Exam 5 Flashcards
Lecture 30
Lyme disease in Animals
What are the characteristics of Borrelia burgdorferi?
Order Spirochaetales, genus Borrellia
Borrellia burgdorferi:
- 0.2-0.5 um wide and 3-20 umm long
- Gram negative
- Stains poorly.
- Better visualized if stained with silver, Giemsa, Wrights, or dark field microscopy
- Obligate pathogen in a variety of vertebrate hosts
How are spirocheates transmitted?
They are transmitted and maintain by ticks
-Infection have a blood-borne phase accompanied or followed by general and localized manifestations
Lyme disease in humans
- Early localized stage (3-30 days post tick bite)
- Red, expanding rash: erythema migrans (EM)
- Fatigue, chills, fever, headache, muscle and joint aches, and swollen lymph nodes.
- Early disseminated stage (dates to weeks post-tick bite)
- Facial or Bell’s palsy
- Severe headaches
- Pain and swelling in large joints
- Shooting pains that interfere with sleep.
Late disseminated stage: months to years post tick-bite)
- Arthritis with severe joint pain and swelling
- Up to 5% of untreated patients may develop chronic neurological complaints months to years after infection. Pain, numbness, tingling, problems with short term memory.
Lyme Disease in Dogs
70-90% of all dogs in endemic areas are seropositive.
- C/S are observed in < 10% of exposed dogs
- Severity and propensity varies inversely with the animal’s immune status
- Clinical syndromes polyarthritis and glomerulopathy
- Lyme arthritis
- Lyme nephritis
Lyme Disease in Horses
50% of all exposed in endemic areas are seropositive
Clinical signs observed in <10% of exposed
C/S:
Chronic weight loss, sporadic lameness, shifting leg lameness, low-grade fever, muscle tenderness, chronically poor performance, swollen joints.
Changes in behavior and skin sensitivity both rapid onset
Neurological signs: depression, dysphagia, head tilt and encephalitis were reported in chronic cases
What are the the vectors and natural hosts of Borrelia species?
Borrelia species: Ixodes vector, Rodents, birds, lizards Reservoir host,
B. anserina: Argas spp. ticks, Birds RH
B. theileri: many tick species, Cattle, sheep, horses.
B. coriaceae: Ornithodoros spp. Cattle, deer.
Clinical Laboratory findings
No specific hematologic or biochemical changes are pathognomonic of borreliosis
- Synovial fluids of lyme arthritic dogs have increased cell count of 5000 to 100,000 cells/uL
- Neutrophils predominating up to 95%
*if a dog in a lyme disease endemic area has leukopenia or thrombocytopenia, these hematologic changes are likely cuased by co-infection with Rickettsial pathogen
Serologic testing for borreliosis
Seropositive = exposure
Does not necessarily mean that the clinical illness is caused by the organism
Serological assays:
- Whole-cell ELISA: Antibody measurement using whole spirochetes. IgG-ELISA positive titer by 4-6 weeks after exposure. Reach highest levels by 3 months and last for two years.
- Antigen preparations not standarized.
- Cross-reactivity with Leptospira and other disease moieties.
- Whole-cell Immunobloting: Helps identify sera that produce false-positive results in whole-spirochaete assays.
- After natural exposure, antibodies develop to proteins in the range of 58, 41, 39, and 23 kDa.
- In general vaccinated dogs show reactivity to 31, 34, 28, and 93 kDa.
- C6 peptide based assays: C6 variable region of the borrelial protein VlsE.
- Can differentiate between vax and not vax dogs naturally infected. C6 does not react with other infectious diseases. Monitor tx response with C6
- SNAP 4Dx Plus
- Multiplex assay
Prevention of Borrellia burgdorferi
- Collars (permethrin or amitraz)
- Topical poweders, shampoos (selamectin, fipronil, permethrin)
- Daily combing and tick removal within 12 hours.
- Tick control of environment, targeting the mice population.
Prevention by vaccines
- Recombinant, subunit vaccine OspA
- Killed, whole-cell, bivalent bacterin (OspA, OspC).
- Duramune
Lec 31
Malignant edema (gas gangrene)
Blackleg
Malignant edema
- Acute, generally fatal toxemia
- Affecting all species and ages of animals
- Usually caused by Clostridium septicum
What is the cause of Malignant edema and what are its characteristics?
- Clostridium septicum
- Found in soil and intestinal content of all species of animals
- Infection generally occurs via contamination of wounds
- Clinical signs develop within 48 hours
- Systematic sigs (fever)
- Localized swelling in muscles and intermuscular connective tissue
- Fatal toxemia often results
- Confirmation by lab testing
- Tx: antimicrobials and supportive therapy
- Control: immunization bacterin and multivalent vaccine
Etiology of Malignant gangrene
- C. chauvoei
- C. perfringes type A
- C. novyi type A
- C. sordellii
Epidimiology
- Infection through contamination of wound containing devitalized tissue, soil, or some other tissue debilitant or dormant spores activation
- Potent Clostridium toxins cause local and systematic signs often resulting in death.
- Severe swelling, edema, necrosis, gangrene.
Risk factors: IM injections in horses, sharing, docking, and lambing in sheep, traumatic parturition, dehorning, castration in cattle.
Clinical signs
- Anorexia, swelling, high fever, local lesions, 6-48 hours after predisposing injury or activation of dormant spores in muscle tissues.
- Large quantities of exudate that infiltrates the intramuscular and connective tissue
- Muscle dark brown or black
- Accumulation of gas in subcutaneous tissue
- Muscle fascias may be present
- Extremely painful infection
- Systematic toxemia
- Local sloughing of skin and tissues
- Rams fighting can result in infection in head region
- Lacerations of vulva during parturition can lead to infection. Marked by edema and severe toxemia 24-48 hours
Diagnosis
- Fluorescent antibody
- Staining of C. septum from a tissue smear
- Bacteria extremely active postmortem, specimen not significant if >24hrs since death.
- PCR assay
- Fine needle aspirates
- Gram stain: gram (+) rods in anaerobic culture
- horses and pigs are susceptible but not to blackleg, important differential diagnosis for anthrax.
Treatment and control
- High dose penicillin, tetracyclines, or broad spectrum antimicrobials early in disease course.
- Vaccination. Bacterins, multivalent vaccines.
- Proper carcass disposal helps prevent soil contamination
Blackleg
Clostridium chauvoei
- Acute
- Highly fatal
- In cattle: no history of wound
- In sheep: wound related
- Febrile
- Worldwide
- Emphysematous swelling and necrotizing myositis that commonly affects large muscles (clostridial myositis)
Clostridium chauvonei
- found naturally in the intestinal tract of animals
- Spores remain viable in the soil for years and purported to be a source of infection
- Outbreaks possible in farms where recent excavation occur or after flooding
- Ingestion of organism
- May remain dormant in organs
Epidemiology
- Cattle: infection is endogenous
- In some cattle restricted to myocardium and the diaphragm. Abnormal breathing and pericardial friction rub.
- lesions develop without wounds. Bruising or excessive exercise may predispose.
- Commonly beef breeds of excellent health and gaining weight.
- Outbreaks are found each day for several days
- Most cases are seen in cattle 6-24 months old, but as young as 6 weeks and as old as 10-12 years
Sheep
- New Zeland, most frequent
- Acute, severe lameness, affecting hind legs, marked depression is common
- Fever initially
- Edematous and crepitant swellings develop in the hip, shoulder, chest, back, neck, or elsewhere, at first, the swelling is focal, hot, painful.
- Skin becomes cold, decreased blood supply to affected areas.
- Death 12-48 hours
Diagnosis
- Rapid febrile disease in well-nourished beed young cattle with large muscle swellings
- Anaerobic culture
- biochemical identification
- fluorescent antibody test is rapid and reliable
- Immunohistochemical testing reliable for clinical samples, but not reliable for environmental samples.
Control
Multivalent vaccine combined C. chauvonei, C. septum, C. novyii. antigens
- Calves 2 months old should be vaccinated twice 4 wks apart, annual booster before spring or summer.
- Cattle should be moved from affected areas
- Carcasses should be destroy by burning or deep burial in a fenced-off area to limit heavy spore contamination of the soil
Lect 32
Bovine Foot Rot or Infectious bovine pododermatitis or Interdigital phlegmon or interdigital necrobacillosis
F. necrophorum aid D. nodosus
Etiology:
-Fusobacterium necrophorum biotypes A and AB. Other organisms can facilitate infection
Epidemiology
- All ages are susceptible
- Infected feet are source of infection
- Transmission highest in wet, humid conditions
Clinical findings
- Sudden onset of lameness and fever
- Typical fissuring, necrotic lesion in the skin at the top of interdigital cleft
- Drop in milk production
Dx
-clinical findings; culture may be done
Tx
- Antimicrobial
- Control: avoidance of abrasive underfoot conditions; foot baths, antimicrobials; vaccination
Etiology and pathogenesis
- injury to the interdigital skin provides a portal of entry for infection
- Maceration of the skin by water, feces, and urine may predispose to injuries
- Fusobacterium necrophorum is the mojor cause
- It can be isolated from feces, which may survive as saprophytes, which may explain why control is so difficult. It can also survive in moist soil
Fusobacterium necrophorum
- Gram (-)
- non-spore-forming
- non-flagellated
- non-motile
- Pleomorphic
- Anaerobic
- Polysaccharides endotoxin capable of necrotizing activity
Other organisms that may be involved:
- Dichelobacter nodosus
- Staphylococcus aureus
- E. coli
- Trueperella pyogenes
- Bacteroides melaninogenicus
Non-spore forming Gram (-) anaerobes
-Dichelobacter nodosus: thick, straight or slightly curved, up tp 6um long and bulge at one or both ends
Colonies: dark central zone, pale granular middle zone, irregular periphery spread with glass appearance.
-Type IV fimbrae major virulence factor
-Essential causal pathogen
-Sources: actively infected sheep
-Organism does not survive in the environment for more than a few days
-Merino breed most susceptible
-Warm and moist conditions favor persistance
-Fusobacterium necrophorum has irregular staining, long non-motile branching filaments.
Colonies: gre, round and shiny
-Gram negateive anaerobes: fetid or putrid odor due to volatile fatty acids
Virulence factors
Synergistic interaction of Fusobacterium necrophorum with
- Trueperella
- Arcanobacterium pyogenes
- Dichelobacter nosodus
Production of heat liable factor by T. pyogenes stimulates F. necrophorum replication
- F. necrophorum Leukotoxin helps T. pyogenes
- F. necrophorum facilitates tissue invasion by D. nodosus
- F. necrophorum is stimulated by a growth factor elevated by D. nodosus
Clinical signs/findings
The incubation period of footrot can be a week
- The fore or more commonly the hindlimbs can be affected, but more than one foot is rarely involved at the same time in mature cows.
- First sign, swelling and erythema of the soft tissues of the interdigital space and the adjacent coronary band
- Typically, the claws are markedly separated, and the inflammatory edema is uniformly distributed between the two digits.
- Extreme pain, rapid onset of disease increasing lameness
- In severe cases, the animal is reluctant to bear weight on the affected foot.
- Fever and anorexia are seen
- The skin of the interdigital space first appears discolored; later, it fragments with exudate production
- As necrosis of the skin progresses, sloughing of the tissue is likely to follow
- Characteristic foul odor
- Weight loss can be severe, decreased milk yield
Treatment and control
- Most treated animals recover in a few days
- Good results with penicillin G, IM, for 3 days
- Should start as soon as signs begin
- Local treatment is essential for some longstanding cases
- foot bath with antiseptic and astringent solution (copper or zinc sulfate)
- Vaccines 60% protection
- High levels of zinc in feed supplemental are beneficial in improving epidermal resistance to bacterial invaders.
Sheep
- Parenteral antibiotics
- Vaccination for sheep multivalent, autogenous mono or bivalent vaccines.
- Destocking of flock affected virulent footrot
Lecture 33
Order Rickettsiales
Family Rickettsiales
Family Anaplasmataceae
Order Rickettsiales
- Gram (-)
- Small, non-motile, pleomorphic, Gram-negative bacteria
- Obligate intracellular pathogens, which replicate only in host cells
- Romanowsky stain in blood smear
- Host specific
- Tropism for particular cell types
- Cause systemic diseases, mainly arthropod-borne, in humans and animals
Family Anaplasmataceae
- Lack cell walls, possess cell membranes
- Have not been culture in vitro
- Tropism for cells of hemopoietic system
Family Rickettsiales
- Cell wall peptidoglycan
- Cultured in specific cell lines or in fertile eggs
- Tropism for vascular endothelium
Anaplasmatacae
Genus Neorickettsia
- Within vacuoles of monocytes, macrophages in lymph tissue, and occasionally in enterocytes
- Flukes serve as vectors and all stages within the life cycle of flukes are infectious
- Transovarial transmission and transstadial
Species:
- N. helmithoeca
- N. risticii
- N. sennetsu
Salmon poisining disease
Neorickettsia helminthoeca Only obligate helminth-borne pathogenic bacterium
SPD: NO TOXIN involved
- Acute systematic disease of canids
- Neorickettsia helminthoeca
- Gram (-) pleomorphic cocci
- Fever, anorexia, weakness, weight loss, lymphadenopathy, typically of cervical and mesenteric lymph nodes
- Canine mononuclear cells are infected after dogs ingest salmoid fish with a fluke, Nanophyetus salminocola, infected with the organism.
- Indigenous to river areas of the US Pacific North West Coast.
Dx
- Serology
- PCR
- Finding trematode eggs in feces
- Travel to US Pacific coast
- Demonstrate organism in LN aspirates
- Serology (IFA or CF)
Tx
- doxycycline
- Tetracyclines
- 90% fatal if left untreated
Prevention
-Avoid raw fish, use emetics if accidentally eaten, NO Vax
