are normal flora of mucous membranes and enter the sterile circulatory and lymphatic systems sometimes during procedures like dentals or minor GI sx. In healthy animal, these bacteria are cleared rapidly (within minutes) and thus sepsis does not occur.
If body is unable to clear, sepsis/septicemia can occur and lead to severe disease.
What are the predisposing or risk factors (stressors) that allow for transient bacteremia to occur regularly and cause CV infection?
1. Immunodeficiencies
- neonates (failure of passive transfer or during waning maternal immunity)
- adults (iatrogenic: chemotherapy, radiation therapy; loss of key organs like splenectomy, organ which plays huge role in filtering the blood; immunosuppressive doses of corticosteroids)
2. Iatrogenic Manipulations
- dental extractions, endoscopic procedures of GIT, ucaths, IVCs, oral, abd, other invasive-type surgeries
- nosocomial infections of ICU pts
3. Nidus of Infection
- abscesses, migrating FBs, penetrating wounds, burns, colitis, gingivitis, stomatitis, pyoderma, UTIs, arthritis
4. Primary Infections (mostly viral)
- viruses that infect the immune system or compromise another body system that increases the chances of pathogenic microorganisms infiltrating
Transiet bacterermia = when microbes that are normal inhabitants of mucous membranes enter bloodstream/circulatory system, usually as a result of one of the above events
How do bacteria enter the CV system?
- direct inoculation (insect bites, contaminated needles, blood transfusions)
- spread from initial site of infection (via vascular system or lymphatics draining that site)
Infectious Valvular Endocarditis
Conditions: a pre-existing injury or functional abnormality of a heart valve with established platelet and fibrin deposition.
Pathogenesis: Bacteremia occurs (transient or infectious) -> the bacteria are able to adhere to the valve via the platelet/fibrin deposition
Sequelae: = emboli, multi-organ infarction, sudden death
Myocarditis
- cause
- example bacteria in cattle
- inflammation of cardiac muscle due to systemic infection with foci of infection within the heart
- Histophilus somni: in cattle, starts in the lungs but later damages myocytes (as well as the brain)
Traumatic Reticulopericarditis (“Hardware Disease”)
- secondary to trauma, sometimes secondary to systemic infection involving other serosal surfaces (e.g., Glasser’s Dz.)
- traumatic reticulopericarditis in cattle: ingestion of nail or wire -> migrates through reticulum and diaphragm into pericardial sac -> heart cannot contract properly -> heart failure, exercise intolerance, tachycardia due to decreased CO
- bacteria from ingested material enter and establish infection in pericardial sac
- polymicrobial infections w/. Trueperella pyogenes and Fusobacterium necrophorum frequently involved
What are 2 ways microbes can cause blood vessel infections
- direct vascular endothelial injury
- immune-complex deposition and inflammation (type III hypersensitivity)
Type III hypersensitivity is a type of immune response in which antigen-antibody complexes accumulate in the tissues and cause inflammation and tissue damage
Omphalitis
inflammation of the umbilicus in neonates involving umbilical aa. and/or vv.
- farm animals and horses
-enteric, inhabitants of mucosal surfaces, environmental contamininants
Omphalophlebitis
inflammation of the umbilical vein and infection can extend into fetal circulation to involve the liver
Navel ill
when septicemia develops from umbilical infections.
Sepsis vs Septicemia
Sepsis = when the immune response to septicemia becomes dysregulated and causes life-threatening organ dysfunction
Septicemia = presence of bacteria and toxins in the blood
Septic Shock vs Sepsis
Sepsis = I.S. responds in overwhelming/improper manner to infection
Septic Shock = subset of sepsis where the underlying circulatory, cellular and metabolic abnormalities are so extreme that they greatly increase the chances of mortaility
What bacteria are the typical causative agent of septicemia?
Enteobacterales: gram negative rod-shaped, facultative anaerobic, non spore-forming bacteria
- release endotoxins that induce inflammation/overdrive of immune system
- Escherichia coli, Salmonella enterica, Yersinia pestis
How is suspected septicemia sampled?
- goal is to collect 1-2 samples from the blood BEFORE starting abx
- collect 3rd sample at trough antimicrobial concentrations / when fever spikes
- must be sterile sample!!
- blood samples are placed into special blood culture media at time of sampling (EDTA KILLS bacteria! never use EDTA tubes)
How is septicemia clinically diagnosed in veterinary medicine?
confirmed presence (or suspicion) of infection together with 2-3 out of the 4 Systemic Inflammatory Response Syndrome (SIRS) criterias — temp., HR, RR, WBC % bands
- Dogs: 2/4 required
- Cats: 3/4 required
How is septicemia treated?
first treat empirically with broad-spectrum abx asap until culture results + supportive therapies to maintain perfusion to vital organs (IVF, nutritional support, system-specific therapy)
How can septicemia be prevented?
Prevent predisposing factors!
- peri-operative antimicrobials
- ensure good quality and quantity of colostrum
- vaccination
Source of Bacillus anthracis
- Inactive spores in soil that can survive in adverse environmental conditions (high temps / desiccation)
- Can survive for VERY long periods of time (> 100 years) in alkaline soil rich in calcium and nitrate
- Found worldwide in endemic areas (africa, asia, southern europe, australia, south america; occasional USA outbreaks)
- Brought to soil surface by flooding, excavation, subsidence or earthworms
How is B. anthracis transmitted?
Herbivores and carnivores: ingestion of spores or bacteria, or via mechanical transmission with biting insects
Humans: scratches or wounds, and inhalation
Virulence Factors of B. anthracis
1. Capsule that confers resistance to phagocytosis
2. Produces 3 types of toxins: protective antigen, edema factor, lethal factor
Protective Antigen allows for EF and LF to enter cells; EF allows for marked tissue edema via impairing PMN function, and LF causes inflammatory cascade resulting in death
Polymorphonuclear neutrophils (PMNs) are the most abundant innate immune cells in the body and act as the first defense against infections.
Different animals have different susceptiblity to Anthrax. Factors include:
- Infective dose
- Different signs to the toxins
**different clinical signs are observed in different species
Which species are most susceptible to Antrhax?
Cattle and sheep - fewer spores need to be ingested to develop infection
least = dogs/cats, with EF
How do the VFs of Anthrax affect cattle and sheep versus pigs?
Cattle and Sheep: resistant to EF while LF often causes septicemia -> sudden death w/ black tarry stool!
Pigs: sus to EF in pharynx while rarely affevted by LF -> death caused by asphyxiation (O2 deprivation) due to pharyngeal swelling
How does anthrax affect goats and horses?
less sus than cattle and sheep, and signs depend on mode of transmission (ingestion = colic/septicemia, local inocculation = mild local edema)
3 forms of anthrax disease observed in humans
What should you do if you suspect Anthrax infection?
report to state vet!!
never perform a necropsy!
What is Anaplasma marginale and its pathogenesis?
A tick-borne, reportable disease that affects CATTLE.
Vector = multiple tick species, including Dermacentor
tick bite -> bacteria enters bloodstream -> infects erythrocytes -> undergo phagocytosis by Mø in spleen (extravascular hemolysis) -> accel. RBC destruction -> hemolytic anemia
Target cell = erythrocytes
Signalment and clinical signs of bovine anaplasmosis
- older cattle
- severe and fatal dz due to hemolytic anemia with 30-50% mortality rate
- fever, pale, icteric mm, splenomegaly
Canine RMSF
- signalment
- clinical signs
- pathogenesis
- young german shepherds, seasonal (march-oct)
- fever, jt pain, lymphadenopathy, petechia, necrosis of nasal planum, paw pads
- tick bite -> bacteria replicate in endothelial cells -> vasculitis -> PLT activation and coag. cascade -> inflammation, edema, leaky vessels, thrombocytopenia
How does Ehrlichia canis differ from Canine RMSF?
E. canis:
- maintained in dog populations (and not small rodents)
- target cell = monocytes and MØ (and not endothelial cells)
- three stages of disease: acute, persistent/subclinical, chronic
Where does avian chlamydiosis primary infect?
Chlamydia psittici
epithelial cells of URT; can sometimes infect LRT & pericardium
How can avian chlamydiosis be prevented?
- reduce stress/minimize handling and transportation
- eliminate carriers; quarantine new birds
- discuss zoonotic concerns with owners
What does epicellular mean with feline hemotropic mycoplasmosis (Mycoplasma haemofelis)?
The bacteria attaches to/grows on the surface of RBCs (erythrocytes)
Pathogenesis of feline hemotropic mycoplasmosis
flea bite -> bacteria infect RBC membrane -> phagocytosis by mø in spleen (EV hemolysis) -> accel. RBC destruction -> hemolytic anemia
How does Bartonellosis henselae (Cat Scratch Dz) affect dogs and cats?
- chronic bacteremia in ≤ 2y/o cats; typically no clinical signs but major reservoir
- dogs: infectious endocarditis
Prevention of bartonellosis
Strict flea control!
