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PSEUDOMONAS

SPECIES VIRULENCE FACTOR DISEASE HABITAT DIAGNOSIS TREATMENT


➢ Possess fimbriae and pili Cattle - Reticulopericarditis • environmental organisms – • Specimens for lab.exam (pus, • Predisposing causes and
– facilitate adherence to - Infertility water, soil and plants respiratory aspirates, mid-stream sources of infection should be
injured epithelial cells - metritis/uteritis • Skin, mucous mem., and in urine, mastitic milk and ear identified and eliminate (if
Pseudomonas with subsequent - cervicitis feces swabs) possible)
aeruginosa colonization - vaginitis • P. fluorescens and P. putida • BAP and MCA inoculated with
➢ Capsule and LPS – - balanoposthitis –occasionally infect suspected material – incubated • Surgical debridement and
– opportunistic protection against - mastitis freshwater fish aerobically at 37oC for 24-48 hrs. drainage should be provided
pathogen, occasionally antiphagocytic (linked to contaminated water used for
cause acute systemic destruction udder washing or to the insertion of Resistance ID criteria for isolates: • combination of:
disease ➢ Extracellular products contaminated intramammary antibiotic • P. aeruginosa is resistant to • Colonial morphology - gentamicin
– major nosocomial produced by some tubes) some disinfectants including • Fruity grape like odor - tobramycin
pathogen in human strains – toxins and Sheep - “green wool” or fleece rot (associated QUATS; chlorine-containing • Pyocyanin production - Carbenicillin
hospitals enzymes with heavy or prolonged rainfall) disinfectants are effective • Oxidase +, lactose – - Ticarcillin
–Important pathogen of • maceration of the skin surface ff.water • Pale colonies in MCA - Amikacin
patients with cystic Extracellular products penetration of the fleece allows colonization • With minimal moisture P. • TSI agar unchanged - Ciprofloxacin
fibrosis 1. Proteases, including elastase by the org., resulting to suppurative aeruginosa can survive for • Biochemical profile - colistin (polymixin E)
- involved in the invasiveness of the dermatitis long periods on water faucets, -
organism and destruction of tissue • The bluish green pigment produced by the utensils, floors, instruments, •Molecular techniques – PFGE, • Vaccination for farmed mink
2. Alginate org discolours the wool baths, humidifiers and PCR and chinchillas
- containing polysaccharide slime - Mastitis medical equipment • Serology (reaction of Somatic
layer - pneumonia (O) antigens)
- contributes to adherence and is - ulcerative keratitis • Pseudomonads are • Pyocin typing (bacteriocin
antiphagocytic - Purulent rhinitis susceptible to ethylene oxide typing)
3. Lecithinases and lipases - otitis or heat (boiling for 20 • active typing
- enhance invasiveness, destroy Pigs - necrotic pneumonia (respiratory minutes) • phage typing
tissue, and contribute to the infection)
inflammatory response - otitis
4. Exotoxin A - enteritis rhinitis
- inhibits protein synthesis, causes Horses - corneal ulceration
tissue necrosis (tissue damage) and - opacification (ulcerative keratitis)
contributes to lethality in severe - genital tract infection
infections; systemic toxicity - pneumonia
5. Exoenzyme S - abortion
– catalyzes the transfer of - guttural pouch infections
adenosine diphosphate-ribose to Dogs and - otitis externa
various guanosine triphosphate- cats - ulcerative keratitis
binding proteins; dissemination of - cystitis
the org. - post-operative septicemia
6. Leukocidin Mink - hemorrhagic pneumonia
- a cytotoxin, acts on cell - septicemia
membranes, inhibiting and mortality rate up to 50%
ultimately destroying neutrophils Chinchillas - pneumonia
and damaging endothelial cells - septicemia
7. Phospholipase C (heat-labile Reptiles - necrotic stomatitis
hemolysin) (captive) ➢ Snakes – the org.is found in the
- destroys lecithin-containing oral cavity, cause necrotic
lipoprotein of the alveolus stomatitis in captive reptiles, kept
(pulmonary surfactant) and thus under poor husbandry
contributes to tissue destruction Fowl - septicemia
and atelectasis - respiratory infections
8. Pyocins
- prevents or reduce colonization
of infected sites by other bacteria Pathogenesis and pathogenicity

• Fimbriae (type IV pili) – initial phase of attachment


• Flagella and LPS – adherence
• Exoenzyme S
• Extracellular slime
• Outer-membrane LPS
• Resistance to complement mediated damage
• Ability to obtain iron from host tissues

BURKHOLDERIA
SPECIES CHARACTERISTICS DISEASE FORMS PATHOGENICITY DIAGNOSIS
Forms of the disease: VIRULENCE FACTOR: • Discharges from lesions,
•obligate pathogen of horses, Glanders • Acute : • Capsule tissue containing early nodules
other solipeds, humans and • is a contagious, usually chronic disease particularly of: septicemic form – •Type III and IV secretion or pus from ulcers are
Burkholderia carnivores - Horses (chronic) o fever systems submitted, blood for serology
• facultative intracellular - mules (acute) o mucopurulent nasal • Quorum sensing mechanisms • The organism grows well on
mallei pathogen that does not occur in - donkeys discharge • Encoding proteins and fimbriae standard laboratory media,
nature • characterized by the formation of tubercle-like nodules o respiratory signs • Able to survive intracellularly, including MCA and blood agar
– found in soil and • Colonies: small, round convex, (granulomas) that frequently break down to form ulcers • Chronic: utilized actin-based motility incubated aerobically at 37oC
translucent yellowish • Sporadic cases of disease occur in the Middle East, India, o Nasal similar to L.monocytogenes for 2-3days
occasionally infects man
• glycerol-enhances growth • Pakistan and China o Pulmonary • Colonies are shallow, round,
and animals
infection is usually via the • Humans and carnivores – susceptible o skin/cutaneous Gross Lesions-Necropsy convex, and opaque and
• Wild rodents – are
respiratory tract (farcy) • Ulcers, nodules, stellate scars in become yellowish green or
reservoirs
• the disease is spread directly Other animals affected • Nasal form upper respiratory brown on aging.
– major pathogen of
from animal to animal and • Cattle, swine, rats, birds are resistant; humans o ulcerative nodules • Pneumonia • In MCA – non-lactose
Equidae; causes both
indirectly by fomites and members of the cat family and carnivores develop on the • Firm rounded miliary nodules fermenter
acute and chronic dss,
are susceptible mucosa of the nasal • Swollen lymph nodes and • On blood agar, colonies tend
lesions in the skin and
• Carnivores – may contract the dss. by eating septum vessels to be slimy.
respi.tract
infected carcases o lower part of the • Cultural; agar enriched with
turbinates glycerol or selective media
o Purulent, blood- TREATMENT • Definitive identification is
Transmission stained nasal Treatment and Control based on a number of
• Ingestion of food or water contaminated by nasal discharges discharge • Test and slaughter policy – in biochemical tests.
of infected Equidae o regional countries where dss.is exotic • Mallein test (analogous to
• Inhalation or skin abrasions – less common lymphadenopathy • Antibiotic therapy is tuberculin testing). Mallein (an
• Carnivores – eating contaminated/infected carcasses inappropriate in endemic areas extract of B. mallei cultures) is
Transmission: Animals o Ulcers eventually • Effective cleaning and injected intradermally (0.1ml)
• Ingestion – Contaminated food and water – Skin exudates, heal leaving star- disinfection of all contaminated below lower eyelid = positive
respiratory secretions shaped scars areas – formalin (1.5%) or an reaction – local swelling and
• Inhalation • Respiratory form iodophor (2%) mucopurulent ocular discharge
• Direct contact o respiratory distress • Trimethoprim- after 24 hrs.
• Fomites – Grooming tools – Harnesses o development of sulfamethoxazole, sulfa and • AIT (Straus reaction)
tubercle-like lesions tetracycline; no bacterins or Laboratory diagnosis:
Transmission: Humans throughout the vaccines used • Serologic tests
• Direct contact with infected animals – Abraded skin – lungs • ELISA
Mucous membranes • Cutaneous form (farcy) • Complement Fixation Test
• Fomites o lymphangitis (CFT)
• Inhalation o nodules occur along • Agglutination
• Ingestion the course of the • HA
• Person-to-person (rare) lymphatic vessels of
• Humans: abscesses, malaise, nasal and mouth ulcers, the limbs
inflammation of joints and fever o Ulcers develop
o discharge a
Who Is At Risk? yellowish pus
• Veterinarians
• Grooms
• Horsemen
• Butchers
• Lab workers
Modes of infection: Pathogenesis and Diagnosis
• Facultative intracellular parasite Melioidosis / Pseudoglanders • Ingestion pathogenicity • Isolation and ID
• Opportunistic pathogen • It is chronic and characterized by purulent granulomatous • Inhalation Implicated in disease production/ • Pus from abscesses and
Burkholderia • Found in tropical and subtropical nodules in the lungs, liver, spleen, lymph nodes, joints and • Wounds and abrasions – VIRULENCE FACTOR: material from nodular material
soils and water in Southeast Asia,
pseudomallei Central Africa and Australia
subcutis skin contamination from • Capsule are submitted
• The acute disease occurs more often in young animals environmental sources • Type III and IV secretion • Blood for serology
• survive up to 30 months in soil • Those with impaired immune systems are susceptible • Outbreaks occur most systems • The organism grows well on
– can survive in the
• Active substances associated: • In spite of extensive lesions, animals may appear normal frequently during or after • Exotoxin BAP and MCA (utilize lactose -
environment for up to 6
endotoxin, exotoxin, proteases and • Lesions of meliodosis are frequently seen in slaughterhouses heavy rainfall and flooding • Dermonecrotic protease incubated aerobically at 37oC
weeks
hemolysin in endemic regions • Lecithinase for 2-3days
– cause chronic
suppurative lesions in • Colonies are smooth and
the lungs and other Treatment and Control mucoid to dry and wrinkled
organs of a wide range • Slaughter of infected animal- in • Growth has a pungent,
of species countries where disease is exotic earthy odor
• Tx is inexpensive and unreliable • Strains are nonhemolytic,
- Tetracyclines motile and oxidase positive
- novobiocin combination Diagnosis
- chloramphenicol • PCR Techniques
- TMPS (trimethoprim- • ELISA, CFT, indirect
sufamethoxazole) hemagglutination tests –
- Imipenem detect serum antibodies •
- Ceftazidime Immunofluorescence assay
• Keep animals on dry pastures • Straus reaction: the organism
and premises is injected intraperitoneally
positive reaction result to
• vaccines are not avail.at present purulent orchitis using guinea
(are being developed in some pig observed in 2-3 days
countries)
• Detection and treatment of
infected animals
HISTOPHILUS, HAEMOPHILUS/AVIBACTERIUM
SPECIES INFORMATION HOST/ DISEASE PATHOGENICITY DIAGNOSIS TREATMENT
- adhere firmly to - Thromboembolic ✓ Isolate affected animals
several host cell meningoencephalitis IN GENERAL: IN H.SOMNI IN CATTLE IN GENERAL: – w/ clinical
types Cattle - Septicemia H. somni, H. parasuis, A. - Cause degeneration of - Diagnostic procedures signs of septicemia,
- cause thrombi - bronchopneumonia paragallinarum macrophages and - Specimens for lab.exam should be monitored
formation (in association with other suppresses neutrophil depend on the clinical closely to detect early
Histophilus - can pathogens)  heterogenous org. function condition and type of lesions signs of signs of the
somni - survive and - sporadic reproductive  their virulence differs - degeneration of vascular - Serological tests – little disease
multiply within tract infections from strain to strain endothelial cellls and diagnostic value
bovine  Some isolates are transmural neutrophil - Either chocolate agar or ANTIBIOTICS:
- monocytes CLINICAL SIGNS: purely commensal infiltration (prominent BAP inoculated with a ✓ Oxytetracycline
- found on the - High fever  H. parasuis serotype findings in TME) streak of S.aureus incubated ✓ Penicillin
brain & - Depression 3 – found in the URT - Outer membrane under 5-10% CO2 at 37oC ✓ Erythromycin
- meninges - Accompanied by  H. somni - avirulent proteins – widespread for 2-3days in a moist ✓ Potentiated
- Commensal of the blindness, lameness preputial isolate lack dissemination of the atmosphere sulphonamides
male and female - and ataxia many putative bacteria ID criteria for isolates: ✓ Commercially available
bovine genital - Sudden death due to virulence factors - small, dewdrop-like colonies bacterins
tracts myocarditis  Variability in strains VIRULENCE FACTORS: after 1 to 2 days
- Also colonize the - Arthritis can have difficulties in - Capsule - Enhancement of growth by
URT - Sporadic cases of diagnosis - Endotoxin CO2
- One of the abortion, endometritis,  Natural habitat of all - Reqt. for X or V growth
bacterial otitis and mastitis strains H. somni, H. The four principal syndromes factors
pathogens parasuis, A. that - Biochemical profile
commonly isolated LESIONS: paragallinarum - is characterize the H.somni - -PCR based tests
from the enzootic - fibrinous meningitis with the host animal disease complex
calf pneumonia arterial thrombosis and (disease occurs are: IN H.SOMNI IN CATTLE:
- Environmental necrosis opportunistically) 1. Respiratory
stress factors - hemorrhages on serous  young or previously involvement - Severe neurological signs in
contribute to the surfaces and unexposed animals (with fibrinopurulent young feedlot cattle
development of - muscles are susceptible to bronchopneumonia and - Multiple foci of
clinical disease - enlarge lymph nodes infections by bacteremia or septicemia ) hemorrhagic necrosis,
- hemorrhagic areas in Haemophilus species 2. Localization in the detectable grossly in
brain  Endotxin CNS affected brains at PME
(with thromboembolic - Confirmation by isolation
meningoencephalitis and ID of org. from CSF,
(TEME) resulting from postmortem lesions (blood,
vasculitis of meningeal brain, liver, spleen, in media
vessels) enriched with yeast extract
3. Fibrinous pleuritis at 10% CO2) and aborted
and arthritis fetuses
4. Genital infection
with vaginitis,
endometritis and
cervicitis
• Epididymitis (young
rams)
Histophilus Sheep
somni *EWES
- Vulvitis
(ovine strain) - Mastitis
- reduced reproductive
performance in ewes
*LAMBS
- septicemia EPIDEMIOLOGY
- arthritis - found in the nasal
- meningitis cavity of many pigs
- pneumonia - onset of disease may
- formerly • Glasser’s disease be associated with Clinical signs ✓ Tetracyclines
Haemophilus Pigs - secondary invader in exposure to stress - I.P. 1-5 days ✓ Penicillin
parasuis respiratory disease such as transport or - C.S.develop in conventionally reared pigs 2-7 days ff.exposure ✓ potentiated
- part of normal (Affecting pigs - Manifests as movement to new to stress factors (e.g.weaning, transportation) sulphonamides
bacterial flora of fr.weaning up - polyserositis and pens - Anorexia, pyrexia, lameness, recumbency and convulsions ✓ Vaccination – bacterins
Glasserella nasopharyngeal to 12 wks.of leptomeningitis - disease may follow - Cyanosis and thickening of the pinnae ✓ Vaccination – An
parasuis mucosa of pigs Age) - respiratory signs are seen other infections such - Pigs may die suddenly w/o signs of illness inactivated vaccine is
but chiefly in older as swine influenza - signs and lesions resemble those of polyserositis caused by available for the
becomes pigs. - chiefly a secondary Mycoplasma hyorhinis prevention of Glasser’s
pathogenic in the invader, the organism - sudden onset, and several pigs are affected at the same time disease and enzootic
presence of • infectious arthritis may be a serious - Affected animals show pyrexia (temperature, 41°C), anorexia, pneumonia
Influenza virus and pneumonia primary pathogen in cough, and dyspnoea) ✓ Immunity is serotype
secondary invader - stresses such as transport, SPF herds - Lameness is also seen, with swollen joints and pigs walking specific
in swine influenza, cold and weaning - Piglets may have with short strides and on tiptoes. ✓ oral medication in
enzootic predispose to the disease colostral immunity, - CNS signs may develop in untreated cases, and discoloration water or food (if
pneumonia and in older pigs and Glasser’s disease of the skin may precede death eating)
other is seen chiefly in pigs - Chronic cases may follow initial infection: chronic arthritis, Injections of:
pneumonia from weaning to 4 intestinal obstruction caused by peritonitis, and heart failure - penicillin–
months of age - Deaths and abortion have been reported in sows suddenly streptomycin,
- disease can be a exposed to Glasser’s disease in SPF herds. - oxytetracycline
complication of other - trimethoprim-sulpha
respiratory diseases DIAGNOSIS
such as enzootic - Diff.dx: Strep.suis and Mycoplasma hyorhinis, Swine
pneumonia and PRRS erysipelas - produce similar clinicopathological changes
- Postmortem findings: fibrinous polyserositis, polyarthritis,
Virulence factors: and meningitis
- Capsule - Isolation and ID of G.parasuis from joint fluid, heart blood,
- Endotoxin – CSF or postmortem tissues
responsible for - PCR and ELISA
thrombi formation - complement fixation tests on serum, and culture of the
organism from joints and other tissues (e.g. the pericardium)
Lesions: serofibrinous - Culture is difficult and requires special media
serositis and synovitis
- formerly named • Chickens • Infectious coryza Virulence factors: Clinical Signs Diagnosis medication of water and
Haemophilus • pheasants - respiratory disease - Outer membrane • mildest form of the  Based on clinical signs (facial feed with:
paragallinarum • Turkeys - Affects URT and proteins – aid in disease swelling) and lesions ✓ sulphonamides
Avibacterium - produce more • guinea paranasal sinuses of colonization - Depression  identification of the bacteria ✓ Erythromycin
severe disease in fowls chickens - Hyaluronic acid - serous nasal discharge in a Gram-stained smear ✓ oxytetracycline
paragallinarum the presence of - morbidity rate is high, capsule – toxic when - Occasional slight facial from sinus
viral or * mainly but mortality rate is low injected to chickens swelling  Confirmation is by isolation Several new-generation
mycoplasmal affects pullets - disease is limited • more severe form and identification - requires antibiotics:
infection and layers; primarily to chickens and - severe swelling of one X (Haemin) and V (NAD) ✓ fluoroquinolones
- disease has both broilers are has no public health Morbidity and Mortality or both infraorbital factors, preferably in raised ✓ Macrolides
acute and chronic occasionally significance - IC is usually sinuses CO2 such as a candle jar are active against infectious
forms and is affected - recovered chickens may characterized by low - edema of the  Immunoperoxidase staining coryza
characterized by carry and shed the mortality and high surrounding tissue, serology: ELISA, HI,
nasal discharge, * Chickens organism for long morbidity which may close one or agglutination and IF Various sulfonamides:
sneezing and become periods - Complicating factors both eyes  Molecular techniques such ✓ Sulfamethazine
swelling of the susceptible at - three serovars, A, B, and such as poor housing, - In adult birds, as restriction endonuclease ✓ Sulfamerazine
face about 4 weeks C, occur and bacterins parasitism, and especially males, the analysis and ribotyping ✓ sulfonamide-
after hatching must contain the inadequate nutrition edema may extend to  PCR trimethoprim
and serovar(s) likely to be may add to severity the intermandibular (sulfadimethoxine)
susceptibility encountered and duration of the space and wattles Differentiate from:
increases with disease - mycoplasmosis Prevention:
age - The disease is more LESIONS: - fowl cholera - Stock coryza-free birds
severe and prolong  limited to the - Laryngotracheitis on an all-in/all-out
* Reservoirs of with resulting infraorbital sinuses - Newcastle disease infectious production policy
infection – increased mortality  presence of copious, bronchitis - Since serovars A, B, and
chronically ill when complicated tenacious, grayish, - avian influenza C are not cross-
and clinically with other diseases semifluid exudate - swollen head syndrome protective, it is
normal carrier such as:  As the disease becomes (ornithobacteriosis) essential that bacterins
birds • fowl pox chronic or other - vitamin A deficiency contain the serovars
• infectious pathogens become present in the target
bronchitis involved, the sinus population
• Laryngotracheitis exudate may become - Vaccines are used in
• Mycoplasma consolidated and turn areas of high incidence.
gallisepticum yellowish Birds recovered from
infection  Conjunctivitis challenge of one sero-
• pasteurellosis  Tracheitis type are resistant to
 Bronchitis others, while bacterins
 airsacculitis only protect against
homologous strain
Post-mortem lesions
 inflammation of nasal
passages and sinuses
 conjunctivitis u eye-lid
adherence
 caseous material in
conjunctiva/
 tracheitis
ACTINOBACILLUS
SPECIES INFORMATION HOST DISEASE PATHOGENICITY DIAGNOSIS TREATMENT
Actinobacillosis in cattle: Bovine cattle • WOODEN TONGUE - induration of the tongue ✓ sodium iodide
actinobacillosis (lesions in tongue, lymph - Hx of grazing rough pasture (parenteral)
- commensal in the oral cavity and nodes, ruminal wall, skin) - Specimens for lab.exam – pus, ✓ potassium iodide (oral)
intestinal tract Sheep, pig - granulomas of biopsy material, and tissues from ✓ Potentiated
Actinobacillus - chronic pyogranulomatous the head, neck, lesions at PM suphonamides
lignieresii inflammation of soft tissues – lungs, lymph - Pyogranulomatous foci containing ✓ Penicillin-streptomycin
induration of the tongue/ timber nodes, wall of the club colonies ✓ Oral isoniazid for 30
tongue stomach Skin - Cultures on BAP and MCA – days
- Lesions occur in the esophageal lesions in sheep incubated aerobically at 37C for 24- ✓ Avoid rough feed or
groove and retropharyngeal lymph 72 hrs pasture
nodes (can lead to intermittent
tympany and enlargement ID criteria for isolates:
retropharyngeal lymph nodes – Horse glossitis - small, sticky, non-hemolytic
cause difficulty in swallowing and colonies on BAP
Dogs Bite wounds
stertorous breathing) - Slow fermentation on MCA
- enter tissues thru erosions or - Biochemical profile
lacerations in the mucosa and skin - Analysis of 16s rRNA gene
- A localized pyogranulomatous sequences –definitive ID
response is assc. with club colonies
containing the bacteria
- Sporadic dss
- Animals w/ timber tongue have
difficulty in eating and drool saliva
- B-hemolytic; causes contagious Pigs Pleuropneumonia Virulence factors - On Blood Agar, colonies of ✓ Chemotherapy based
pleuropneumonia in swine ((hemorrhagic pneumonia)) a. Endotoxin/LPS – responsible Actinobacillus pleuropneumoniae on AST
Actinobacillus - stress factors like cold weather for thrombi formation and will cluster around V factor- ✓ Prophylactic
pleuropneumoniae facilitate spread; common in intensive interlobar edema producing colonies. This is known as administration of
farms b. Hemolysin - disarms lung satellitism antibiotics to in-contact
macrophages - Subclinical carrier pigs – harbour the pigs
Transmission: inhalation of droplets c. glycoprotein – allow deeper organisms in the RT and tonsillar ✓ Polyvalent bacterins
penetration of organism into tissues ✓ Avoid predisposing
lungs - Blood-stained froth present around factors – poor
the nose and mouth ventilation, chilling and
Pathogenesis and pathogenicity - Concurrent infections with overcrowding
• Acute infection presents as Pasteurella multocida and
necrotizing fibrino- mycoplasmas may exacerbate the
hemorrhagic pneumonia condition
• Capsule – virulent strains - postmortem areas of consolidation
• Fimbriae and other and necrosis are found in the lungs
adhesins along with fibrinous pleurisy
• 4 related cytotoxins – - Blood-stained froth may be found in
repeats-in-structural-toxin trachea and bronchi
(RTX) cytolysin family -
damage cell membranes by - Hx of ventilation failure or
producing pores environmental temp.decrease
• Iron uptake systems - Specimens for lab exam – tracheal
• Sustained inflammatory washings or lung tissue (affected
response – a major factor portion)
in rapid tissue necrosis - Biotype 1 require V factor (NAD)
;neutrophils release lytic - Serological techniques – ELISA
enzymes - Immunofluorescent techniques or
PCR based techniques
- Strain typing techniques – PCR-
restriction fragment length
polymorphism
- present in URT of sows and piglets Pigs - Septicemia - specimens cultured on MCA and BAP – - Tx should be based on
- Infected by aerosols or possibly (under 3 - pneumonia incubated at 37oC for 1-3 days AST
Actinobacillus through skin abrasions mos. of - endocarditis ID Criteria for isolates: ✓ ampicillin
- Dss.is charac.by septicemia and rapid age) - metritis - sticky hemolytic colonies on BAP ✓ Carbenicillin
suis death & Older - arthritis - Pink, Lactose-fermenting colonies ✓ potentiated
- mortality rate – 50% pigs on MCA sulphonamides
- Petechial and ecchymotic - Septicemia - Biochemical profile ✓ Tetracyclines
hemorrhages in many organs - pneumonia - Analysis of 16S rRNA gene - Contaminated pens
- Commensal in horses (URT) Foals & associated with sequences – definitive ID shld.be disinfected u
Adult abortion - No commercial
- neonatal death of vaccines available
foals
- resp.and genital
infection
- respiratory and genital infection
- localizes in epididymis and testis of Ram - Ovine epididymitis - Specimens for lab.exam should - Vaccine is not available
rams - Polyarthritis include pus, biopsy material or - Prophylactic
Actinobacillus -
-
transmitted by semen
Found in prepuce lambs
- posthitis
Polyarthritis -
tissue obtained at postmortem
Serological examination:
antibiotics in feed or
water
seminis - Epididymitis occurs ff. and ascending Immunofluorescence technique,
opportunistic infection Ewes, abortion CFT, ELISA
goats,
cows
laying - Salphingitis
Actinobacillus hens - peritonitis
salphingitis

- found in the reproductive and Foals - Sleepy foal - Hx of the dss occurring on the ✓ Streptomycin
intestinal tracts of mares disease premises in previous seasons ✓ tetracyclines
Actinobacillus - Two subsp.of A. equuli: subsp. (shigellosis, - Clinical signs in a neonatal foal ✓ ampicillin
equuli and subsp. haemolyticus viscosum - specimens cultured on MCA - Supportive
equuli infection) and BAP – incubated treatment – blood
- joint ill aerobically at 37oC for 1-3 days transfusion and
• Subsp.equuli - associated with - nephritis ID Criteria for isolates: bottle-feeding with
acute, potentially fatal - septicemia - sticky colonies with variable colostrum
septicemia of newborn foal - enteritis hemolysis on BAP - Mares w/c have
(sleepy foal dss.) Mares Abortion - Lactose-fermenting colonies on had affected foals
• subsp. haemolyticus – known adult - Purulent nephritis MCA should be
to produce an RTX toxin horses - meningitis - Biochemical profile monitored closely
- Foals which recover from the Piglets - Septicemia - PCR – for direct detection of at subsequent
acute septicemic phase may - arthritis the org. foalings
develop polyarthritis, nephritis, - purulent nephritis - Good hygiene
enteritis or pneumonia pigs - Arthritis - Prophylactic
- Petechiation on serosal surfaces calves - Enteritis antibiotic therapy
and enteritis –foals dying 24hrs - Endocarditis - No commercial
- enteritis vaccines available
Actinobacillus ram Ovine epididymitis
actinomycetemcomitans Humans Endocarditis
periodontal disease
humans URT infection
Actinobacillus sow Abortion
ureae
FUSOBACTERIUM
SPECIES INFORMATION HOSTS DISEASE PATHOGENICITY DIAGNOSIS TREATMENT
Fusobacterium - Commensal in the Cattle Calf diptheria/ Bovine Diphtheria Rough feed Major Virulence factors: Diagnosis for Black Calf diptheria - Potentiated
alimentary tract and - Presents as necrotic pharyngitis or producing mucosal 1. endotoxin spot of teat/ black sulphonamides
necrophorum on mucous laryngitis in calves under 3 mos.of damage --- important in the genesis pox of the teat - Tetracyclines
membranes age of hepatic abscesses and - Various Hepatic Chlortetracycline in
- Four biotypes or - Infections are - The org. enter thru induces an intense primary necrobacillosis feed
biovars: A, B, endogenous - abrasions in the mucosa of the neutrophilia media, one
AB, C pharynx or larynx cause by ingestion 2. potent leukotoxin with hemin Bull nose Potentiated
- Biotypes A and 3 BIOTYPES of coarse feed --- active against ruminant and (Necrotic sulphonamides
B – recovered - Biotype A (F. Bovine rumenitis-liver abscess complex/Hepatic necrobacillosis neutrophils but also act menadione, rhinitis)
from bovine liver necrophorum subsp. - Hepatic abscessation 2 degrees to rumenitis - mostly in against macrophages and blood agar, Black spot of - Amoxicillin
abscesses necrophorum) feedlot animals hepatocytes baked blood teat/ black pox - Ampicillin
- Biotype B – –more virulent; has - Feeding of rations high in carbohydrates and the resulting 3. Hemolysin agar of the teat - clavulanic acid-
ruminal contents greater hemolytic activity rapid intraluminal fermentation can lead to the --- a dermonecrotic toxin (enhances amoxicillin
and lesions - Biotype B (F. development of ulcers 4. Hemagglutinin pigment - tetracyclines
- biotype A is necrophorum subsp. - with Trueperella pyogenes invade the tissues, and --- function as adhesins and prod), - chloramphenicol
more virulent funduliforme) occasional emboli which reach the liver via portal vein promote adherence to, and selective agar - metronidazole
than biotype B - Biotypes C strains initiate abscess formation invasion of ruminant to suppress - clindamycin
- biotype AB – were given the name Bovine Foot rot epithelial cells facultative - cephalosporins
intermediate - Fusobacterium Bovine Contagious dermatitis 5. adhesins (pili) anaerobes, - Tylosin – most
between subsp. Post-partum metritis Dystocia 6. platelet aggregation and bile effective drug
biotypes A and pseudonecrophorum Hepatic abscessation Sudden dietary factor esculin agar
- B, rarely isolated now F. varium – non- change leading to 7. proteases for the B.
from animals pathogenic acidosis and 8. Dnase fragilis group
rumenitis 9. LPS
Black spot of teat/ black pox of the teat Trauma to region 10. other extracellular
enzymes
- Presents as a localized area of adjacent to teat
necrosis with black scab formation sphincter • Capsulated of F.
due to invasion by F. necrophorum necrophorum –
- Can contribute to stenosis of more virulent
sphincter and mastitis
- Exert pathogenic
Horses Thrush (hoof) Poor hygiene and
- Necrotic condition of the equine hoof wet housing effects when
anatomical barriers
- Commonly affects the hind feet conditions
are breached to allow
- Charac.by a foul-smelling discharge in
invasion of underlying
the sulci close to the frog
tissues
Necrobacillosis of lower limbs Poor hygiene
- most infections are
Pigs Bull nose Trauma to nasal
mixed – two or more
(necrotic rhinitis) mucosa
bacterial spp.
- affects young pigs
interacting
- Suppuration and necrosis of the
synergistically
snout
- Trueperella pyogenes
- Suppuration and necrosis of the
produce heat labile
snout
factor and
Fusobacterium
- involvement of the nasal and facial necrophorum
bones can result in permanent facial produces leukotoxin
deformity - D. nodosus (growth
factor) and F.
Ulcerative stomatitis necrophorum (tissue
invasion)
- a 2 DEGREE bacterial
Necrotic enteritis invader, invades and
multiplies in the
Sheep Ovine contagious foot rot anaerobic
Ovine infective bulbar necrosis environment provided
Ovine interdigital dermatitis by damaged tissue
Rabbit Necrobacillosis
Chicken sequel to fowl pox virus infection

BACTEROIDES
SPECIES INFORMATION HOSTS DISEASE
Bacteroides fragilis - commensal bacteria that normally lives in the human ***lambs and calves accumulation of fluid in ligated intestinal
gastrointestinal tract loops
- can become pathogenic under circumstances involving
disruption of the normal intestinal mucosa such as ** Diarrhea
trauma, or surgery - calves
- Some strains produce ***enterotoxin - Lambs
- fragilysin an extracellular zinc metalloprotease - Foals
- ** Enterotoxigenic strains - piglets
- humans
- mastitis
Humans - abscesses

Bacteroides - cause bovine foot rot synergistic with F. necrophorum Bovine bovine foot rot
melaninogenicus
DICHELOBACTER
SPECIES INFORMATION HOSTS DISEASE PATHOGENICITY DIAGNOSIS TREATMENT
- obligate parasite of Ovine ovine foot rot - Virulence: - Gram staining - Foot trimming
digital epithelium of associated with - Culture on selected should be carried out
sheep production of medium containing - Formalin, copper, or
Dichelobacter - 1 degree cause of proteolytic enzymes horse blood, yeast, zinc sulfate footbaths
contagious foot rot – breakdown of eugon agar and and 10 % tincture of
nodosus of sheep keratin lincomycin chloromycetin
Bovine bovine contagious - Acidic and basic - Loffler’s methylene Antibiotics:
interdigital dermatitis extracellular serine blue ✓ Penicillin
proteases and - Cultural procedures ✓ Tetracycline
elastase are not carried out ✓ Chloramphenicol
- Disease is ✓ Clindamycin
aggravated by moist ✓ Tylosin
environmental ✓ Streptomycin
conditions in ✓ erythromycin
temperature of 10 - Prevention: alum
degree C or greater precipitated, oil
adjuvant vaccine
- Control is difficult in
more temperate
countries
Porphyromonas associated with F. cattle foot lesions
necrophorum
levii
Prevotella species associated with other cattle foot lesions
anaerobes

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