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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
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, nonprogressive 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 nonimmune 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
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
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)
History of exposure to stress with sudden onset of respiratory disease 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)
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)
Species of veterinary importance: F. tularensis Genus: Francisella
Gram-negative, coccobacillary rods Genus: Francisella
Non-motile, obligate aerobes Genus: Francisella
No growth on MacConkey agar Genus: Francisella
Oxidase-negative, catalase-positive Genus: Francisella
Facultative intracellular pathogen Genus: Francisella
Survival in environment 4 months Genus: Francisella
Wildlife reservoirs and arthropods important in epidemiology Genus: Francisella
Causes 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
Lymphadenitis (local or generalized) is a constant finding and septicemia is common; pale necrotic foci in enlarged superficial lymph nodes; miliary lesions in the liver and spleen; primary pulmonary lesions due to aerosol inhalation have been described i 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)
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, bronchitis 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 genital tract of stallions(urethral fossa), mares(clitoral fossa)and foals Genus: Taylorella
First reported as clinical entity 1977 in thoroughbred in Britain,Ireland, reported in other European countries,USA,Australia,Japan Contagious equine metritis
Highly contagious, localize venereal disease characterize by mucopurulent vulvular discharge cause temporary infertility in mare Contagious equine metritis
Economic importance, disrupts breeding program on thoroughbred stud farms Contagious equine metritis
Infected stallions and mares are the main reservoirs of infection Contagious equine metritis
Transmission usualy occur during coitus (also by contaminated instrument) Contagious equine metritis
Spontaneous ascending infection in mare doesn’t occur, T. equigenitalis must be deposited in 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 isolated from >75% of offspring of infected mares at 2to4 weeks of age,these offspring & mares that have recovered may act as source of infection Contagious equine metritis
Preejaculatory 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 produce 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 stallion(minority of infected nares)remain asymptomatic,infected mares develop copious mucopurulent vulvular discharge without systemic disturbance in few days of service by a carrier stallion, discharge may continue 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
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 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
Small, gram negative rods (coccobacillus) Genus: Bordetella
Growth on nonenriched media & MacConkey Genus: Bordetella
Motile (peritrichous flagella) Genus: Bordetella
Oxidase and catalase positive Genus: Bordetella
Strict aerobes Genus: Bordetella
B. bronchiseptica is hemolytic and B. avium is nonhemolytic Genus: Bordetella
Toxigenic strains agglutinate mammalian RBCs Genus: Bordetella
Commensals of upper respiratory tract Genus: Bordetella
Causes respiratory disease in mammals and birds Genus: Bordetella
Affinity for ciliated epithelium Bordetella
Bordetella 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
Bordetella bronchiseptica Species of veterinary importance
Atrophic rhinitis in pigs,Canine infectious tracheobronchitis(kennel cough)in dogs, Pneumonia in kitten,Resp infection in horses,URI in rabbit,Bronchopneumonia in lab rodents Bordetella bronchiseptica
Coryza in turkeys (Turkey coryza) Bordetella avium
Pneumonia in lambs Bordetella parapetussis
Also known as kennel cough Canine infectious tracheobronchitis
One of the most prevalent respiratory disease complexes of dogs Canine infectious tracheobronchitis
Most important participating pathogens, Canine parainfluenza virus 2(PI-2)and Canine adenovirus 2 (CAV-2) Canine infectious tracheobronchitis
Other microbial pathogens involved,Canine distemper virus,CAV-1,Canine herpesvirus 1, Reoviruses 1,2,3 and Mycoplasma species Canine infectious tracheobronchitis
Most important bacterial pathogen, Bordetella bronchiseptica Canine infectious tracheobronchitis
Tx, respiratory secretion(direct or aerosol) mechanical transfer on footwear or clothing, contaminated feeding utensils (fomites)common in kennels,petshops & animal shelters Canine infectious tracheobronchitis
Morbidity may reach 50%, mortality is low Canine infectious tracheobronchitis
Organism may remain in respiratory tract and shed for several months after recovery Canine infectious tracheobronchitis
Clinical sign in 3to4 day,persist to 14days, coughing,gagging with mild serous oculonasal discharge,active,alert & nonfebrile,usually selflimiting unless complicated by bronchopneumonia(unvaccinated pup) Canine infectious tracheobronchitis
Toxigenic strains of B. bronchiseptica are widely distributed in pig herds Atrophic rhinitis
Can cause turbinate hypoplasia without distortion of snout in young piglet(4 weeks of age) Atrophic rhinitis
Infection of B. bronchiseptica may facilitate colonize of toxigenic strains of P. multocida with subsequent development of severe atrophic rhinitis with distortion of snout Atrophic rhinitis
Predisposing factors: overcrowding and poor ventilation Atrophic rhinitis
Most severe form of atrophic rhinitis: concurrent infection of B. bronchiseptica and P. multocida Atrophic rhinitis
Causative agent: Bordetella avium Turkey coryza
Highly, contagious upper respiratory tract disease of turkey poults Turkey coryza
High morbidity and low mortality Turkey coryza
Transmission: direct contact; aerosols and environmental sources Turkey coryza
Characterized by mucus accumulation in the nares, swelling in the submaxillary sinuses; beak breathing, excesive lacrimaton and sneezing Turkey coryza
Predisposes 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 Moraxella bovis
Causative agent of Infectious bovine keratoconjunctivitis (“pinkeye”) Genus:MORAXELLA
Important ocular disease of cattle and occurs worldwide Genus:MORAXELLA
Short, 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
Aerobic, non-motile Moraxella bovis
Usually catalase- and oxidase-positive Moraxella bovis
Unreactive with sugar substrates Moraxella bovis
Virulent strains are fimbriated and hemolytic Moraxella bovis
Susceptible for desiccation Moraxella bovis
Found on mucus membranes of carrier cattle Moraxella bovis
Highly contagious disease, usually in animals under 2 years of age Infectious bovine keratoconjunctivitis (IBK)
Economic loss due to decreased weight gain in beef breeds, loss of milk production, disruption of breeding programs & treatment costs Infectious bovine keratoconjunctivitis (IBK)
Transmission: direct contact, aerosols, thru flies acting as vectors Infectious bovine keratoconjunctivitis (IBK)
Virulence attributed to the fimbriae, which allow adherence of the organism to the cornea Infectious bovine keratoconjunctivitis (IBK)
Initially manifests as blepharoplasm, conjunctivitis and lacrimation Infectious bovine keratoconjunctivitis (IBK)
Progresses to keratitis, corneal ulceration, opacity and abscessation, leading sometimes to panophthalmitis and permanent blindness Infectious bovine keratoconjunctivitis (IBK)
Can be unilateral or bilateral Infectious bovine keratoconjunctivitis (IBK)
Cattle with very little eye pigmentation are more severely affected Infectious bovine keratoconjunctivitis (IBK)
Hereford 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)
Jersey cattle are highly susceptible to Pinkeye. Prominence of their eyes may expose them to more intense sun light Infectious bovine keratoconjunctivitis (IBK)
High solar radiation is a predisposing factor Infectious bovine keratoconjunctivitis (IBK)
Lower incidence in dairy breeds compared to beef herds Infectious bovine keratoconjunctivitis (IBK)
Characteristically affects a number of animals in a herd Infectious bovine keratoconjunctivitis (IBK)
Lacrimal 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)
Cultures of virulent strains agglutinate in saline Infectious bovine keratoconjunctivitis (IBK)
Smears from colonies reveal short, plump, gram-negative rods, usually in pairs Infectious bovine keratoconjunctivitis (IBK)
Catalase- and oxidase- positive Infectious bovine keratoconjunctivitis (IBK)
Antimicrobial therapy subconjunctivally or topically early in the disease Infectious bovine keratoconjunctivitis (IBK)
Fimbriae-derived bacterins available in some countries of uncertain efficacy Infectious bovine keratoconjunctivitis (IBK)
Management-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)
Prophylactic use of intramuscular oxytetracycline for animals at risk Infectious bovine keratoconjunctivitis (IBK)
Vitamin 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
Predilection for reproductive organs (both male & female) Brucella sp
Infected animals serve as reservoirs of infection (often persists indefinitely) Brucella sp
Organisms shed by infected animals can remain viable in moist environment for several months Brucella sp
Usually 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 initiate via mucous membrane and spread through blood, lymphatics. Following this bacteremia, the organism colonizes tissue such as lung,placenta,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
Causative agent of bovine brucellosis Brucella abortus
organism usually ingested (venereal contact, penetration thru skin abrasions, inhalation or transplacental transmission). Brucella abortus
Localized in supramammary gland or testes (tissue with high level of erythritol (polyhydric alcohol),which act as growth factor for brucellae. Brucella abortus
Few clinical signs during early phases Brucella abortus
Causes abortion or weak calves, orchitis and epididymitis in bulls Brucella abortus
Abortion storms may be encountered in susceptible herds Brucella abortus
Usually occurs after the 5th month of gestation Brucella abortus
Large numbers excreted in fetal fluids for 2 to 4 weeks following abortion Brucella abortus
Infection of calves is of limited duration Brucella abortus
May be excreted intermittently in milk for a number of years Brucella abortus
Effect of brucellosis: Decreased fertility; reduced milk production; abortions Brucella abortus
Clinical sign nonspecific, although abortion in first calf heifers & replacement animals may be suggestive Brucella abortus
MZN positive coccobacilli in smears of cotyledons, fetal abomasal contents and uterine discharge Brucella abortus
Colony appearance(small,smooth, glistening, bluish & translucent)MZN pos, Agglutination with high titered antiserum,rapid urease pos Brucella abortus
Serological tests,Milk ring test and Rose-Bengal plate test (useful screening tests); CF and Indirect ELISA are widely used confirmatory tests; Competitive ELISA using monoclonal antibodies is highly specific, capable of detecting all Igs and can be used Brucella abortus
Immunity is predominantly cell-mediated Brucella abortus
Vaccination, Three types of vaccines Brucella abortus
1)Attenuated strain 19 female calves up to 5 months of age.2)45/20 adjuvanted bacterin – less effective.3)RB51 strain stable, rough mutant, provides good protection against abortion, no seroconversion Brucella abortus
Treatment not practical Brucella abortus
National eradication, detection & slaughter Brucella abortus
Causes Undulant fever in humans Brucella abortus
Causative agent of caprine and ovine brucellosis Brucella melitensis
commonly encountered in Mediterranean countries, Middle East, central Asia and parts of South America (not U.S.A) Brucella melitensis
Goats are more susceptible than sheep Brucella melitensis
Clinical disease resembles bovine brucellosis Brucella melitensis
Late stage abortion and orchitis Brucella melitensis
Causes Malta Fever in humans Brucella melitensis
Serology Test & slaughter policy Brucella melitensis
Occurs worldwide Brucella ovis
Infects only sheep Brucella ovis
Characterized by epididymitis and orchitis in rams & placentitis in ewes Brucella ovis
Venereal transmission is important Brucella ovis
Abortions less frequent Brucella ovis
Rams are more susceptible than ewes & can shed organisms for up to 4 years Brucella ovis
Not pathogenic to humans Brucella ovis
Causative agent of porcine brucellosis Brucella suis
Occurs occasionally in the USA, more prevalent in Latin America and Asia Brucella suis
Prolong bacteremia with chronic inflammatory lesions in reproductive organ of sows & boars Brucella suis
Abortion (0 – 80%) & reduced litters Brucella suis
Associated with lameness and spondylitis (localization in bones & joints) Brucella suis
Sterility is a common outcome of infection Brucella suis
Venereal TX is important (shed in high numbers in semen); Infected herd quarantined & depopulated Brucella suis
Causative agent of canine brucellosis Brucella canis
Worldwide (large kennels & breeders) Brucella canis
Venereal transmission is important Brucella canis
Causes late abortion, orchitis, epididymitis and sterility in dogs (often is subclinical) Brucella canis
Chronic cases Dyskospondylitis resulting in lameness & paralysis Brucella canis
Treatment,confined to animals not intended for breeding,combination of tetracycline and aminoglycoside may be effective given early Brucella canis
Neutering infected animals reduces risk of transmission; no vaccines available Brucella canis
Susceptible to B. abortus, B. melitensis and B. suis (rarely to B. canis) Brucellosis in humans
Transmission occurs thru contact with secretions or excretions of infected animals Brucellosis in humans
Routes of entry: skin abrasions; inhalation and ingestion Brucellosis in humans
Raw milk and dairy products made with unpasteurized milk important sources (laboratory accidents can also be involved) Brucellosis in humans
Abortion is a not a feature of human infection Brucellosis in humans
Undulant fever caused by B. abortus: Moderately severe, fluctuating pyrexia, malaise, fatigue, muscle & joint pains Brucellosis in humans
Osteomyelitis is the most common complication Brucellosis in humans
Malta fever caused by B. melitensis & infections with B. suis are much more severe Brucellosis in humans
B. canis infection is usually mild Brucellosis in humans
Antimicrobial therapy: early stage of infection Brucellosis in humans
Hypersensitivity reaction: infection or accidental inoculation of live vaccine Brucellosis in humans
Causative agent of bovine campylobacteriosis C. fetus subsp. venerealis
Highly adapted to the bovine reproductive tract C. fetus subsp. venerealis
Transmitted during coitus (venereal transmission) C. fetus subsp. venerealis
Organisms survive in glandular crypts of the prepuce and bulls may remain infected indefinitely C. fetus subsp. venerealis
Disease characterized by temporary infertility associated with early embryonic death and sporadic abortion C. fetus subsp. venerealis
About 1/3rd of infected cows become carriers (persists in the vagina) --- extension of infection to the uterus results in development of endometritis and salphingitis C. fetus subsp. venerealis
Causative agent of ovine genital campylobacteriosis (also C. jejuni) C. fetus subsp. fetus
Occurs worldwide and is one of the most common causes of ovine abortion in some countries C. fetus subsp. fetus
C. fetus subsp. fetus is found in the feces of sheep and cattle (C. jejuni is found in the feces of birds and mammals) C. fetus subsp. fetus
Transmission is by fecal-oral route C. fetus subsp. fetus
During pregnancy, localization in the uterus may occur following bacteremia, with subsequent necrotic placentitis results in abortion late in pregnancy, stillborn lambs or weak lambs C. fetus subsp. fetus
Round, necrotic lesions with pale raised rims and dark depressed centers are evident on the liver surface in aborted lambs C. fetus subsp. fetus
Aborted ewes are major source of infection for susceptible animals in a flock (up to 20% of ewes in a susceptible flock may abort) C. fetus subsp. fetus
Recovered ewes are immune for at least 3 years and flock fertility in subsequent breeding season is usually good C. fetus subsp. fetus
Causative agent of canine intestinal campylobacteriosis C. jejuni
Diarrhea in dogs and other animals (confirmation is difficult because healthy animals shed the organisms in their feces). Presence of large numbers from fecal smears or rectal scrapings is indicative of infection C. jejuni
May contribute to the severity of enteric diseases in dogs caused by viruses, Giardia sp. and helminths C. jejuni
Young and debilitated or immunosuppressed animals are particularly at risk C. jejuni
Enrofloxacin is effective in eliminating fecal shedding of Campylobacter species C. jejuni
Dogs shedding C. jejuni are potential source of human infection C. jejuni
Causative agent of Avian hepatic hepatitis C. jejuni
Birds commonly harbor in their intestinal tracts and shed the organisms in their feces C. jejuni
Chicks acquire infection from feed, water and litter when introduced into contaminated premises C. jejuni
Infection in chickens and turkeys is usually asymptomatic and are principal source of infection of humans following carcass contamination at slaughter C. jejuni
Characterized by substantial loss in egg production; hemorrhage and multifocal necrosis in the liver C. jejuni
Dihydrostreptomycin sulfate in feed early is beneficial C. jejuni
Causative agent of human intestinal campylobacteriosis C. jejuni
Is the major and most frequent cause of food poisoning in many countries C. jejuni
Zoonotic and food-borne infection C. jejuni
Poultry meat is the major source of human infection C. jejuni
Fever, abdominal pain and diarrhea sometimes with blood are common C. jejuni
Antibiotic resistance, particularly to fluoroquinolones, is a major public health concern C. jejuni
Curved, gram-negative rods Genus: Lawsonia
Obligate intracellular pathogens Genus: Lawsonia
Microaeophilic Genus: Lawsonia
No growth on inert media (cell-free media) Genus: Lawsonia
Growth in tissue culture prepared from enterocytes Genus: Lawsonia
Can be cultured in specific cell cultures Genus: Lawsonia
Rat enterocyte cell line (IEC 18) Genus: Lawsonia
Continous - Henle 407 cells Genus: Lawsonia
Causative agent of proliferative enteritis in pigs Genus: Lawsonia
Enteric disease in weaned pigs (6 to 12 weeks of age) Genus: Lawsonia
Characterized by proliferative and inflammatory changes in the terminal small intestine and large intestine Genus: Lawsonia
Clinical signs: Ranges from chronic intermittent diarrhea with reduction in weight gains to acute hemorrhagic enteropathy Genus: Lawsonia
Genus: Lawsonia Species of veterinary importance Lawsonia intracellularis
Sudden death associated with severe disease (milder form of the disease, animals recover without treatment) Genus: Lawsonia
Characteristic lesions in the ileum, cecum and colon include thickening of the wall, mucosal necrosis and in severe cases clotted blood in the lumen; enlargement of the mesenteric lymph nodes is a feature of the disease Genus: Lawsonia
Family: Leptospiraceae Genus: Leptospira
Family: Spirochaetaceae Genus: Borrelia, Brachyspira/Serpulina, Treponema
Spiral, motile with endoflagella (located within the periplasm, attached to cell-wall at each end of the organism Spirochaetes
Labile in the enviornment & sensitive to desiccation Spirochaetes
Although Gm-ve (stains poorly) Spirochaetes
Some grow in liquid media (most require specialized media) Spirochaetes
Many produce zoonotic infections Spirochaetes
Protoplasmic cylinder- the region containing the cytoplasmic and nuclear regions. Spirochaetes
Cytoplasmic wall- contains peptidoglycan and is fairly rigid. Spirochaetes
Outer sheath- the outer cell envelope which contains LPS Spirochaetes
Flagella also called axial fibrils. Periplasmic flagella are to the protoplasmic cylinder at a point called the basal insertion plate Spirochaetes
Found in aquatic environments Leptospira sp
Systemic infections (many species) Leptospira sp
Shed in urine Leptospira sp
Transmission by arthropod vectors Borrelia sp
Systemic infections (many species) Borrelia sp
Grow slowly in specialized culture media Borrelia sp
Intestinal spirochaetes (some important enteropathogens of pigs) Brachyspira/Serpulina sp
Can be demonstrated in stained fecal smears or in silver stained histopathological sections Brachyspira/Serpulina sp
Anaerobic or microaerophilic Treponema/Serpulina/Brachyspira
Corkscrew rods 5- 20um long Treponema/Serpulina/Brachyspira
Stains well with giemsa stain Treponema/Serpulina/Brachyspira
Commensal of oral cavity, intestinal tract, and urinary tract Treponema/Serpulina/Brachyspira
Aerotolerant. Brachyspira hyodysenteriae
Loosely coiled (2-3 turns/cell). Brachyspira hyodysenteriae
7-8um long with taper at one end. Brachyspira hyodysenteriae
Catalase negative. Brachyspira hyodysenteriae
Gray white colonies with complete hemolysis in 2-5 days Brachyspira hyodysenteriae
Selective medium has an extract of pigs feces and spectinomycin and rifampin Brachyspira hyodysenteriae
Causative agents of swine dysentery (bloody scours) Brachyspira hyodysenteriae
fecal oral transmission Brachyspira hyodysenteriae
colonization of the colon Brachyspira hyodysenteriae
Release of endotoxin and hemolysin Brachyspira hyodysenteriae
Inflammation leads to hemorrhage of the large intestine Brachyspira hyodysenteriae
Severe, bloody diarrhea with rapid weight loss Brachyspira hyodysenteriae
Variable mortality (about 30%) due to dehydration, recovered animals are carriers for life Brachyspira hyodysenteriae
History, clinical signs & gross lesions may indicate swine dysentery Brachyspira hyodysenteriae
Easily confused with other scours. Brachyspira hyodysenteriae
Necropsy shows marked hemorrhagic lesions confined to the large intestine Brachyspira hyodysenteriae
An accumulation of undigested food. Brachyspira hyodysenteriae
Necrotic material and thick mucus in colon and feces. Brachyspira hyodysenteriae
Microscopic exam of mucosal scrapings. Brachyspira hyodysenteriae
A recently described spirochaete in pigs that causes a similar but less severe disease than B. hyodysenteriae Brachyspira pilosicoli
The disease is usually referred to as porcine intestinal spirochaetosis Brachyspira pilosicoli
Diarrhea with mucus but no blood and low mortality Brachyspira pilosicoli
Pigs usually recover in 2-3 weeks, but are delayed in reaching market weight Brachyspira pilosicoli
Many are non-pathogenic & are commensals Genus: Borrelia
Gram negative Genus: Borrelia
Loose helical coils (3-10 turns /cell) Genus: Borrelia
3-20 micro-meter in length Genus: Borrelia
Stains well with Giemsa stain Genus: Borrelia
Require complex growth medium Genus: Borrelia
Anaerobic Genus: Borrelia
Tick and louse transmission Genus: Borrelia
Important species: B. burgdorferi & B. anserina Genus: Borrelia
Causative agent of Lyme disease in humans, dogs, horses, mice & deer B. burgdorferi
Species divided into 4 genomic species based on geographic distribution & genotypes. B. burgdorferi sensu stricto is the principal genotype present in North America B. burgdorferi
Tick transmission: Ixodes sp. B. burgdorferi
Spirochete transmission during feeding requires at least 48 hrs. B. burgdorferi
Dogs: not all animals develop clinical illness despite seroconversion B. burgdorferi
Clinical signs: fever, lethargy, arthritis, cardiac, renal or neurological disturbance B. burgdorferi
(USA: arthritis; Europe & Japan: neurological) B. burgdorferi
Cause Avian spirochetosis in chickens, turkeys, geese, ducks & pheasants B. anserina
Transmitted by fowl ticks (Argas sp)transovarian transmission between ticks; contact transmission; infected material B. anserina
Affects primarily younger birds B. anserina
Clinical signs are acute: septicemia, fever, yellowish-green diarrhea, rapid emaciation, drowsiness & weakness, swollen spleen, death in 3-4 days B. anserina
can be demonstrated in blood & tissues using Giemsa stain B. anserina
Acute disease with significant economic loss in flocks in tropical & subtropical countries B. anserina
Leptospirosis has 2 phases Leptospiremia and fever for 7 days, Leptospuria for 2-3 months
Entry is through mucous membranes. Leptospira interrogans
Following clearance of leptospires from the blood, the organism localizes in the kidney, lungs, liver, eyes, and reproductive tract Leptospira interrogans
Primary replication occurs in the liver. Leptospira interrogans
Acute leptospirosis: damage to RBC membranes and endothelial cells along with hepatocellular injury produce hemolytic anemia, jaundice, hemoglobinuria & hemorrhage Leptospira interrogans
Cattle: fever, diarrhea, anorexia, infertility, abortion, and icterus. Leptospira interrogans
Pigs usually subclinical. Associated with icterus, anemia, and abortions. Leptospira interrogans
Horses rare infections associated with fever, anorexia, and icterus; abortions Leptospira interrogans
Dogs depression, vomiting, diarrhea or constipation, muscle stiffness, bad breath. Acute nephritis (pups) & chronic renal disease (adults); Acute hepatitis & jaundice (icterus Leptospira interrogans
Cattle- hardjo, pomona: Abortions Different animal species have important principal L. interrogans serovars
Sheep- pomona, hardjo (occasionally): Acute hemolytic disease Different animal species have important principal L. interrogans serovars
Swine – pomona, bratislava: Septicemia in piglets Different animal species have important principal L. interrogans serovars
icterohaemorrhagiae: Peracute haemorrhagic disease & acute hepatitis with jaundice Dogs: canicola: Acute nephritis (pups) Chronic renal disease (adults);
Horses: pomona: Abortions L. grippotyphosa-recurrent uveitis moon blindness
Foxes, squirrels, raccoons: grippotyphosa: Septicemia & abortions Different animal species have important principal L. interrogans serovars
is an occupational disease of abattoir workers, dairy & pig farmers, veterinarians & those engaged in manual work related to sewage and drainage Leptospirosis
Is Zoonotic Leptospirosis
Gram-negative, anaerobic Pathogenic anaerobic non-spore-forming Gm-ve bacteria
Endospores not produced Pathogenic anaerobic non-spore-forming Gm-ve bacteria
Enriched media required for growth Pathogenic anaerobic non-spore-forming Gm-ve bacteria
Majority are commensals on mucosal surfaces (principally alimentary tract) Pathogenic anaerobic non-spore-forming Gm-ve bacteria
Synergism with other bacteria in mixed infections Pathogenic anaerobic non-spore-forming Gm-ve bacteria
Dichelobacter sp. (Formerly classified as Bacteriodes sp.) & Fusobacterium sp. (>50%) Pathogenic anaerobic non-spore-forming Gm-ve bacteria
Footrot in sheep D. nodosus as Primary pathogen
Interdigital dermatitis in cattle D. nodosus as Primary pathogen
Interdigital necrobacillosis in cattle F. necrophorum as Primary pathogen
Interdigital dermatitis in sheep F. necrophorum as Primary pathogen
Primary pathogen in a number of disease conditions in farm animals Fusobacterium necrophorum
Mixed bacterial infections are commonly implicated in foot lesions in domestic ruminants and pigs Fusobacterium necrophorum
Cattle: Calf diphtheria: Bovine liver abscess; Black spot of teat; Bovine interdigital necrobacillosis (necrotizing interdigital dermatitis) Fusobacterium necrophorum
Horses: Thrush Fusobacterium necrophorum
Pigs: Necrotic rhinitis (Bull nose) Fusobacterium necrophorum
Necrotic pharyngitis or laryngitis in calves under 3 months of age Calf diphtheria
Enters via abrasions in mucosa of pharynx or larynx often caused by ingestion of rough feed Calf diphtheria
Clinical signs: Fever, depression, anorexia, excessive salivation, respiratory distress & foul smell from mouth Calf diphtheria
If untreated: may develop fatal necrotizing pneumonia Calf diphtheria
Thick, straight or slightly curved, bulging at one or both ends. Appearance of colonies is variable (virulent strains – dark central zone with pale granular middle zone & ground glass appearance) Dichelobacter nodosus
Irregularly staining, slender, non-branching filaments. Colonies are gray, round & shiny ( some are hemolytic ) Fusobacterium necrophorum
Minute colonies in 2 to 7 days, fried egg appearance Mycoplasmas
colony morphology umbonate Mycoplasmas
Contagious bovine pleuropneumonia (CBPP ) M. mycoides subsp. mycoides (small colony type)
Severe, contagious, highly fatal disease of cattle Contagious bovine pleuropneumonia (CBPP )
Causative agent: M. mycoides subsp. mycoides (small colony type); large colony type – causative agent of pleuropneumonia of goats & sheep Contagious bovine pleuropneumonia (CBPP )
Clinical signs: Sudden onset of fever, anorexia, depression, drop in milk yield, accelerated respiration & coughing, characteristic stance with head & neck extended & elbows abducted; expiratory grunting & mucopurulent nasal discharge may be present Contagious bovine pleuropneumonia (CBPP )
In the U.S, it is listed under FOREIGN ANIMAL DISEASES & is a reportable disease Contagious bovine pleuropneumonia (CBPP )
Enzootic pneumonia in pigs Mycoplasma hyopneumoniae
Often subclinical Mycoplasma hyopneumoniae
Chronic respiratory distress Mycoplasma hyopneumoniae
transient diarrhea Mycoplasma hyopneumoniae
Reduced weight gain Mycoplasma hyopneumoniae
Damages the cilia of the respiratory epithelium Mycoplasma hyopneumoniae
Lung lesions observed at slaughter Mycoplasma hyopneumoniae
vaccination reduces lesions and salvages feed efficiency Mycoplasma hyopneumoniae
Chronic respiratory disease in chickens and infectious sinusitis in turkeys M. gallisepticum
Infectious synovitis in turkeys and chickens M. Synoviae
Airsacculitis in turkey poults M. meleagridis
Arthritis in chickens M. Iowae
No evidence as primary causative agent of disease in cats,M. felis,Present in va,Conjunctivitis,M. gateae,Commensal of the oropharynx,Polyarthritis Canine and Feline Mycoplasmas
Contagious caprine pleuropneumonia (CCPP) in goats M. capricolum subsp. capripneumoniae (F38)
Aerosol transmission M. capricolum subsp. capripneumoniae (F38)
Ciliostatic M. capricolum subsp. capripneumoniae (F38)
Rapid onset of fever, cough, and lethargy M. capricolum subsp. capripneumoniae (F38)
Death in 2-3 days M. capricolum subsp. capripneumoniae (F38)
reportable & foreign animal disease M. capricolum subsp. capripneumoniae (F38)
Minute, non-motile, Gm-negative Order: Rickettsiales
Obligate intracellular pathogens, replicate only in cells Order: Rickettsiales
Demonstrated in blood smears by Romanowsky stains Order: Rickettsiales
Host specificity & tropism for particular cell types Order: Rickettsiales
Extracellular survival brief (except Coxiella burnetii) Order: Rickettsiales
Systemic diseases, mainly arthropod-borne, in humans and animals Order: Rickettsiales
Cowdria,Coxiella,Ehrlichia,Rickettsia, Neorikettsia Family: Rickettsiaceae
Anaplasma,Eperythrozoon,Haemobartonella, Aegyptianella Family: Anaplasmataceae
Organisms in this family are referred to as rickettsiae Family: Rickettsiaceae
In common with Gm-ve bacteria, rickettsiae have peptidoglycan in their cell walls Family: Rickettsiaceae
Cultured in specific cell lines or embryonated eggs Family: Rickettsiaceae
Tropism for vascular endothelium or leukocytes Family: Rickettsiaceae
Lack cell walls, possess cell membranes Family: Anaplasmataceae
Have not been cultured in vitro Family: Anaplasmataceae
Tropism for erythrocytes Family: Anaplasmataceae
Rod-shaped or small, pleomorphic, Gm-ve Genus: Rickettsia
Host cell-dependent obligate intracellular pathogens of eukaryotic cells (makes them difficult to culture or reach with antibiotics) Genus: Rickettsia
Predilection for endothelial cells of small blood vessels Genus: Rickettsia
Enter host cells by phagocytosis Genus: Rickettsia
Transmitted by arthropod vectors Genus: Rickettsia
Veterinary importance: Rickettsia rickettsii Genus: Rickettsia
Causative agent of Rocky Mountain Spotted Fever (RMSF) Rickettsia rickettsii
Hosts: Humans, dogs Rickettsia rickettsii
Geographical distribution: North, Central and South America Rickettsia rickettsii
Vectors: Ticks North America: Dermacentor variabilis and Dermacentor andersoni Rickettsia rickettsii
Vectors: Ticks Central and south America: Rhipicephalaus sanguineus and Amblyomma cajennense Rickettsia rickettsii
Clinical signs:Fever, depression, conjunctivitis,retinal hemorrhages,muscle & joint pain,coughing,dyspnoea & edema of the extremities.Neurological disturbance occur in 80% of affected dogs:stupor,ataxia,neck rigidity, seizures and coma. In sev Rickettsia rickettsii
RMSF should be considered in dogs with systemic disease, with exposure to ticks in endemic areas Rickettsia rickettsii
IFA or ELISA to demonstrate a rise in antibody titer (antibodies are not demonstrable until at least 10 days after infection Rickettsia rickettsii
A marked thrombocytopenia and leukopenia may be present in acute phase of the disease Rickettsia rickettsii
D/D: Acute canine monocytic ehrlichiosis Rickettsia rickettsii
Species of veterinary importance: Coxiella burnetii Genus: Coxiella
Grows preferentially in the acid environment of phagolysosomes Genus: Coxiella
Localizes and replicates in cells of the reproductive tract and mammary glands of the ruminants Genus: Coxiella
Stains well with aniline dyes Genus: Coxiella
In MZN-stained smears from ruminant placental tissues: clusters of small, red-staining coccobacilli Genus: Coxiella
Causative agent of Q fever with sporadic abortion in ruminants Coxiella burnetii
Hosts: Ruminants, humans Coxiella burnetii
Geographical distribution: worldwide Coxiella burnetii
Vectors: Ticks (most infections are acquired by inhalation of aerosols) Coxiella burnetii
An occupational hazards for vets., farmers, abattoir workers & others in contact with farm animals & their products Coxiella burnetii
Rare outbreaks of Q fever have been reported in cats Coxiella burnetii
Human infections: Ingestion of contaminated milk & milk products Coxiella burnetii
Most infections in animals are subclinical Coxiella burnetii
In ruminants, infection may also result in infertility or birth of weak offspring Coxiella burnetii
Placentitis or endometritis may be evident Coxiella burnetii
Fetal lesions include hepatitis, myocarditis and interstitial pneumonia Coxiella burnetii
Can be cultured in yolk sac of 5-7 day old embryonated eggs Coxiella burnetii
Segregation of animals and careful disposal of placentas and aborted fetuses are essential, once diagnosis has been confirmed Coxiella burnetii
Inactivated egg-yolk vaccine are available for non-pregnant animals Coxiella burnetii
A vaccine for lab & abattoir workers at high risk is also available Coxiella burnetii
reportable and zoonotic Coxiella burnetii
Species of veterinary importance: Cowdria ruminantium Genus: Cowdria
Replicates in reticuloendothelial cells, particularly macrophages, and in vascular endothelial cells, especially those in the central nervous system Genus: Cowdria
Can have a rapid onset or can be chronic Genus: Cowdria
Causative agent of Heartwater (cowdriosis) Cowdria ruminantium
Hosts: Ruminants (severe disease) Cowdria ruminantium
Geographical distribution: Sub-Saharan Africa and Caribbean islands Cowdria ruminantium
Vectors: Ticks (Amblyomma sp.) Cowdria ruminantium
Damage to vascular endothelium results in increased permeability and widespread petechial hemorrhage Cowdria ruminantium
Sudden onset of fever Cowdria ruminantium
Neurological signs are common and include chewing movements, twitching of eyelids, high-stepping gait, circling and recumbency, associated with high mortality Cowdria ruminantium
In sub-acute disease, lesions include hydropericardium, hydrothorax, pulmonary edema and congestion. Splenomegaly and extensive mucosal and serosal hemorrhages may be evident Cowdria ruminantium
Obligate intracellular parasites of white blood cells Genus: Ehrlichia
All are vector-borne transmitted (but not all vectors have been identified) Genus: Ehrlichia
Approximately 1-3 weeks after exposure, cause mild to severe leukopenia and anemia which can be acute or chronic Genus: Ehrlichia
Infection predisposes for secondary infections Genus: Ehrlichia
Can demonstrate organism in blood smears Genus: Ehrlichia
E. equi (Equine granulocyte ehrlichiosis) Genus: Ehrlichia species of vet importance
E. risticii (Potomac horse fever) Genus: Ehrlichia species of vet importance
E. canis (Canine monocytic ehrlichiosis) Genus: Ehrlichia species of vet importance
E. platys (Canine cyclic thrombocytopenia) Genus: Ehrlichia species of vet importance
Others: E. bovis (Bovine ehrlichiosis); E. ovina (Ovine ehrlichiosis); E. phagocytophilia (Tick-borne fever in ruminants); E. ewingii (Canine granulocytic ehrlichiosis) Genus: Ehrlichia species of vet importance
Causative agent of Canine monocytic ehrlichiosis Ehrlichia canis
Hosts: Dogs Ehrlichia canis
Geographical distribution: Tropical and subtropical regions Ehrlichia canis
Vectors: Ticks (Rhipicephalus sanguineus) Ehrlichia canis
After detachment from an infected host, ticks can transmit the agent to susceptible dogs for up to 5 months. Dogs often remain carriers for > 2 years after recovery from acute disease Ehrlichia canis
Clinical signs: Can progress thru acute, subclinical and chronic phases Ehrlichia canis
Acute phase: mild to severe, characterized by fever, thrombocytopenia, leukopenia and anemia. Most affected dogs recover but some progress to a subclinical phase. Ehrlichia canis
Subclinical phase: lasts months or years, low blood cell values but with minimal clinical signs Ehrlichia canis
A minority of the dogs later develop a severe form of the disease known as tropical canine pancytopenia. Persistent bone marrow depression, along with hemorrhages, neurological disturbance, peripheral edema and emaciation are characteristic of this phase Ehrlichia canis
Progression to this chronic phase may be influenced by factors such as breed susceptibility, immunosuppression & virulence of the strain Ehrlichia canis
Causative agent of Canine cyclic thrombocytopenia Ehrlichia platys
Hosts: Dogs Ehrlichia platys
Geographical distribution: Worldwide (mainly USA, Israel) Ehrlichia platys
Vectors: Ticks suspected Ehrlichia platys
Target cells for replication are platelets Ehrlichia platys
Bacteremia and thrombocytopenia episodes lasts for a couple of weeks & recur at 1-3 week intervals Ehrlichia platys
Causative agent of Tick-borne fever of domestic and wild ruminants Ehrlichia phagocytophila
Endemic in some European countries Ehrlichia phagocytophila
Main vector: Tick (Ixodes ricinus) Ehrlichia phagocytophila
Recovered animals remain infected for up to 2 years and act as reservoirs of infection for ticks Ehrlichia phagocytophila
Induce abortion in association with systemic disease in sheep and cattle Ehrlichia phagocytophila
Causative agent of Salmon poisoning disease (acute & frequently fatal disease) Genus: Neorickettsia N. helminthoeca
Hosts: Dogs Genus: Neorickettsia N. helminthoeca
Geographical distribution: West coast of North America Genus: Neorickettsia N. helminthoeca
Vectors: Flukes (Nanophyteus salmincola) Genus: Neorickettsia N. helminthoeca
Transmitted by ingestion of raw salmon containing infected flukes Genus: Neorickettsia N. helminthoeca
Infects and replicates within macrophages Genus: Neorickettsia N. helminthoeca
Fever, anorexia, weakness and depression followed by persistent vomiting and bloody diarrhea Genus: Neorickettsia N. helminthoeca
Death occurs in 7-10 days (high mortality of 90%) Genus: Neorickettsia N. helminthoeca
Animals which survive are usually resistant to reinfection Genus: Neorickettsia N. helminthoeca
History of exposure in endemic areas, clinical signs and presence of fluke ova in the feces are suggestive of infection Genus: Neorickettsia N. helminthoeca
Organism can be demonstrated in macrophages in lymph node aspirates by Giemsa stain Genus: Neorickettsia N. helminthoeca
D/D: Canine parvovirus & distemper virus Genus: Neorickettsia N. helminthoeca
Cause Elokomin fluke fever Genus: Neorickettsia N. elokominica
Common in West coast of North America Genus: Neorickettsia N. elokominica
Dogs, bears, racoons & ferrets Genus: Neorickettsia N. elokominica
Transmitted by flukes (Nanophyetus salmincola) Genus: Neorickettsia N. elokominica
Morphologically indistinguishable from N.helminthoeca Genus: Neorickettsia N. elokominica
Disease milder than salmon poisoning disease Genus: Neorickettsia N. elokominica
Infection may be concurrent with N. helminthoeca Genus: Neorickettsia N. elokominica
No cross-protection between the two organisms Genus: Neorickettsia N. elokominica
Causative agent of Potomac horse fever Ehrlichia risticii
Hosts: Horses (Fatal disease) Ehrlichia risticii
Geographical distribution: North America, Europe Ehrlichia risticii
Vectors: Flukes suspected Ehrlichia risticii
Occurs during summer Ehrlichia risticii
Infects epithelial cells of the crypts in the colon (also monocytes & macrophages) Ehrlichia risticii
Clinical signs: Fever, anorexia, depression, colic, leukopenia & laminitis; transplacental transmission may induce abortion Ehrlichia risticii
Eperythrozoon (surface of RBC) Family: Anaplasmataceae
Anaplasma (within vacuoles in RBC) Family: Anaplasmataceae
Haemobartonella (surface of RBC) Family: Anaplasmataceae
Aegyptianella (within vacuoles in RBC) Family: Anaplasmataceae
Gm-ve, obligate parasites of erythrocytes, which leads to anemia; no replication in other tissues; worldwide distribution Family: Anaplasmataceae
Arthropod vectors & contaminated instruments Family: Anaplasmataceae
E. ovis: Sheep, goats (Eperythrozoonosis) Genus: Eperythrozoon
E. suis: Pigs (Swine eperythrozoonosis) Genus: Eperythrozoon
Causative agent is A.marginale Bovine Anaplasmosis (gall sickness)
Affects cattle in tropical and subtropical regions (most US exposure is in the Gulf Coast states) Bovine Anaplasmosis (gall sickness)
Vectors: Ticks (Boophilus sp.) and biting diptera; contaminated instruments can also be a source of infection Bovine Anaplasmosis (gall sickness)
Characterized by fever, anemia and icterus Bovine Anaplasmosis (gall sickness)
Young animals: mild (carrier); adult: severe (50% mortality) Bovine Anaplasmosis (gall sickness)
Located inside RBCs close to cell membrane Bovine Anaplasmosis (gall sickness)
Clinical signs: include depression & reduced milk yield; marked anemia & jaundice in the absence of hemoglobinuria & weight loss is pronounced (severe emaciation) Bovine Anaplasmosis (gall sickness)
H. felis (Feline haemobartonellosis --- Feline infectious anemia) Genus: Haemobartonella
H. canis (Canine haemobartonellosis) Genus: Haemobartonella
Worldwide; rod-shaped obligate parasite of RBCs Genus: Haemobartonella
Often associated with mild to subclinical infections Genus: Haemobartonella
Causative agent of Feline infectious anemia (Feline haemobartonellosis) Haemobartonella felis
Occurs worldwide; found on the surface of RBCs; exact mode of transmission is uncertain (biting arthropods suspected); common in free-roaming tom cats 1-3 years of age; perinatal transmission to kittens has been recorded; recovered cats may remain asympto Haemobartonella felis
Disease varies in clinical presentation: Haemobartonella felis
Peracute form: profound anemia associated with immunosuppression, overwhelming parasitaemia, resulting in rapid death Haemobartonella felis
Acute form (most common): fever, anemia, depression, weakness and occasionally jaundice Haemobartonella felis
Chronic form: anemia, lethargy and marked weight loss Haemobartonella felis
Immunosuppression from FeLV infection often results in the development of severe feline infectious anemia Haemobartonella felis
Diagnosis: Giemsa stained blood smears; IF; hematolgy (reduced pcv & evidence of regenerative anemia Haemobartonella felis
Treatment: Doxycycline initiated early & continued for 21 days is effective: severely affected cats may require blood transfusion Haemobartonella felis
Control: flea control & careful selection of donors for blood transfusion Haemobartonella felis
Causative agent: Bartonella henselae (thin gram-negative slightly curved rods) Cat-scratch disease (CSD)
Grows only on blood-enriched media & may take 3 to 4 weeks Cat-scratch disease (CSD)
Carried by healthy cats & transmitted by cat flea Ctenocephalides felis Cat-scratch disease (CSD)
Causes no clinical signs in cats, infection is common in kittens Cat-scratch disease (CSD)
Humans: signs develop 1 to 3 weeks after scratch or bite of a cat and include lymphadenitis & systemic signs such as fever, malaise & headaches Cat-scratch disease (CSD)
Usually resolves without treatment, but complications may occur Cat-scratch disease (CSD)
Causes bacillary angiomatosis in immunocompromised individuals (can be fatal) & requires prolonged antimicrobial therapy (erythromycin, rifampicin, doxycycline & gentamycin are most effective). Cat-scratch disease (CSD)
Chlamydophila psittaci: Birds --- Pneumonia & airsacculitis, intestinal infection & diarrhea, conjunctivitis, pericarditis, encephalitis Chlamydia & Chlamydophila
Chlamydophila psittaci: Humans (secondary hosts) --- Psittacosis/Ornithosis, abortion, conjunctivitis Chlamydia & Chlamydophila
Chlamydophila abortus: Sheep --- Enzootic abortion in ewes (EAE); Goats, Cattle & Pigs --- Chlamydial abortion Chlamydia & Chlamydophila
A common upper respiratory and conjunctival infection of cats, especially kittens Feline chlaymidiosis (pneumonitis)
Direct transmission between cats and is highly contagious Feline chlaymidiosis (pneumonitis)
Can be severe but is rarely fatal Feline chlaymidiosis (pneumonitis)
Difficult to distinguish from other feline respiratory diseases Feline chlaymidiosis (pneumonitis)
Clinical signs: appear in around 1 week & progress for about 2 weeks--- coughing, fever, anorexia, ocular/nasal discharge; recovery takes 1-2 months ( cats continue shedding); keratitis & corneal scarring may occur Feline chlaymidiosis (pneumonitis)
Susceptible to several antibiotics. All contact cats should be treated at the same time Feline chlaymidiosis (pneumonitis)
MLV are available (prevents clinical disease but does not prevent infection or shedding of organisms) Feline chlaymidiosis (pneumonitis)
A small number of cases of conjunctivitis in humans involving C.felis have been reported--Zoonotic Feline chlaymidiosis (pneumonitis)
Major cause of reproductive failure in sheep. Cattle, goats and pigs are also susceptible Enzootic abortion of ewes (EAE)-Chlamydophilia abortus--Zoonotic reportable
Primarily a disease of intensively managed flocks & is economically significant disease Enzootic abortion of ewes (EAE)-Chlamydophilia abortus--Zoonotic reportable
Infection occurs primarily by ingestion Enzootic abortion of ewes (EAE)-Chlamydophilia abortus--Zoonotic reportable
Characterized by abortion during late pregnancy or birth of premature weak lambs Enzootic abortion of ewes (EAE)-Chlamydophilia abortus--Zoonotic reportable
Clinical signs: affects particularly the digestive & respiratory tracts, severity varies with the strain of C. psittaci , species & age of birds Avian chlamydiosis
Important p.m findings: Hepatosplenomegaly, airsacculitis & peritonitis Avian chlamydiosis
Is zoonotic & is a reportable disease Avian chlamydiosis
Infection of humans is by inhalation of infected droplets or dusts Avian chlamydiosis
Pulmonary involvement is common Avian chlamydiosis
Meningitis or meningoencephalitis may develop in severely affected individuals Avian chlamydiosis
Avian psittacosis: psittacine birds Avian chlamydiosis
Ornithosis: other avian species Avian chlamydiosis
Avian chlamydiosis: preferred designation Avian chlamydiosis
Worldwide problem of major economic impact Avian chlamydiosis
Infection is usually acquired by inhalation or by ingestion & subclinical infection is common Avian chlamydiosis
Created by: alljacks



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