Spirochetes Flashcards
Match the Order Spirochaetales with its family and species.
- Brachyspiraceae
- Spirochaetaceae
- Leptospiraceae
A. Borrelia, Treponema
B. Leptospira
C. Brachyspira (Serpulina)
1 - C
2 - A
3 - B
What is the morphology of spirochete?
Flagella in periplasmic space (located inside the body), axial filaments/endoflagella (insert at the end of protoplasmic cylinder), capable of moving in environment with 5-15x higher viscosity (translational, rotating, and flexing motion).
What are the characteristics of Genus Brachyspira?
Gram negative, beta-hemolytic, O2 tolerant, anaerobic, loosely coiled, motile spirochete.
What kind of disease does Genus Brachyspira cause?
Acute to chronic, highly infectious disease.
Commonly found in grower and finisher pigs (8-16wks).
Multiple species infected.
Who does swine dysentery that is caused by B. Hyodysenteriae affect?
Actively growing pigs (6-12wks)
What disease does B. pilosicoli cause?
Intestinal spirochetosis in animals and humans
What are the virulence factors of Brachyspira?
Cytotoxin/Hemolysin
LPS
How is Brachyspira transmitted?
Fecal-oral (asymptomatic carriers of pigs - farm to farm; mechanical vectors - boots, vehicles, birds)
What is the pathogenesis of Bradyspira?
Not completely understood
Synergistic action between B. hyodysenteriae and other anaerobes found in swine colon/cecum required for disease.
B. yodysenteriae is attracted to hog mucin > invades intestinal crypts and disrupts colonic epithelium > progressive erosion of superficial epithelium, excess mucus production, edema, and hemorrhage of the lamina propria with pseudomembrane prod. > death from dehydration.
Absorption of bacterial endotoxin through damaged colonic mucosa > thrombosis.
Where are the lesions for B. hyodysenteriae? What disease does it cause? What are the symptoms if there are any?
Lesions in large intestines ONLY (sharp line of demarcation). Fibrinonecrotic pseudomembranous colitis (granular, hyperemic mucosa in advanced cases). Bloody diarrhea (gray to strawberry colored feces), dehydraton, and weight loss.
What is morbidity for B. hyodysenteriae? mortality? How can you detect asymptomatic shedders?
Morbidity: ~90%
Mortality: ~40%
Difficult to identify
What are the diagnosis for B. hyodysenteriae?
Direct staining: Wright's Giemsa, Victoria blue Stain Observation of coiled spirochetes Anaerobic culture PCR Histopath and silver staining
What is treatment and control for B. Hyodysenteriae?
Treatment: Antibiotics (infected pigs develop immunity)
Control: Whole cell bacterin vaccines
What does Treponema pallidum cause in humans? What does it cause in cows?
Hmans: Syphilis
Cows: Papilomatous digital dermatitis (PDD)
What is Papilomatous digital dermatitis (PDD) also known as? Why is this a disadvantage for farmers?
HAIRY HEEL WARTS (HHW), Heel warts, Strawberry Foot Disease.
Growing cause of lameness, economic loss due to treatment costs, decreased milk production, lower efficiacy, premature culling.
What are the treatments for T. pallidum? What are the disadvantages of these treatments?
Antibiotic, Formaldehyde foot baths.
T. pallidum can be resistant to antibiotics and foramaldehyde is toxic.
Who is the primary host for Treponema paraluis-cuniculi? What disease does it cause?
Rabbits.
Rabbit syphilis/Vent diseases.
Where are the lesions of rabbit syphilis? How is it spread?
Initial lesions: perineum and genitalia
Perineal and face
Transmission: direct or venereal contact
Describe the lesions that are caused by T. paraluis-cuniculi.
Epidermal hyperplasia with erosions, ulcers; infiltrates of plasma cells, heterophils, and macrophages.
T/F. Definitive diagnosis of T. paraluis-cuniculi is by demonstration of spirochetes in typical lesions.
True.
How is Borrelia transmitted? What are the characteristics of it?
ARTHROPOD
Grow slowly in specialized media (microaerophilic), linear chromosome!
T/F. Treponema can be cultivated in vitro.
False. NOPE
T/F. B. anserina causes lyme disease. B. burgdorferi causes avian borreliosis. B. recurrentis causes relapsing fever borreliae.
False. (true for B. recurrentis)
B. anserina: avian borreliosis
B. burgdorferi: lyme disease
What are the virulence factors for Borrelia? How about B. burgdorferi?
LPS
Antigenic variation in major outer surface lipoproteins (OSP)
B. burgdorferi: midgut of ticks/culture (Osp C to Osp A) to salivary gland of tick (Osp A to Osp C) to mammals in early infection (Osp C)
How was Lyme Disease identified? How many genomospecies of B. burgdorferi are there? This bacteria is reported in which animal species?
A cluster of arthritis cases was diagnosed in children near Old Lyme.
11 genomospecies.
Reported: humans, dogs, horses, cattle, sheep
T/F. There is a genetic (strain) diversity among genotypes of ticks (ixodes).
True.
T/F. Lyme disease is a problem in humans, dogs, horses, cattle, sheep.
False.
Only humans and dogs.
How is lyme disease transmitted?
Ticks feed on animal with high level of bacteremia > spirochete up-regulates expression of an outer surface protein (essential for virulence) in ticks > Spirochete moves from midgut to salivary glands.
This requires ~50 hrs.
T/F. Lyme Disease is the most common vector borne bacterial disease in humans.
True
T/F. B. burgdorferi does not respond to antibiotic, fatal, communicable.
False. Responds to antibiotic, non-fatal, non-communicable.
T/F. Lyme disease is both geographically and seasonally limited. It is both over-reported and under-diagnosed.
False. It IS geographically and seasonally limited but UNDER-reported and OVER-diagnosed.
What is the pathogenesis for lyme disease?
Inoculation into the skin > spirochetes multiply A LOT in the skin > bloodstream > joints, brain, nerves, eyes, heart, liver, kidney.
Incubation period: 2-6 months
T/F. Symptoms are very severe in canine lyme disease.
False. Infection is subclinical (95%)
If there are clinical signs in canine lyme disease, what are they?
Fever, acute arthritis, arthralgia, and lameness. Anorexia, lethargy, and depression can be seen.
How do you diagnose lyme disease?
Direct detection of organism in tissues, culture/isolation (slow), SEROLOGY! SNAP test (point of care test), Western, paired titer, multiplex ELISa for dogs and horses.
How do you interpret lyme disease test results?
Clinical signs and positive: infected
Healthy and negative: not infected
Clinical signs and negative: underlying disease, retest
Healthy and positve: subclinical may be possible
TREATMENT in endemic areas
What is the treatment and control of lyme disease?
Vaccines (bacterin, subunit Osp A) > does not prevent infection (antibodies must be delivered to the tick because killing of the bacteria will occur in the tick).
Vector control in dogs
DOXYYYY for dogs
Which family is Leptospira in?
Leptospiraceae
T/F. Leptospira: Isolates of one serovar belongs to only on type of genomospecies. Isolates of one genomospeices belong to only type of serovar.
False. Isolates of one serovar belong to different genomospecies. Isolates of one genomospecies belong to different serovars.
T/F. Leptospira: There are >250 serovars on carbohydrate component of the bacterial lipopolysaccharide, organized in ~23 serogroups, ~22 genomospecies.
True
T/F. Too many serovars in leptospira > maintained in the liver > constantly secreted with liver enzymes > animal to animal/human contact > animals and humans can get infected.
False. Maintained in the renal tubule > constantly secreted through urine > survive in ponds, rivers, surface waters, moist soils, mud > direct contact with urine or contaminated water > infection
Leptospira is considered as a “one health problem”. Why is this?
Humans: flu like symptoms (complications from renal, pulmonary, hepatic, CNS disease), Livestock: disease of production and reproduction, Companion animals: disease similar to humans.
What are the virulence factors of Leptospira?
Cell associated: endoflagella, outer membrane proteins, LPS
Extracellular: hymolysins, cytotoxins
What is the pathogenesis of Leptospira?
Penetrates epithelial barriers > bacteremia > enter liver, kidney, spleen, CNS, genital tract > antibodies develop > maintenance hosts: kidneys > long term shedding or incidental hosts: recovery with short term shedding in urine or severe disease.
What are signs of Leptospirosis in dogs?
Renal or hepatic injury, uveitis, pulmonary hemorrhage, abortion
Signs of hepatic and renal failure, including icterus.
What is the diagnosis for Leptospira in dogs?
Detection of the agent: Fluorescent antibody staining, PCR
Detection of host response: microscopic agglutination test, ELISA
What is mortality for leptospirosis? What happens to dogs that survive the infection?
Mortality: 11-27%
Chronic renal failure (33-40%)
Explain Serology (Microscopic agglutination test) of Leptospira.
Measures antibody titers to serovars (uses live Leptospira serovars).
Serovar selected based on geographic prevalence.
Considered as GOLD STAND TEST.
Used for definitive diagnosis by performing MAT on a paired sera (acute and convalescent): x4 increase.
Serovar specific but cross-reactivity is common (Paradoxical titiers in acute cases).
What are ideal samples for antemortem diagnosis of Leptospira to maximize the sensitivity?
Blood and urine: PCR/FA
Serum: MAT
Serum, EDTA blood, urine should be sent to lab for PCR, FA, and MAT
What is treatment for Leptospirosis in dogs?
Supportive care (fluids, nutrition, blood products), antimicrobials (acute vs. carrier), penicillins (acute; ampi/amoxi), Doxy (minimize carrier state, prophylaxis state).
How can you prevent Leptospirosis in dogs?
Agglutinating antibody titers are not predictive of protection of urinary shedding!! Humoral response (mediated through antibodies), vaccine (old: 2 serovars; new: 2 additional serovars), antibodies are serovar specific, minimize exposure to contaminated surface waters.
What are clinical signs of leptospirosis in cattle and ruminants? Lactating cows?
fever, hemolytic anemia, jaundice, pulmonary congestion; occasionaly meningitis and death.
Lactating cows: agalactia with small quantities of blood-tinged milk.
What are diagnosis for leptospirosis in ruminants?
Urine FA and PCR, Collect mid stream urine (after administration of diuretic: Lasix), ship overnight under refrigeration conditions, Serum for MAT testing, chronically infected cows have low titiers.
T/F. Incidental infections of leptospirosis in cattle/ruminants with serovar Pomona results in chronic disease.
False. ACUTE!
How do you treat/prevent Leptospirosis in ruminants?
Tetracycline, sustained-release ceftiofur.
Vaccines for L. borgpetersenii
Dry cows: vaccination + tetracycline
Annual vaccination in closed herd/low incidence area, twice-yearly vaccine in an open herd/high incidence area.
T/F. Leptospiral Borgpetersennii serovar hardjo is host adapted in cattle resulting in reproductive failure due to embryonic death and repeat breeding.
True.
What causes Leptospirosis in horses? What are clinical signs?
Serovars Pomona and Grippotyphosa.
Clinical signs: abortions, systemic illness in foals, Equine Recurrent Uveitis (periodic opthalmia, moon blindness).
What causes leptospirosis in pigs? What is the clinical signs in pigs? California Sea Lions?
Pigs: Pomona and Bratislava > Reproductive failure (infertility, sporadic abortion).
California Sea Lions: Pomona
What are the clinical symptoms of Leptospirosis in humans?
Weil’s disease (hepatic and renal failure)
Incubation period: 2-25d; occurs 1 week after recovery from an initial febrile illness.
Subclinical, a mild, influenze-like illness.
T/F. Most widespread zoonotic disease of leptospirosis occurs in humans.
True.
T/F. Acute to chronicle, high infectious disease caused by B. Hyodysenteriae is the most common in older animals.
False.
Grower and finisher pigs (8-16 wks)
Which specie causes Lyme disease?
B. Burgdorferi
Which genus is Lawsonia intracellularis in?
Brachyspira
T/F. Lawsonia intracellularis are curved rods, obligate intracellular pathogen of enterocytes.
True
How does Lawsonia Intracellularis transmission occur?
Fecal oral
Intestinal tract and environment, rodents
Who are the reservoirs of Lawsonnia intracelluaris?
What is the name of the disease that is caused by Lawsonia Intracellularis?
Porcine Proliferative Enteropathy
Who does Porcine Proliferative Enteropathy affect?
Primarily porcine and equine
T/F. Experimental inoculation of germ-free swine leads to disease.
False.
Interaction with unknown natural flora are required for disease (Experimental inoculation of germ-free swine does not lead to disease).
