Spiral Bacteria Flashcards
Campylobacter species-General characteristics
gram negative gull winged on gram stain motile with flagella at both ends microaerophilic (5% oxygen max) Like enriched media Non-fermentative (unlike enterobacteria) Oxidase positive Commensals of intestinal tract in adult animals pathogenic in repro tract and enteric tracts (mostly in young animals)
Campylobacter fetus ss. fetus- diseases caused
sporadic abortion in sheep (often late in gestation)
transmitted by contaminated food or water
sporadic abortion in cattle, goats, pigs and horses
Bloodstream infection in humans (usually but not always with underlying immuno-compromise)
C. fetus ss. fetus- how the bacteria causes abortion
organism acquired by fecal contamination and grazing. organisms invades gut tissues–> bacteremia–>tropism for placenta
Invades fetus and kills it
Abortion in the 3rd trimester results from placentitis–> aborted mummified fetus
C. fetus ss fetus abortion presentation
mummified fetus
necrotic donut-like lesion in liver d/t bacteremia
C. fetus ss fetus ovine abortion pathogenesis- S protein
High molecular S weight protein completely covers the surface of the bacterium (similar to a capsule, but not made of polysaccharides).
S-proteins fail to bind complement–> avoid opsonisation–> prevents phagocytosis by neutrophils.
S-layer mutants are of reduced virulence in disease model.
S-layer shields LPS, perhaps as a means of decreasing immunogenicity.
C. fetus ss. venerealis- disease it causes and how it’s transmitted
causes bovine venereal campylobacteriosis aka sexually transmitted bovine infectious infertility.
transmitted by infected bulls through normal breeding or AI
Organism is recovered from glans penis and distal urethra of infected bulls
Causes an ascending infection in cows from vagina to cervix to uterus to oviducts.
causes TEMPORARY infertility- eventually protective immunity develops (IgA in vaginal mucous and IgG in uterus) and normal repro function is restored.
Abortion is <10% of infected cows.
Pathogenesis of BVC
bacteria persists in vagina of cow due to antigenic shifts in the immuno-dominant antigens of the S-layer proteins (sapA)
genomic re-erranges of the locus – invertible segment that allows different versions to flip in and out
sapA promoter on invertible segment can flip and allow change in expression from S-layer protein gene cassettes.
Develop an IR to all the different versions the organism can present.
Intestinal campylobacter in dogs (C. jejuni)
causes acute diarrhea in puppies and other young animals. Typically develops diarrhea after buying of the dog
Typical history of recently acquired puppy developing bloody or watery diarrhea followed by owner or child getting diarrhea –> zoonotic.
Healthy animals may shed C. jejuni with no symptoms
May be a part of a mixed infection
C. upsaliensis
also causes acute diarrheal dz in dogs- can be acquired by humans.
C. jejuni infection presentation
colitis with localized hemorrhage and inflammation, lots of mucus production.
C. jejuni and C. coli in animals
C. jejuni is part of normal intestinal flora in birds–> no disease association with poultry
C. coli is normal intestinal flora in pigs
C. jejuni and C. coli may cause acute diarrhea in young animals but not in older animals. in the 70s it was discovered that these organisms cause acute diarrhea in humans.
C. jejuni and C. coli in man
most frequently identified cause of acute infective bacterial diarrhea in man.
zoonosis- acquired from animals via food, or direct contact (mainly from poultry)
Campylobacter enteritis in man
incubation ~3 days severe abdominal pain small volume of blood diarrhea, or watery diarrhea with blood, or just watery diarrhea fever malaise, myalgia rigors, high fever, delirium.
Campylobacter infection- how does man get it?
it’s food borne! poultry, raw meat, unpasteurized milk, untreated water, shellfish (fecally contaminated)
broiler chickens are the main source of infection
Lab ID of campylobacter species
use of selective media containing ABX cocktail to suppress fecal commensals.
grow at 37 or 42 degrees (42 is body temp of chicken)
microaerophilic atmosphere (5% O2, 5%CO2, 5%H, 85% N)
confirm by smear and gram stain
identify using API
ABX sensitivity testing possible
Culture characteristics of campylobacter
spreading colony, looks very wet, characteristic smell.
Helicobacter pylori
spiral organisms in stomach ulcers in man. suggested that it may be important in the pathophysiology of chronic active gastritis and peptic ulceration in man.
Main cause of duodenal and gastric ulceration, and is an important risk factor for gastric adenocarcinoma and lymphoma
Spirochaetes
Spiral, flexible, gram negative rods- although we can’t stain with gram stain, we have to stain with silver.
Arranged in spirals, with flagella (axial fibrils) originating at each end and curling around the body within the outer envelope
Highly motile- virulence factor
Borrelia-general characteristics
large spirochetes, live in the blood
aerobic, or sometimes microaerophilic
Borrelia- important species
B. anserina: tick transmitted in birds by Argas perscius- (tropical dz)
B. burgdorferi (lyme): tick transmitted- north america
in europe, also B. afzellii, B. garinii- cause joint infxn and CNS disease
Lyme Borereliosis
Late 1970’s Old lyme ct- discovered due to a higher than expected incidence of childhood arthritis. most prevalent tick-borne disease in the US, europe and parts of asia.
Lyme disease- stages
Incubation period ~7-14 days
Skin sign: erythema migraines (not everone get this skin stage). spirochetes multiply in the skin and enter the circulation– spreading lesion. rash appears days to weeks after a tick bite
Second Stage: musculoskeletal signs (migratory joint, muscle pains), rare CNS signs, cardiac damage (meningitis, myocarditis–very serious signs of inflammation)
Canine lyme borreliosis
Sudden onset of non-specific symptoms: lethargy, inappetance, fever, swollen LN, acute arthritis and increased synovial fluid
Inflamamtion in joint space
-high synovial fluid cell counts (90% PMN), fibrin
Swollen, edematous LN
Also, CNS infection can progress: cervical pain, depression, anorexia, seizures
Fatal renal disease: lyme specific immune complexes and complement deposition in glomeruli.
Diagnosis is clinical/serological (antibodies- confirmed with western blot)
Epidemiology of lyme
human/canine encroachment into habitat of deer. spread from deer, mice to humans/dogs by bite of soft ticks
Infection rate in nymphs 10-25%, infection rate in adult ticks no infection.
Can get intrauterine transmission in dogs.
If tick hasn’t been on very long, risk of transmission is very low.
Prevention, control and therapy of lyme
ABX therapy in acute infection
- successful for primary disease
- secondary or tertiary disease rx often unsuccessful. If disease progresses, ABX too late for CNS/myocarditis/joints–tx with steroids.
- doxycycline, amoxicillin
- duration usually 4 weeks (slow multiplication and in vivo persistence)
- dogs clinically recover in 24-48 hours.
Leptospira
very fine (0.2 micrometers in diameter, 10 micrometers long)
tightly coiled with hooked ends
aerobic
fastidious and easily destroyed yet can survive in environment.
highly motile
Leptospira species
8 pathogenic species, >200 serovars
disease in humans, domestic animals
zoonosis; rodents, domestic animals
Most widespread zoonosis? suggested– widespread in developing countries
Major pathogens= interrogans and borgapetersenii
Serogroups of veterinary important
L. interrogans canicola (interstitial nephritis in dogs)
L. interrogans icterohemorrhagiae (weil’s disease, leptospiral jaundice)— carried by rats, most associated with humans. zoonotic disease causes renal failure and liver dz.
L. interrogans pomona- pigs
L. borgpetersenii/hardjo- cows
L. interrogans hardjo- cows
Epidemiology of lepto- Animals
Many serovars apparently host-adapted
disease relatively mild, sporadic
venereal transmission, lifelong colonization of genitourinary tract (like to live in kidney)
-hardjo in cattle, tarassovi (swine)
Others are NON-host adapted
cause catastrophic infections: abortion storms, death of adults
brief carrier state- lifelong in survivors
serovars pomona (swine, cattle) and canicola (dogs)
Epidemiology of lepto- humans
temperate climates
-few serovars- associated with farm animals and rodents
-infection via direct contact: infected farm animals (urine, aerosols in milking parlors, milk of infected cows)
Tropical climates: many serovars, many reservoirs, exposure via environmental contamination
urban environment: rodent-borne lepto frequently misdiagnosed.
Pathogenesis of lepto
Enter through cuts, abrasions, conjunctivae
Evade local defenses, produce bacteremia: shorter (host-adapted strains) or longer (non adapted)
proliferate in liver, kidneys, spleen, meninges
Antibodies and complement eliminate leptospires from blood stream, tissues other than brain eye and kidneys, multiply in PCT. excreted in urine by asymptomatic reservoir hosts.
Pig lepto
Bratislava (host-adapted): clinical picture similar to hardjo in cattle
Pomona (non-adapted): infection similar to pomona in cattle–> abortion storms, fever, icterus, anemia, metritis, meningoencephalitis, death
Source may be wildlife (skunks, raccoons, opossums, deer)
horse lepto
Horses:
- bratislava adapted: mild, sporadic infection of adults, late-term abortions
- pomona, kennewicki non-adapted: fever, icterus, abortion.
Dog lepto
bratislava (adapted): mild disease, infertility, weak pups
Canicola (non-adapted): high fever, myalgia, blood vomit
vascular damage; DIC, melena, epistaxis, petechial hemorrhage
renal localisation- leptospiruria by 2 weeks PI
acute nephritis progresses to chronic interstitial nephritis, renal failure.
Brachyspira
Anaerobic, large spirochetes, grow on blood agar to cause varying degrees of Beta hemolysis.
Live in LI of animals and birds where some cause inflammation, diarrhea dysentery (small volume bloody diarrhea with tissue inflammation).
Brachyspira hyodysenteriae
Large spirochete, clearly visible in gram stained smears
7-14 filaments originating from each end
beta hemolytic colonies on blood agar after 48 hours in anaerobic conditions
infects porcine large intestine to cause swine dysentery.
B. pilosicoli
smaller than B. hyodystenteriae with 4-5 filaments overlapping centrally
less hemolytic
several different types
causes spirochetal diarrhea in pigs, chickens, dogs and humans
Not blood, cf. swine dysentery—just causes acute D, not invasive into tissue
Colonises colonic epithelium to give false brush border- vast numbers of spirochetes adhering to the mucosal border.
