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•Very small, gram-negative rods Pasteurella and Mannheimia species
•Optimal growth on enriched media Pasteurella and Mannheimia species
•Non-motile, oxidase-positive, facultative anaerobes Pasteurella and Mannheimia species
•Most species are catalase-positive Pasteurella and Mannheimia species
•Some specie grow on MacConkey agar Pasteurella and Mannheimia species
•Bipolar staining is prominent in smears from lesions, using Giemsa method Pasteurella and Mannheimia species
•Commensals in the upper respiratory tract Pasteurella and Mannheimia species
•Respiratory pathogens Pasteurella and Mannheimia species
Species of veterinary importance Pasteurella multocida
Gram – rods small w/bipolar staining (Giemsa),Non-hemolytic PASTEURELLA
Pigs Sneezing, epixstasis, lateral deviation of snout. Young more susceptible; rarely fatal. VACCINATE! Associated w/bordatella bronchisepta: predisposes to PM infectionincr severity P. multocida Atrophic Rhinitis
*Turkeys,chickens Swollen, pus filled wattles, blood stained mucus, consolidated lungs, synovitis, fluid in body cavities, hemorrhages. Acute septicemia-often fatal. Highly contagious dz of domestic/wild birds P. multocida Fowl Cholera =avian pasteurellosis
Cattle,Buffalo(more susceptible)Laryngeal edema to parotid,brisket;fever,resp stress, recumbency-endotoxemia,death<24hrs.Acute septicemia w/high mortality;PM:widespread petechiae,edema P. multocida Hemorrhagic Septicemia Exotic/reportable
Rabbits Nasal discharge, sneezing, coughing, conjunctivitis, subQ abscessation Common, recurring purulent rhinitis D/D B.bronchiseptica Overcrowding, chilling, transport, poor ventilation. P. multocida Snuffles
Cattle, Pigs, Sheep P. multocida Pneumonia
•Very small, gram-negative rods Pasteurella and Mannheimia species
•Optimal growth on enriched media Pasteurella and Mannheimia species
•Non-motile, oxidase-positive, facultative anaerobes Pasteurella and Mannheimia species
•Most species are catalase-positive Pasteurella and Mannheimia species
•Some specie grow on MacConkey agar Pasteurella and Mannheimia species
•Bipolar staining is prominent in smears from lesions, using Giemsa method Pasteurella and Mannheimia species
•Commensals in the upper respiratory tract Pasteurella and Mannheimia species
•Respiratory pathogens Pasteurella and Mannheimia species
Species of veterinary importance Pasteurella multocida
Atrophic rhinitis in pigs; Fowl cholera in poultry; Haemorrhagic septicemia in cattle and buffaloes; Snuffles in rabbits; Pneumonia in cattle, pigs and sheep Pasteurella multocida
Septicemia in sheep (5 to 12 months) Pasteurella trehalosi
Bovine pneumonic pasteurellosis (shipping fever) Mannheimia haemolytica
Septicemia in sheep (< 3months) Mannheimia haemolytica
•Causative agent: P. multocida (toxigenic strains) --- severe, progressive form of atrophic rhinitis Atrophic rhinitis of pigs
•Bordetella bronchiseptica may cause mild, non-progressive turbinate atrophy without significant distortion of the snout (presence may predispose to infection with toxigenic strain of P. multocida and increase the severity of the disease) Atrophic rhinitis of pigs
•Young pigs are more susceptible (but non-immune pigs of any age can be infected) Atrophic rhinitis of pigs
•Clinical signs: Excessive lacrimation, sneezing and occasional epistaxis Atrophic rhinitis of pigs
•Snout gradually becomes shortened and wrinkled and as the disease progresses, a distinct lateral deviation of the snout develops Atrophic rhinitis of pigs
•Is rarely fatal Atrophic rhinitis of pigs
•Affected pigs are usually underweight and damage to the turbinate bones may predispose to secondary bacterial infections of the lower respiratory tract Atrophic rhinitis of pigs
•Is a primary avian pasteurellosis caused by P. multocida (capsular type) Fowl cholera
•Highly contagious disease of domestic and wild birds Fowl cholera
•Causes acute septicemia and often fatal Fowl cholera
•Turkeys are more susceptible than chickens Fowl cholera
•Postmortem lesions: hemorrhages on serous surfaces and accumulation of fluid in body cavities Fowl cholera
•Swollen wattles, sternal bursae and joints are often seen Fowl cholera
•Acute septicemic form of the disease --- characteristic bipolar-staining organisms detected in blood smears Fowl cholera
•P. multocida can be isolated from blood, bone marrow, liver or spleen ( difficult from chronic lesions) Fowl cholera
•Medication of feed or water with sulfonamides or tetracyclines given early will reduce mortality Fowl cholera
•Polyvalent adjuvant bacterins are widely used Fowl cholera
Autogenous vaccines ca be used if commercial vaccines are ineffective. MLV are also available Fowl cholera
•Causative agent: P. multocida (serotype B in Asia, Middle East and some southern European countries; serotype E in Africa) Haemorrhagic septicemia
•Is a reportable disease in the U.S and in countries where it is considered exotic Haemorrhagic septicemia
•Acute, potentially fatal septicemia mainly affecting buffaloes and cattle (buffaloes are more susceptible) Haemorrhagic septicemia
•Predisposing factors: overwork, poor body condition and monsoon rains Haemorrhagic septicemia
•Explosive outbreaks occur if an active carrier is introduced into a stressed susceptible population Haemorrhagic septicemia
•Clinical signs: Death can occur without prior signs within 24 hrs of infection; sudden onset of fever, respiratory distress, characteristic edema of the laryngeal region, edema may extend to the throat, parotid regions and to the brisket Haemorrhagic septicemia
•Recumbency is followed by death due to endotoxemia Haemorrhagic septicemia
•Mortality are usually >50% and can be 100% Haemorrhagic septicemia
•Diagnosis/Treatment/Control: Haemorrhagic septicemia
•History of acute disease with high mortality in endemic area suggest presumptive diagnosis of the disease Haemorrhagic septicemia
•Gross pathological lesions: widespread petechial hemorrhages, enlarged hemorrhagic lymph nodes and blood-tinged fluid in the pleural cavity and the pericardial sac Haemorrhagic septicemia
•Giemsa-stained blood smears from a recently-dead animal --- bipolar-staining organisms Haemorrhagic septicemia
Isolation, identification and serotyping of P. multocida isolate is confirmatory Haemorrhagic septicemia
•Diagnosis/Treatment/Control: Haemorrhagic septicemia
•Antibody titer of 1:160 or > in an indirect HA test is indicative of recent exposure to the pathogen Haemorrhagic septicemia
•Antibiotic therapy early is effective (although susceptible to penicillin, tetracycline are more often used) Haemorrhagic septicemia
•Slaughter policy of affected and in-contact animals are pursued in countries where the disease is exotic Haemorrhagic septicemia
•Vaccines: Bacterins and MLV are available Haemorrhagic septicemia
•Latent carriers detected by immunochemical techniques on samples of tonsillar tissue Haemorrhagic septicemia
•Common, recurring, purulent rhinitis, caused by P. multocida Snuffles in rabbits
•B. bronchiseptica may sometimes cause similar clinical signs ( important for D/D) Snuffles in rabbits
•Clinical disease often precipitated by stress factors such as overcrowding, chilling, transportation, concurrent infection, poor ventilation ( high levels of ammonia) Snuffles in rabbits
•Characterized by purulent nasal discharge, sneezing and coughing with conjunctivitis, otitis media and subcutaneous abscessation Snuffles in rabbits
•Antibiotic may be useful but no vaccines available Snuffles in rabbits
•Caused by M. haemolytica (although P. multocida has also been isolated) Bovine pneumonic pasteurellosis (Shipping fever)
•Characterized by severe bronchopneumonia and pleurisy, most commonly in young cattle within weeks of being subjected to stress ( transportation to feedlots and close confinement) Bovine pneumonic pasteurellosis (Shipping fever)
•Several respiratory viruses (parainfluenza virus 3, bovine herpes virus 1 and bovine respiratory syncytial virus may predispose to bacterial invasion Bovine pneumonic pasteurellosis (Shipping fever)
•Characteristic PM lesions: Cranial lobes of the lungs are red, swollen and consolidated with often overlying fibrinous pleurisy Bovine pneumonic pasteurellosis (Shipping fever)
•Clinical signs: Sudden onset of fever, depression, anorexia and serous nasal discharge (mixed infections --- cough and ocular discharge) Bovine pneumonic pasteurellosis (Shipping fever)
•Morbidity can be 50% with mortality (1 –10%) Bovine pneumonic pasteurellosis (Shipping fever)
•Diagnosis/Treatment/Control: Bovine pneumonic pasteurellosis (Shipping fever)
•History of exposure to stress with sudden onset of respiratory disease Bovine pneumonic pasteurellosis (Shipping fever)
•Gross pathological findings Bovine pneumonic pasteurellosis (Shipping fever)
•Cytospin prep. from bronchoalveloar lavage --- large numbers of neutrophils Bovine pneumonic pasteurellosis (Shipping fever)
•Isolation of M. haemolytica from bronchoalveolar lavage or lung tissue is confirmatory Bovine pneumonic pasteurellosis (Shipping fever)
•Affected animals must be isolated and treated early Bovine pneumonic pasteurellosis (Shipping fever)
•Oxyteracycline, potentiated sulfonamides and ampicillin are effective Bovine pneumonic pasteurellosis (Shipping fever)
•Minimize stress factors (castration, dehorning, branding should be done several weeks before transportation). Vaccination against respiratory pathogens should be completed at least 3 weeks before transportation Bovine pneumonic pasteurellosis (Shipping fever)
•Vaccines (modified leukotoxin and surface antigens) may induce protection Bovine pneumonic pasteurellosis (Shipping fever)
nSpecies of veterinary importance: F. tularensis Genus: Francisella
nGram-negative, coccobacillary rods Genus: Francisella
nNon-motile, obligate aerobes Genus: Francisella
nNo growth on MacConkey agar Genus: Francisella
nOxidase-negative, catalase-positive Genus: Francisella
nFacultative intracellular pathogen Genus: Francisella
nSurvival in environment – 4 months Genus: Francisella
nWildlife reservoirs and arthropods – important in epidemiology Genus: Francisella
nCauses tularaemia in animals and humans Genus: Francisella
Highly virulent Type A strain; confined to North America; cause classical tularaemia in animals and humans; reservoirs – rabbits, rodents, birds and deer F. tularensis subsp. tularensis
Less virulent Type B strain; present in North America and Eurasia; cause less serious disease in animals and humans; reservoirs – aquatic mammals (beavers and muskrats) F. tularensis subsp. holarctica
•Ticks ( Dermacentor variabilis, Dermacentor andersoni and Amblyomma americanum) and the deerfly (Chrysops discalis) Francisella tularensis
•Direct transmission between domestic animals is uncommon Francisella tularensis
•Common in endemic areas (outbreaks are relatively rare) Tularaemia in domestic animals
•Disease has been reported in sheep, horses and young pigs Tularaemia in domestic animals
•Adult pigs and cattle are relatively resistant Tularaemia in domestic animals
•Dogs and cats can be infected and seroconvert without clinical signs of the disease Tularaemia in domestic animals
•Usually occurs through skin abrasions or by arthropod bites Francisella tularensis
•Can also acquire by inhalation or by ingestion Francisella tularensis
•Facultative intracellular pathogen – can survive in macrophages (inhibits phagosome /lysosome fusion) Francisella tularensis
•Characterized by fever, depression, stiffness and other manifestations of septicemia Francisella tularensis
•Although clinical signs are non-specific, heavy tick infestation in severely ill animals in endemic regions may be suggestive of tularaemia Francisella tularensis
•Specimens: Blood for serology; scrapings from ulcers; lymph nodes aspirates; biopsy material or postmortem samples from affected tissues Francisella tularensis
•Agglutination titers (1:80 or >) is presumptive with rising antibody titer indicative of active infection Francisella tularensis
•FA technique – tissues, exudates or cultures Francisella tularensis
•Isolation must be carried out in biohazard cabinet, with special precautions when handling Francisella tularensis
•Glucose-cysteine-blood agar ( with antibiotics if contaminated samples) and incubated at 37 deg. C for up to 7 days Francisella tularensis
•Identification criteria: Small, grey, mucoid colonies with narrow zone of incomplete hemolysis after 3 to 4 days of incubation; IF to confirm; Slide agglutination test; PCR Francisella tularensis
•Effective antibiotics: Amikacin, streptomycin, imipenum-cilastatin and the fluoroquinolones Francisella tularensis
•High relapse rate may occur if treated with bacteriostatic antibiotics Francisella tularensis
•No commercial vaccines available Francisella tularensis
•Ectoparasite control is essential (Removal of ticks from dogs and cats) Francisella tularensis
•Serious and potentially fatal infection, often presents as a slow-healing ulcer accompanied by lymphadenopathy Tularaemia in humans
•Individuals at risk are hunters, trappers, veterinarians and laboratory workers (should take precautions when handling suspect animals or materials) Tularaemia in humans
A modified live vaccine available for personnel working with F. tularensis in specialized labs Tularaemia in humans
•Species of veterinary importance: Histophilus
•Haemophilus somnus: Cattle Histophilus
•Thrombotic meningoencephalitis (TME); septicemia; bronchopneumonia (in association with other pathogens); sporadic reproductive tract infections Histophilus
•Haemophilus somnus (ovine strains): Histophilus Sheep
•Epididymitis in young rams; vulvitis, mastitis and reduced reproductive performance in ewes; septicemia, arthritis, meningitis and pneumonia in lambs Histophilus
•Species of veterinary importance: •Haemophilus parasuis: Pigs
•Glasser’s disease; secondary invader in respiratory disease Histophilus
•Haemophilus paragallinarum •Infectious coryza in chickens
•Causative agent: H. somnus Thrombotic meningoencephalitis (TME)
•Normal bacterial flora of the male and female bovine genital tracts ( can also colonize the upper respiratory tract Thrombotic meningoencephalitis (TME)
•Environmental stress factors predispose for development of clinical disease Thrombotic meningoencephalitis (TME)
•Transmission: direct contact or aerosols Thrombotic meningoencephalitis (TME)
•25% of cattle have antibodies to H. somnus Thrombotic meningoencephalitis (TME)
•Clinical signs: Septicemia --- many organ systems involved Thrombotic meningoencephalitis (TME)
•High fever, depression, blindness, lameness and ataxia; sudden death --- myocarditis; survivors of acute phase --- arthritis Thrombotic meningoencephalitis (TME)
•Sporadic cases of abortion, endometritis, otitis and mastitis Thrombotic meningoencephalitis (TME)
•Severe neurological signs in young feedlot cattle may be indicative of TME Thrombotic meningoencephalitis (TME)
•Multiple foci of hemorrhagic necrosis in the brain at PM is a consistent finding Thrombotic meningoencephalitis (TME)
•Vasculitis, thrombosis and hemorrhage detected histologically in brain, heart and other organs Thrombotic meningoencephalitis (TME)
•Confirmation is by isolation and identification of H. somnus from CSF, postmortem lesionsor aborted fetuses Thrombotic meningoencephalitis (TME)
•Animals with clinical signs of septicemia should be isolated and those at risk closely monitored for early signs of the disease Thrombotic meningoencephalitis (TME)
•Although oxytetracycline is commonly used, penicillin, erythromycin and potentiated sulfonamides are also effective Thrombotic meningoencephalitis (TME)
•Bacterins may reduce morbidity and mortality if given I month before anticipated outbreaks Thrombotic meningoencephalitis (TME)
•Causative agent: H. parasuis Glasser’s disease
•Characterized by polyserositis and leptomeningitis and sometimes polyarthritis Glasser’s disease
•Affects usually pigs from weaning up to 12 weeks of age Glasser’s disease
•Normal flora of the upper respiratory tract Glasser’s disease
•Piglets acquire the organism from the sows shortly after birth --- direct contact or aerosols Glasser’s disease
•Maternal-derived antibodies prevent development of clinical signs and active immunity usually established by 7 to 8 weeks of age Glasser’s disease
•Anorexia, pyrexia, lameness, recumbency and convulsions are characteristic features of the disease Glasser’s disease
•Cyanosis and thickening of the pinnae are often encountered Glasser’s disease
•May die without any signs of illness Glasser’s disease
•Streptococcus suis and Mycoplasma hyorhinis will produce similar clinicopathological changes (Important for D/D) Glasser’s disease
•PM findings: Fibrinous polyserositis, polyarthritis and meningitis Glasser’s disease
•Isolation and identification of H. parasuis from joint fluid, heart blood, CSF or PM tissues is confirmatory Glasser’s disease
•Causative agent: H. paragallinarum Infectious coryza of chickens
•Affects the upper respiratory tract and paranasal sinuses of chickens Infectious coryza of chickens
•Economic importance: Weight loss in broilers and loss in egg production in layers Infectious coryza of chickens
•Chronically ill and clinically normal carrier birds act as reservoirs of infection Infectious coryza of chickens
•Transmission: direct contact, aerosols or contaminated drinking water Infectious coryza of chickens
•Chickens susceptible at about 4 weeks of age and susceptibility increases with age Infectious coryza of chickens
•Mild form --- depression, serous nasal discharge and slight facial swelling Infectious coryza of chickens
•Severe form --- swelling of one or both infraorbital sinuses and edema of the surrounding tissues which may extend to the wattles; marked drop in egg production; PM findings: a copious, tenacious exudate in the infraorbital sinuses, tracheitis, bronchiti Infectious coryza of chickens
Facial swelling is a characteristic finding Infectious coryza of chickens
Isolation and identification of H. paragallinarum from infraorbital sinuses is confirmatory Infectious coryza of chickens
Immunoperoxidase staining to demonstrate the organism in the tissues of the nasal passages and sinuses Infectious coryza of chickens
Serological tests: ELISA, AGID tests Infectious coryza of chickens
Medication of water and feed with oxytetracycline or erythromycin given early in outbreak Infectious coryza of chickens
•An all-in/all-out management program with replacement birds from coryza-free stock Infectious coryza of chickens
•Good management of poultry units minimizes the risk of infection Infectious coryza of chickens
•Bacterins useful in farms where the disease recurs Infectious coryza of chickens
•Vaccines should be given about 3 weeks before outbreaks of coryza is anticipated Infectious coryza of chickens
•Species of veterinary importance: T. equigenitalis Genus: Taylorella
•Causative agent of Contagious equine metritis (CEM) Genus: Taylorella
•Short gram-negative rods and non-motile Genus: Taylorella
•Optimal growth on chocolate agar Genus: Taylorella
•Microaerophilic, requires 5-10% CO2 Genus: Taylorella
•Catalase-, oxidase- and phosphatase- positive Genus: Taylorella
•Does not grow on MacConkey agar Genus: Taylorella
•Found in the genital tracts of stallions (urethral fossa), mares (clitoral fossa) and foals Genus: Taylorella
•First reported as a clinical entity in 1977 in thoroughbreds in Britain and Ireland; subsequently reported in other European countries, USA, Australia and Japan Contagious equine metritis
•Highly contagious, localized venereal disease characterized by mucopurulent vulvular discharge causing temporary infertility in mares Contagious equine metritis
•Economic importance: disrupts breeding programs on thoroughbred stud farms Contagious equine metritis
•Infected stallions and mares are the main reservoirs of infection Contagious equine metritis
•Transmission: Usually occurs during coitus (may also be introduced by contaminated instruments) Contagious equine metritis
•Spontaneous ascending infection in mares doesn’t occur and T. equigenitalis must be deposited in the uterus to establish infection Contagious equine metritis
•Foals born to infected dams may acquire infection in utero or during parturition Contagious equine metritis
•T. equigenitalis has been isolated from >75% of the offspring of infected mares at 2 to 4 weeks of age and these offspring and mares which have recovered clinically may act as a source of infection Contagious equine metritis
•Pre-ejaculatory fluid and semen may be contaminated with T. equigenitalis from the urethral fossa Contagious equine metritis
•Evidence of prevalence of strains of differing pathogenicity exists Contagious equine metritis
•After introduction of pathogenic organism into the uterus, they replicate and induce an acute endometritis Contagious equine metritis
•Initially, mononuclear cell and plasma-cell infiltration predominates (a feature rarely observed in acute bacterial endometritis) Contagious equine metritis
•Later, migration of neutrophils into the uterine lumen produces a profuse mucopurulent exudate Contagious equine metritis
•Pathogens may persist in the uterus, acute endometrial changes subside within a few days Contagious equine metritis
•Clinical signs: Infected stallions (minority of infected nares) remain asymptomatic; infected mares develop copious mucopurulent vulvular discharge without systemic disturbances within a few days of service by a carrier stallion; the discharge may contin Contagious equine metritis
•A copious, mucopurulent discharge 2 to 7 days after service may indicate CEM Contagious equine metritis
•Specimens should be collected before and during breeding season Contagious equine metritis
•Swabs (double-guarded swab) from mares: Clitoral fossa, endometrium at estrus Contagious equine metritis
•Swabs from foals (<3 months of age): Clitoral fossa (fillies); penile sheath and tip of the penis (colts) Contagious equine metritis
•Swabs from stallions: Urethra, urethral fossa, penile sheath and pre-ejaculatory fluid Contagious equine metritis
•Identification criteria: Contagious equine metritis
•Colony characteristics --- small, smooth, yellowish-grey with entire edge Contagious equine metritis
•Positive catalase, oxidase and phosphatase tests Contagious equine metritis
•Slide agglutination test using high-titered antiserum on the culture Contagious equine metritis
•FA test, rendered specific following absorption with M. haemolytica Contagious equine metritis
Latex agglutination test kit ( available commercially) Contagious equine metritis
•Is a reportable disease in many countries Contagious equine metritis
•Control regimens are based on lab. detection of asymptomatic carriers and clinical infections in animals used for breeding Contagious equine metritis
•Appropriate, routine hygienic methods on stud farms to prevent lateral spread Contagious equine metritis
•If CEM is detected on stud farms, breeding services should be stopped immediately Contagious equine metritis
•Animals treated for CEM, should be tested to be free from pathogen Contagious equine metritis
•No vaccines available for CEM Contagious equine metritis
lSmall, gram – negative rods (coccobacillus) Genus: Bordetella
lGrowth on non-enriched media & MacConkey Genus: Bordetella
lMotile (peritrichous flagella) Genus: Bordetella
lOxidase- and catalase- positive Genus: Bordetella
lStrict aerobes Genus: Bordetella
lB. bronchiseptica is hemolytic and B. avium is non-hemolytic Genus: Bordetella
lToxigenic strains agglutinate mammalian RBCs Genus: Bordetella
lCommensals of upper respiratory tract Genus: Bordetella
lCauses respiratory disease in mammals and birds Genus: Bordetella
lAffinity for ciliated epithelium
lBordetella toxins: 1. Heat labile toxin: 2. tracheal cytotoxin
1. Heat labile toxin: Dermonecrotoxic toxin (induces skin necrosis, impairs osteogenesis),Smooth muscle of vessel,Arterial constriction
2. Tracheal cytotoxin: Inhibits ciliary action, Destruction of ciliated cells
stimulates cytokine release, fever LPS - endotoxin Genus: Bordetella
"Inhibits phagocytosis, Inhibits phagosome-lysosome fusion
" Adenylate cyclase - haemolysin (Except B. avium) Genus: Bordetella
lBordetella bronchiseptica: lSpecies of veterinary importance:
Atrophic rhinitis in pigs; Canine infectious tracheobronchitis (“kennel cough”) in dogs; Pneumonia in kittens; Respiratory infections in horses; Upper respiratory tract infections in rabbits; Bronchopneumonia in laboratory rodents lBordetella bronchiseptica:
Coryza in turkeys (Turkey coryza) lBordetella avium:
Pneumonia in lambs lBordetella parapetussis:
lAlso known as kennel cough Canine infectious tracheobronchitis
lOne of the most prevalent respiratory disease complexes of dogs Canine infectious tracheobronchitis
lMost important participating pathogens: Canine parainfluenza virus 2 (PI-2) and Canine adenovirus 2 (CAV-2) Canine infectious tracheobronchitis
lOther microbial pathogens involved: Canine distemper virus; CAV-1; Canine herpesvirus 1; Reoviruses 1, 2 and 3 and Mycoplasma species Canine infectious tracheobronchitis
lMost important bacterial pathogen: Bordetella bronchiseptica Canine infectious tracheobronchitis
lTransmission: respiratory secretions (direct or aerosols); mechanical transfer on footwear or clothing, contaminated feeding utensils (fomites) --- common in kennels, pet shops and animal shelters Canine infectious tracheobronchitis
lMorbidity may reach 50%, mortality is low Canine infectious tracheobronchitis
lOrganisms may remain in the respiratory tract and shed for several months after clinical recovery Canine infectious tracheobronchitis
lClinical signs: develop within 3 to 4 days and persists up to 14 days. Characterized by coughing, gagging with mild serous oculonasal discharge; active, alert and non-febrile; usually self-limiting unless complicated by bronchopneumonia ( unvaccinated pu Canine infectious tracheobronchitis
lToxigenic strains of B. bronchiseptica are widely distributed in pig herds Atrophic rhinitis
lCan cause turbinate hypoplasia without distortion of the snout in young piglets (4 weeks of age) Atrophic rhinitis
lInfection with B. bronchiseptica may facilitate colonization of toxigenic strains of P. multocida with the subsequent development of severe atrophic rhinitis with distortion of the snout Atrophic rhinitis
lPredisposing factors: overcrowding and poor ventilation Atrophic rhinitis
lMost severe form of atrophic rhinitis: concurrent infection of B. bronchiseptica and P. multocida Atrophic rhinitis
lCausative agent: Bordetella avium Turkey coryza
lHighly, contagious upper respiratory tract disease of turkey poults Turkey coryza
lHigh morbidity and low mortality Turkey coryza
lTransmission: direct contact; aerosols and environmental sources Turkey coryza
lCharacterized by mucus accumulation in the nares, swelling in the submaxillary sinuses; beak breathing, excesive lacrimaton and sneezing Turkey coryza
lPredisposes for secondary bacterial infections (E. coli) --- more serious with high mortality Turkey coryza
Upper respiratory tract,Frothy discharge from eye, Lacrimation,Sneezing, Excessive upper respiratory mucus production,Cough,Tracheal collapse Bordetella avium
Species of veterinary importance: moraxella genus lMoraxella bovis
lCausative agent of Infectious bovine keratoconjunctivitis (“pinkeye”) Genus:MORAXELLA
lImportant ocular disease of cattle and occurs worldwide Genus:MORAXELLA
lShort, plump gram-negative rods, usually in pairs Genus:MORAXELLA
Optimal growth in enriched media (growth enhanced by the addition of serum to media) Genus:MORAXELLA
lAerobic, non-motile Moraxella bovis
lUsually catalase- and oxidase-positive Moraxella bovis
lUnreactive with sugar substrates Moraxella bovis
lVirulent strains are fimbriated and hemolytic Moraxella bovis
lSusceptible for desiccation Moraxella bovis
lFound on mucus membranes of carrier cattle Moraxella bovis
lHighly contagious disease, usually in animals under 2 years of age Infectious bovine keratoconjunctivitis (IBK)
lEconomic loss due to decreased weight gain in beef breeds, loss of milk production, disruption of breeding programs & treatment costs Infectious bovine keratoconjunctivitis (IBK)
lTransmission: direct contact, aerosols, thru flies acting as vectors Infectious bovine keratoconjunctivitis (IBK)
lVirulence attributed to the fimbriae, which allow adherence of the organism to the cornea Infectious bovine keratoconjunctivitis (IBK)
lInitially manifests as blepharoplasm, conjunctivitis and lacrimation Infectious bovine keratoconjunctivitis (IBK)
lProgresses to keratitis, corneal ulceration, opacity and abscessation, leading sometimes to panophthalmitis and permanent blindness Infectious bovine keratoconjunctivitis (IBK)
lCan be unilateral or bilateral Infectious bovine keratoconjunctivitis (IBK)
lCattle with very little eye pigmentation are more severely affected Infectious bovine keratoconjunctivitis (IBK)
lHereford and Holstein, Shorthorn cattle very susceptible - because they lack pigment around the eyes. Angus are less affected. Zebu and Brahma are apparently not affected). Infectious bovine keratoconjunctivitis (IBK)
lJersey cattle are highly susceptible to Pinkeye. Prominence of their eyes may expose them to more intense sun light Infectious bovine keratoconjunctivitis (IBK)
lHigh solar radiation is a predisposing factor Infectious bovine keratoconjunctivitis (IBK)
lLower incidence in dairy breeds compared to beef herds Infectious bovine keratoconjunctivitis (IBK)
lCharacteristically affects a number of animals in a herd Infectious bovine keratoconjunctivitis (IBK)
lLacrimal secretion is most suitable for lab. exam. & must be processed promptly (extreme susceptibility to desiccation). For transportation, swabs should be placed in 1 to 2 ml of sterile water & should be cultured within 2 hrs of collection Infectious bovine keratoconjunctivitis (IBK)
lCultures of virulent strains agglutinate in saline Infectious bovine keratoconjunctivitis (IBK)
lSmears from colonies reveal short, plump, gram-negative rods, usually in pairs Infectious bovine keratoconjunctivitis (IBK)
lCatalase- and oxidase- positive Infectious bovine keratoconjunctivitis (IBK)
lAntimicrobial therapy subconjunctivally or topically early in the disease Infectious bovine keratoconjunctivitis (IBK)
lFimbriae-derived bacterins available in some countries of uncertain efficacy Infectious bovine keratoconjunctivitis (IBK)
lManagement-related methods are important in the control of IBK --- isolation of affected animals, reduction of mechanical irritants, use of insecticidal ear tags and control of concurrent diseases Infectious bovine keratoconjunctivitis (IBK)
lProphylactic use of intramuscular oxytetracycline for animals at risk Infectious bovine keratoconjunctivitis (IBK)
lVitamin A supplementation may be benificial Infectious bovine keratoconjunctivitis (IBK)
Brucella abortus Bovine brucellosis
Brucella melitensis: Caprine & ovine brucellosis
Brucella suis: Porcine brucellosis
Brucella canis: Canine brucellosis
Brucella ovis: Ovine epididymitis
small, gram neg, coccobacilli Genus Brucella
MZN positive Genus Brucella
Non-motile, cat pos, oxi pos, urease pos Genus Brucella
intracellular pathogen Genus Brucella
lPredilection for reproductive organs (both male & female) Brucella sp
lInfected animals serve as reservoirs of infection (often persists indefinitely) Brucella sp
lOrganisms shed by infected animals can remain viable in moist environment for several months Brucella sp
lUsually species specific ( cattle: B. abortus; sheep/goats*: B. melitensis; Pigs: B. suis; Sheep: B. ovis; Dogs: B. canis Brucella sp
-Facultative intracellular pathogens of macrophges and endothelial cells. Genus: Brucella
-Brucellae are associated with reproductive tract infections and abortions. Genus: Brucella
-Infection initiates via mucous membranes and spread through the blood and the lymphatics. Following this bacteremia, the organism colonizes tissues such as the lung, placenta, and secretory glands Genus: Brucella
-There is a long (1-2 month) incubation period where the animal appears normal. Genus: Brucella
world-wide distribution. Brucella abortus
. Wild ruminants severe as reservoirs Brucella abortus
. Smooth strains are virulent. Brucella abortus
. “Not” stable in the environment. Easily killed by pasteurization and disinfectants. Brucella abortus
. Shed in large quantities in milk, urine and placenta. Brucella abortus
. Grows as white colonies on blood agar. Virulent strains are usually smooth Brucella abortus
Created by: alljacks