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Yersinia species

non-lactose fermenting, gram negative rods

Motile- i.e. those that cause enteric disease(not y. pestis)

Y. pestis (plague), Y. enterocolitica, Y. pseudotuberculosis (enteric disease, septicemia) pathogenic for animals and man.

Y. ruckeri causes perioral hemorrhage inflammation in fish

Demonstrate bipolar staining (look like safety pins) in Giemsa stained smears from animal tissues



Yersinia species ecology

Y.pseudotuberculosis and Y. enterocolitica in intestinal tract of wild mammals, birds, and domestic animals--reservoir of infection of foodborne pathogens in humans

All may be reservoirs of infection

Many avian species may act as amplifier hosts and may transfer organisms mechanically

Both organisms grow in wide temp. range (4-42)

In endemic areas, wild rodents are important reservoirs of Y. pestis. Fleas, especially Zenopsylla cheopis (oriental rat flea) transmit infection to man and other animals. 



Y. enterocolitica

pigs and other domestic animals, wildlife: subclinical enteric infections, occasionally enteritis

ewes: sporadic abortion

humans: gastroenterocolitis 


Y. pseudotuberculosis

farmed deer, sheep, goats, cattle, buffaloes, pigs: enteritis in young animals, subclinical infections common in older animals, mesenteric lymphadenitis

nb: mesenteric lymphadenitis- swollen mesenteric LNs-->severe abdominal pain-->masquerades as appendicitis 

cattle, sheep, goats: sporadic abortion

g. pigs and other lab animals: focal hepatic necrosis, septicemia

caged birds: septicemia

humans: entercolitis, mesenteric lymphadenitis


Y. pestis

humans: bubonic and pneumonic plague

rodents: sylvatic plague

cats: feline plague. 


Pathogenesis of Yersinia

pathogenic enteric yersinia invade some cells (M cells) of peyers patches and prevent uptake by other cells (phagocyte)

virulence: 70kb plasmid. plasmid and chromosomal encoded virulence factors required for survival and inhibit phaogcytosis by PMNs and macrophages.

TTSS secretes effector proteins into phagocytic cells- "YOPS"

Survival of Y. enterocolitica and Y. pseudotuberculosis is enhanced by anti-phagocytic proteins (Yops) secreted by organism (via TTSS) which interferes with normal functioning of neutrophils and macrophages in host.

This system allows extracellular bacteria adhering on surface of cells to secrete and inject bacterial effector proteins called Yops into the cytosol of the target cell in order to disable or alter function.

In GI mucosa, bacteria prevent phagocytosis, replicate in mesenteric lymph nodes with the development of necrotic lesions and neutrophil infiltration. 


Clinical infections of yersinia

Y. pseudotuberculosis causes enteric infections which are often subclinical. Enteric disease caused by Y. pseudo is common in farmed deer in Australia and NZ (also, sheep, goats and cattle under 1 year)

Septicemia (pseudotuberculosis) occurs in lab rodents and aviary birds

Overcrowding, sudden, feather ruffling, necrotic foci in liver PM. 

Treatment is seldom feasible due to acute nature of the disease

In rodents, organism introduced through contact with contaminated food or wild rodents. 

Diarrhea and weight loss leads to emaciation and death. some die suddenly from septicemia. 


Generally: yersinia pseudotuberculosis causes enteric disease in younger animals. Adults immune to disease but not carriage. 


Clinical infections of Y. enterocolitica

wild and domestic animals may act as a reservoir for what is primarily a human enteric pathogen.

pig is a natural reservoir for y. enterocolitica serotype 03 biotype 4 which is an important pathogen in humans. --common in intensive pig production 


Diagnosis of yersinia enterocolitica and y. pseudotuberculosis

histo exam of intestinal lesions

culture from feces, pus or tissue

plated on macconkey for growth at 37 or room temp


cold enrichment



Plague- yersinia pestis 

caused by gram negative bacteria yersinia pestis (3 biotypes)

zoonotic infection in rodents, transferred by fleas

organism in blood of rodents, blood+organism taken up by fleas and flea bites human (or dog or cat)

Endemic in Africa, Asia, USA (southwest and pacific coast plague foci) (prairie dogs, ground squirrels, antelope, chipmunks, wood rats, deer mice)

potential bioterror weppon (pneumonic plague- person to person spread by airborne route). 


Sylvatic and urban cycles of yersinia

Sylvatic: infective flea-->man 

wild rodent--> direct contact with man

Urban: domestic rodent and infective flea can both infect man 


Susceptibility to yersinia pestis

susceptibilities of different wild rodent species to plague mortality vary greatly.

praire dog of western N.america is extremely susceptible

epizootics among colonies of these animals spread very quickly and may cause greater than 99% mortality

other rodents, such as kangaroo rats in N. america can be infected but are relatively resistant and apparently suffer few ill effects. 

Certain species have both highly susceptible and relatively resistant populations. 


Clinical infection of y. pestis

can infect both dogs and cats in endemic areas. cats are particularly susceptible and may be a source of infection for owners and attending vets

Usually acquired by ingesting infected rodents

bubonic, septicemic, pneumonic

cats with pneumonic plague are a source of human infection through aerosol generation and should be euthanized.

human infection acquired through cat scratches and bites and fleas from infected cats. 


Plague syndromes in man

bubonic: fever, painful lymphadenopathy (bubo)

Septcemic: fever, hypotension with or w/out bubo

Pneumonic: cough, hemoptysis (expectoration of blood), with or w/out bubo

Meningitis: fever, nuchal rigidity usually with bubo


Virulence factors specific to Y. pestis

Fraction 1 (F1) antigen: capsule (made of polypeptide NOT polysaccharide) around bacteria- plasmid encoded- prevents opsonisation

HPI for Iron acquistion (also Ye, Yp)

Ymt protein on plasma is a phospholipase D required for survival in flea midgut

Hms locus required for efficient transmission to sub cut. sites. Bacilli lacking hms replicate in flea midgut but don't lodge en masse in proventriculus. Hms delivers infectious dose by bypassing organisms in proventriculus.

Pla is plasmid encoded and is essential for Y. pestis to disseminate from sub cut site of inoculation to LNs or blood. Pla is enzymes that allows dissemination 


Treatment and control of y. pestis

cats with suspected plague in isolation

IV tetracycline or choloramphenicol for bubonic

endemic areas: dogs and cats routinely treated for fleas

rodent control

effective human and animal surveillance

incidence in animal population

avoid sick/dead animals; avoid endemic areas or outbreak areas


insect repellents

isolate human cases (and contacts)

treat human cases with ABX


Pseudomonas aeuroginosa and Burkholderia species

gram negative rods

obligate aerobes (cf enterobacteria which are facultative anaerobes)

oxidize (don't ferment) CHOs

oxidase and catalase positive

motile by one or more polar flagella (B. mallei non motile)

grow well on MacConkey agar

P.aeuroginosa produces diffusible pigments (pyocyanin, pyoverdin)

P. aeruginosa is an opportunist pathogen- doesn't cause disease within normal immune system- cause severe disease in neutroopenic animals 

B. mallei causes glanders (in horses), B. pseudomallei causes melioidosis (v. virulent, mimics TB)


Clinical conditions arising from pseudomonas aeruginosa infections

Cattle: mastitis, metritis, pneumonia, dermatitis, enteritis (calves)

Sheep: mastitis, fleece-rot, pneumonia, otitis media

Pigs: respiratory infections, otitis

Horses: genital tract infections, pneumonia, ulcerative keratitis

Dogs, cats: otitis externa, cystitis, pneumonia, ulcerative keratitis

Mink: hemorrhagic pneumonia, septicemia

Chinchillas: pneumonia, septicemia

Reptiles (captive): necrotic stomatitis 



pseudomondas are environmental organisms occuring worldwide in water, soil, vegetation

P. aeuroginosa may also be found on skin, mucous membranes and in feces

B. pseudomallei lives in soil where it may infect man and animals. Wildely distributed in tropical and subtropical regions of southeast Asia and australia

B. mallei may survive in environment up to 6 weeks, but it's reservoir is infected equidae. 


P. aeruginosa infections

Causes a wide range of opportunistic infections

predisposing factors with many of thse infections is defective or altered host defenses.

bovine mastitis linked to contaminated water for udder washing or insertion of intrammary abx

fleece rot in sheep (assoc. with prolonged rainfall)- reported in UK and australia- suppurative dermatitis. pyocyanin pigment produce by P. aeruginosa discolors the wool.

P. aeruginosa found in oral cavity of snakes causing necrotic stomatitis in reptiles kept under poor husbandry conditions. 


Virulence factors of p. aeuroginosa

these virulence factors are only important in immunocompromised animal.


survival in diverse environments and large number of virulence factors

toxins and pigments: endotoxin, pyocyanin, pyorubin, alpha oxyphenazine, fluorescein, pyocins, exotoxin a, exotoxin s

enzymes: elastase, phospholipase C, collagenase, gelatinase, lecithinase, alkaline protease, neutral protease, cytotoxin

binding proteins and capsules: fimbriae, alginate, pyochelin 


diagnosis of p. aeruginosa

specimens for lab diagnosis include pus (green pus sometimes), respiratory aspirates, MSU, mastitic milk, ear swabs

characteristic green-ish/teal color

pyocyanin production

NLF on MacConkey agar

oxidase postiive, tsi negative

API 20e

green sheen- grow on normal blood agar with characteristic smell 


Treatment and control

predisposing causes and sources of infection ID'ed and eliminated

P. aeruginosa VERY resistant to MANY abx so lab susceptibilty testing needs to be performed.

vaccines for farmed mink and chinchillas .


Glanders- Burkholderia mallei

gram negative rod

rare: once worldwide but now in middle east, india, pakistan, china, mongolia

contagious disease of equids characterized by formation of nodules and ulcers in respiratory tract and skin.

humans and carnivores also susceptible to infection- potential bioterrorism agent

transmission by ingestion of food or water contaminted by nasal discharges of infected horses; also by inhalation or skin abrasions. 


Clinical features

acute septicemia with fever, mucopurulent nasal discharge and respiratory signs

chronic disease more common presenting as nasal, pulmonary and cutaneous forms

ulcerative nodules develop on mucosa of the nasal turbinates and nasal septum

animals may die after months or recover and shed organisms from RT or skin. 

pathogenesis isn't well defined. 

treatment: test and slaughter; ABX inappropriate as treated animals may carry organism and transmit, cleaning and disinfection of contaminated areas. 


Macs infected with b. mallei--organism goes into vacuole then escapes using actin to move from cell to cell. 


Melioidosis- Burkholderia pseudomallei

endemic in soil and water in south east asia (vietnam time bomb- latent infection, can pop-up decades later) and tropical australia

infection from ingestion, inhalation or skin abrasion from soil/water contact

opportunisticpathogen- stress/immunocompromise predisposes to clinical disease- particularly likes diabetes

many animal species, including man, susceptible. subclinical infections occur in which organism may remain latent and then reactivate.

infection may be acute or chronic, septcemic, respiratory (mimic tb), disseminated and characterized by abscess formation. 

culture on blood agar or ashdowns( soil isolate- dry purple colonies) medium 

culture on blood agar is dry, wrinkled and smells like soil 



gram negative rods

grow at room temp

NLF, oxidase postivie

primarily pathogens of reptiles and fish although some can infect mammals and birds

A. hydrophila: Beta hemolytic--> enteritis and food poisoning in man

A. salmonicida: brown pigment, furunculosis in salmonids. 



TTSS of yersinia similar to E. coli and salmonella

Injectisome=needle complex at cell surface. Injectisome injects effector proteins which go into the macrophages.

Lots of yops have enzymes-->interefere with macrophage cell signaling.

other yops inhibit CK secretion to delay inflammatory response or induce apoptosis in macrophages.