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===Overview===
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#REDIRECT[[:Category:Spirochaetes]]
 
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*Two families exist, ''Leptospiraceae'' and ''Spirochaetaceae''
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*''Leptospiraceae'' include the pathogens of the genus ''Leptospira''
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*''Spirochaetaceae'' include the pathogens of the genera ''Borrelia'', ''Brachyspira'' and ''Treponema''
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*Many cause zoonotic infections
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===Characteristics===
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*Spiral or helical Gram-negative bacteria
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*Motile organisms via endoflagella
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*Poor survival in the environment and sensitive to dessication
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*Stain poorly with Gram stain
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*Most require specialised media for growth
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*Serology required for identification
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===''Leptospira''===
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*Motile, helical bacteria found in aquatic environments
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*Require liquid media for culture
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*Cause leptospirosis in all animals, which can range from mild urogenital tract infections to systemic diseases
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*Organisms persist in kidney tubules or genital tract of carrier animals and are shed in urine
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*Transmission via direct contact
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*Serovars are fairly host-specific, causing mild disease in the maintenance host, with shedding in the urine
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*Maintenance hosts may transmit the infection to incidental hosts, which are less susceptible to infection, but develop serious disease
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* May cause severe systemic disease, resulting in [[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Bacterial septicaemia and enteritis|enteritis]]
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*Pathogenesis and pathogenicity
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**Depends on virulence of the serovar and susceptibility of the host
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**Leptospires invade tissues through moist skin or via mucous membranes, aided by their motility
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**Leptospires may invade via receptor-mediated endocytosis
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**They disseminate through the body via the blood stream
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**Antibodies clear organisms from the blood stream after about 10 days of infection
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**Organisms may persist in the renal tubules, uterus, eye or meninges
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**Evade phagocytosis possibly via macrophage apoptosis
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**Damage red blood cell membranes and endothelial and liver cells, leading to haemolytic anaemia, jaundice, [[Pigmentation and Calcification - Pathology#Haemoglobin|haemoglobin pigmentation]], haemoglobinuria and haemorrhage in acute leptospirosis
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*Diagnosis
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**Clinical signs and history of exposure
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**Dark-field microscopy of urine may detect organisms
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**Isolation from blood or urine by culture or animal inoculation
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**Identificaiton or certain serovars using DNA probes and serology
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**FLuorescent antibody technique for identification in tissues
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**Silver impregnation
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**Molecular techniques such as PCR
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**Serology using microscopic agglutination test or ELISA
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*Clinical infections
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**Cattle and sheep
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***Cattle are maintenance hosts for ''L. borgpetersenii'' serovar ''hardjo''
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***''L. interrogans'' serovar ''hardjo'' is host-adapted to cattle
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***Acute disease in susceptible heifers, with fever and agalactia of all quarters; abortion and stillbirth may occur
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***Diagnosed by rising antibody titre in paired serum samples
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***Infection in sheep may cause abortion and agalactia
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***Urinary excretion can be reduced by administering dihydrostreptomycin or amoxycillin
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***Incactivated vaccines are of questionable efficacy
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***Serovars ''pomona, grippotyphosa'' and ''icterohaemorrhagiae'' cause pyrexia, haemoglobinurea, jaundice, anorexia, uraemia due to renal damage and death in calves and lambs
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**Horses
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***Clinical disease rare
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***May be maintenance host of serovar ''bratislava'', which causes abortion and stillbirth
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***Incidental hosts for serovar ''pomona'', suffering from abortion and renal disease
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***Chronic leptospirosis may cause an immune-mediated anterior uveitis
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**Pigs
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***The rodent-adapted serovars ''icterohaemorrhagica'' and ''copenhagenii'' cause acute disease in pigs
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***Severe disease in young pigs
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***Serovar ''pomona'' is the host-adapted species, and may be shed in the urine
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***Infections may cause abortions and stillbirths
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***Pigs are maintenance hosts for serovars ''tarassovi'' and ''bratislava'', which may cause reproductive failure
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**Dogs and cats
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***Serovars ''canicola'' and ''icterohaemorrhagica'' cause leptospirosis in dogs, but are vaccinated against
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***Serovars ''pomona'' and ''grippotyphosa'' are becoming important
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***The host-adapted serovar ''canicolar'' causes acute renal failure in puppies; a chronic uraemic syndrome may follow
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***Incidental infections with serovar ''icterohaemorrhagica'' or ''copenhagenii'' cause renal failure
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***''L. icterohaemorrhagiae'' may cause [[Pigmentation and Calcification - Pathology#Hepatic (Toxic) Icterus|hepatic jaundice]]
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***Serovar ''bratislava'' causes abortion and infertility in dogs, which may be the maintenance host
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***Infections uncommon in cats
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===''Borrelia''===
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*Longer, wider, helical spirochaetes with a linear chromosome and linear and circular plasmids
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*Obligate parasites transmitted by arthropod vectors
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*Cause systemic infections in many animals and humans
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*Slow growth in specialised culture media
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*Lyme disease
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**Caused by ''Borrelia burgdorferi''
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**Reported in humans, dogs, horses, cattle, sheep
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**Ticks are the vector, which acquire the infection from small rodents, the reservoir hosts
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**Ticks transmit the infection to large mammals such as deer and sheep
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**''Ixodes ricinus'' is the most common tick vector in Europe
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**Pathogenesis
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***Virulence of the borreliae requires a change in expression of an outer membrane protein following ingestion of blood by the tick
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***Borreliae multiply in the blood stream of susceptible hosts and disseminate throughout the body
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***Localisation in joints, brain, nerves, eyes and heart can occur
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***The associated lesions may be in part caused by the host immune response
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**CLinical signs
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***May be subclinical in endemic areas
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***Clinical manifestation depends on the site of localisation of organisms
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***Disease in dogs may cause fever, lethargy, arthritis, cardiac, renal or neurological disturbance
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***Horses suffer similar clinical signs but also lameness, uveitis, nephritis, hepatitis and encephalitis
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***Cattle and sheep may suffer from lameness
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**Diagnosis
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***Laboratory confirmation difficult due to low numbers of organisms and fastidious growth requirements
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***History of exposure to ticks in an endemic region and clinical signs
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***Rising antibody titre to ''Borrelia burgdorferi'' detected by ELISA
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***Immunofluorescence
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***Culture in Barbour-Stoenner-Kelly medium for 6 weeks under microaerophilic conditions
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***PCR
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**Treatment and control
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***Amoxycillin and oxytetracycline in the acute phase; prolonged treatment in the chronic phase
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***Tick control and removal
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***Vaccines including whole cell bacterins and recombinant subunit vaccines available for dogs
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===Avian spirochaetosis===
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*Caused by ''Borrelia anserina''
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*Acute, endemic disease of birds in tropical and subtropical regions
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*Chickens, turkeys, pheasants, ducks and geese susceptible
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*Transmitted by soft ticks of the ''Argas'' family, but also via contact with infected material such as blood and tissues
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*Transmitted transovarially and trans-stadially via the tick population
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*Outbreaks during peak tick activity during warm, humid conditions
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*Fever, anaemia and wight loss occurs, with development of paralysis later
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*Immunity is serotype specific
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*Diagnosis using dark-field microscopy of buffy coat smears or immunodluorescence of blood or tissues
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*Giemsa-stained smears and silver impregnation of tissues
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*Isolation of borreliae by inoculation of embryonated eggs or chicks
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*Antibiotic treatment
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*Inactivated vaccines available
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===''Brachyspira'' and ''Serpulina''===
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*Anaerobic, intestinal spirochaetes, found in normal and diseased pigs
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*Enterophogens of pigs
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*''B. hyodysenteriae, B. pilosicoli, B. innocens, Serpulina intermedia'' and ''S. murdochii'' occur in pigs
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*Carrier pigs shed ''B. hyodysenteriae'' for up to 3 months, acting as a source of infection for healthy pigs
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*Demonstrated in stained faecal smears or silver-stained histopathology sections
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*Cultured anaerobically on selective blood agar
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*Spirochaetes differentiated by pattern of haemolysis on blood agar as well as molecular techniques
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*Pathogenesis
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**Motility in mucous allows colonisation of pig intestine
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**Haemolytic and cytotoxic activiity important for virulence
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**Attachment of ''B. pilosicoli'' to epithelial cells of colonic mucosa disrupts their function and leads to their shedding and oedema
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*Clinical infections
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**''B. hyodysenteriae'' causes [[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Swine Dysentery|swine dysentery]]
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**''B. pilosicoli'' causes porcine intestinal spirochaetosis
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**Infection is acquired via contaminated faeces
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**Disease spreads slowly through the herd
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**Dogs, rats, mice and flies may act as transport hosts
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**''B. hyodysenteriae'' survives several weeks in moist faeces
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*Clinical signs
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**''B. hyodysenteriae'' causes dysentry in weaned pigs 6-12 weeks old; pigs lose condition and become emaciated; appetite is decreased; large amount of mucous may be present in the faeces; low mortality; poor feed conversion ratio
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**''B. pilosicoli'' causes less severe signs than swine dysentry; reduced feed conversion rates occur
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*Diagnosis
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**History, clinical signs and gross pathology
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**Anaerobic culture on blood agar with added antibiotics for at least 3 days
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**''B. hyodysenteriae'' causes complete haemolysis whereas other spirochaetes cause partial haemolysis
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**Immunofluorescence, DNA probes and biochemical tests
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**Serology using ELISA can be used on a herd basis
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**PCR
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[[Brachyspira hyodysenteriae]]
 
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