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Flashcards in Test 3- Spirochetes Deck (37):

Which of the following is incorrect about paucibacillary lesions?

A. seen in mycobacterial infections

B. This is due to lack of cell mediated immunity

C. Few Bacteria are seen in these lesions

D. Result in milder disease

B- in these lesions- cell mediated response


CELL MEDIATED IS THE KEY FACTOR in controlling the lesion


Use of mulitple antimicrobial agents in treating mycobacterial infections is to...


2 reasons

Minimize development of antimicrobial resistance


to cover all of the locations- extracellular or intracellular


Which mycobacterium species is mycobactin dependent for its growth?

M.  avium subsp paratuberculosis




Which mycobacterium spp is widely present in soil and water?

M. avium complex


M. Bovis, leprae, and tuberculosis can be present because they can be obligate pathogens



Spirochete Morphology

• Capable of movement in environments with 5-15 times higher viscosity (translational, rotating, and flexing motion)

• Flagella in the periplasmic space

Axial filaments/endoflagella which insert at the end of protoplasmic cylinder

Number of flagella varies upon genus


Genus Brachyspira

Gram-negative(have LPS), strongly beta hemolytic, oxygen tolerant, anaerobic, loosely coiled, motile spirochete

Acute to chronic, highly infectious disease, most commonly found in grower and finisher pigs (8-16 weeks)

Multiple species of Brachyspira can colonize the porcine colon and cause disease typical of swine dysentery

• Can affect multiple species

Very heterogeneous species with many pathogens

B. Hyodysenteriae
Causes swine dysentery
Actively growing pigs (6-12 weeks of age)

B. pilosicoli; Causes Intestinal spirochetosis in animals and humans

Others with controversial role in diseases

B. intermedia, B. mudochii, B. innocens, B. canis


Virulence Factors and Transmission of Brachyspira

Virulence factors

Cytotoxin/Hemolysin LPS

Transmission is fecal-oral

Asymptomatic carrier pigs are the most important mode of transmission from farm to farm; mechanical vectors (boots, coveralls, vehicles, migratory animals and birds)


Pathogenesis of Brachyspira

Pathogenesis is complex and not completely understood

There is synergistic action between B. hyodysenteriae and other anaerobes normally found in the swine colon and cecum (mainly Bacteroides and Fusobacterium) required for clinical disease

Motile Brachyspira hyodysenteriae is chemotactically 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 production > death from dehydration (malabsorption of water and electrolytes)

Thrombosis may occur due to absorption of bacterial endotoxins from gram-negative bacteria through the damaged colonic mucosa


Lesions and Symptoms of Brachyspira

Lesions in the large intestine only, often sharp line of demarcation at the ileocecal junction. Fibrinonecrotic pseudomembranous colitis with a granular, hyperemic mucosa in advanced cases

Bloody diarrhea, dehydration, and weight loss which was refractory to antibiotic therapy. Secretory diarrhea with gray to strawberry-colored feces and dehydration

Morbidity ~90%, Mortality ~40%
Can last for several weeks
Asymptomatic shedders are difficult to identify


What is a ddx of brachyspira?



Diagnosis of Brachyspira

Direct staining and observation of loosly coiled spirochetes in clinical specimens (Fecal samples or tissues are stained with Wright’s Giemsa, Victoria Blue stain)

Anaerobic culture
Histopathology and Silver staining
(This condition must be differentiated from Salmonellosis)


Treatment and Control of Brachyspira

• Tiamulin, tylosin, gentamicin, nitrofurazone, lincomycin

Infected pigs develop immunity
• Whole cell bacterin vaccines are available



• Treponema pallidum
• Syphilis in humans
• Can not be cultivated in vitro


Papillomatous digital dermatitis (PDD)

“Hairy Heel Warts” (HHW) (also known as Heel warts, Strawberry Foot Disease

Growing cause of lameness of cows in the U.S. dairy industry.

Economic loss due to treatment costs, decreased milk production,

lower reproductive efficiency, and premature culling.

Affects around more than 40 % of US dairy Herds

Treponema brennaborense???


Treatment of PDD

“Spraying feet of dairy cattle with antibiotic (tetracycline or lincomycin) solutions while they are in the milking parlor has generally been found to be the most cost effective method of treating HHW on a herd basis”

“Formaldehyde foot baths”

What are the problems associated with these two commonly used treatment methods?


formalin problems- carcinogen


Treponema paraluis-cuniculi

Rabbit syphilis or Vent diseases in rabbits self-limiting disease

perineal and facial lesions;
infection may increase susceptibility to other infection Spread by direct or venereal contact- USALLY AROUND THE NOSE
Initial lesions are on the perineum and genitalia

Epidermal hyperplasia with erosions, ulcers; infiltrates of plasma cells, heterophils and macrophages.

Definitive diagnosis is by demonstration of spirochetes in typical lesions




Transmitted via arthropod vector

Grow slowly in specialized media (microaerophilic)

Linear chromosome( most have spherical)
 B. burgdorferi: Lyme disease
 B. anserina: avian borreliosis
 B. recurrentis: relapsing fever borreliae


Borrelia virulence Factors


Antigenic Variation in Major outer surface lipoproteins (OSP)- MAIN ONE


In B. burgdorferi:
Osp C to Osp A in midgut of ticks & in culture

Osp A to Osp C in salivary gland of tick
Osp C in mammals early in infection


Lyme Disease

Identified in 1975 when a cluster of arthritis cases was diagnosed in children near Old Lyme, CT

 Borrelia burgdorferi (sensu lato)> 11 genomospecies  (3 from humans in US: burgdorferi, garneri, afzelii)

 Genetic (strain) diversity among genotypes

 Ixodes scapularis (eastern US

 Ixodes. pacificus (western US)
 Reported in humans, dogs, horses, cattle, sheep


Who plays a big role in transmitting Lyme Disease to humans and animals?

Deer, and white footed moose


Lyme Disease Transmission

 Ticks become infected only when feeding on animal with sufficiently high level of bacteremia and only feed once prior to each molting

  After tick ingests blood, spirochete up-regulates expression of an outer surface protein, which is essential for virulence in mammals

  Spirochete moves from midgut to hemolymph to salivary glands

  Transmission of spirochaete requires ~ 50 hrs.


Lyme Disease prevalenae

Most common vector borne bacterial disease in humans US. (>20,000 human cases reported per

Antibiotic responsive, Non-fatal

Geographically and seasonally limited

Both under-reported and over-diagnosed

Clinical syndromes vary depending upon

infecting genotype, age, immune status


Lyme Disease Pathogenesis

After inoculation into the skin,spirochetesmultiplytohighest numbers in the skin and disseminate via the bloodstream>Organisms spread through blood to joints, brain, nerves, eyes, heart, liver, kidneyIncubation period: 2 – 6 mo.


Canine Lyme Disease

Infection usually subclinical (95%)

Exposure common in endemic areas- Typical clinical signs in dogs are fever, acute arthritis, arthralgia and lameness. Sometimes accompanied by anorexia, lethargy and

depression. 344-7 )

(Appel 1990, Compendium Cont Educ Pract Vet 12: 617-26; Levy & Magnarelli 1992, J Am Vet Med Assoc 200:

CNS, heart, renal lesions and uveitis are less frequently reported and not reproduced experimentally in dogs


Dx of Lyme Disease

  Direct detection of organism in host tissues(Poor sensitivity)

  Culture and isolation(slow)

  Serology- remember only tells exposure

  Western Blot

  SNAP test (EIA) – point of care test

  Multiplex ELISA for dogs and horses(OSPA, OSPB, OSPC)

 Paired titer helpful(antigenic variation is a problem)


How to interupt Test results

 Clinical signs and Positive test: infected

  Healthy and negative test: not infected

  Clinical signs and negative test: evaluate for underlying disease, retest

  Healthy and positive test:likely to be infected subclinically.

  In endemic area treatment is preferred,innon-endemic

usually not pursued

Should Healthy Dogs be Screened?
ACVIM Small Animal Consensus Statement: = could not reach a consensus Provided a list of pros and cons in testing this population


Treatment and Control

Vector control in dogs

Vaccine for dogs (bacterin, subunit Osp A)reduces (~3%) incidence of disease in endemic region, does not prevent infection.- VACCINE ACTS IN TICK'S BODY- Stops replication in the tick

Antibodies against OSP A antigen act on found on organisms present in midgut of ticks, vaccine may block transmission by interfering with OspA to OspC conversion. ie. antibodies produced in the dog must be delivered to the tick to exert this effect


Letospira Classification

>250 serovars based on carbohydrate component of the bacterial lipopolysaccharide- maintanied in the renal tubuloles

Organized in ~23 serogroups

(~22 genomospecies)

Serovar and species concept not always in agreement isolates of one serovar may belong to different genomospecies isolates of one genomospecies may belong to different serovars


Leptispira Habitat

  • Pathogenic species maintained in the renal tubules or genital tract of reservoir animals

  • Reservoir animals excrete the bacteria through urine and contaminate the environment (water)

  • Pathogenic species survive for short period of time in ponds, rivers, surface waters, moist soil, mud

  • Direct contact with urine or contaminated water results in infection in susceptible hosts


BIGGEST host for leptospira



What is the main target organ for Leptopira?

Kidney and liver


Leptospira is a _____

Leptospira is a ONE HEALTH PROBLEM

HUMANS: Flu like illness and protean manifestations

Complications from renal, pulmonary, hepatic and CNS disease

IN LIVESTOCK : Disease of  production and reproduction


 Disease similar to humans


Virulence Factors of Leptospira

Cell associated:

- endoflagella- helps with motility
- outer membrane proteins - LPS

- hemolysins (in some serovars)

- protein cytotoxins?


Pathogenesis of leptospira

Penetrates epithelial barriers (incubate 4-20 days) Bacteremia (for up to 7 days)
Enter liver, kidney, spleen, CNS, genital tract Antibodies develop (extent and duration varies)

 In Maintenance hosts--- Long term shedding; doesn't make them sick

Incidental hosts----- Recovery with short term shedding in urine- some have severe disease


Leptospirosis in Dogs


LESIONS IN KIDNEYS- Tublointenstintal injury

Mild or no signs of disease, to severe illness or death.

Acute febrile illness

Renal or hepatic injury, uveitis, pulmonary hemorrhage, abortion.

(polyuria, polydipsia, dehydration, vomiting, diarrhea, inappetence, lethargy, or abdominal pain)

Signs hepatic and Renal failure, including icterus.

Bleeding abnormalities and disseminated intravascular coagulation(DIC)

Dogs surviving acute renal tubulointerstitial injury may have residual chronic kidney injury that progresses over months to years, culminating in signs of decompensated chronic kidney disease.





Papillomatous digital dermatitis( PDD)

aka Hairy Heel Warts or Strawberry foot disease

Treponema brennaborense???