Gram Positive Flashcards
Staphylococcus
Gram + cocci in clusters Facultative anaerobes Non motile, non spore forming Catalase + Commensals on skin and mucus membranes -upper respiratory tract (nose) -lower urogenital tract -GI tract Humans animals and stable in environment Part of normal host associated microbiota Opportunistic
Virulence factors and pathogenesis
Colonization of mucus or minor skin trauma
Overcome innate immune response
Inflammation, destruction of PMNs, may survive in phagocytes
Pathology: pus formation, abscesses, local necrosis
Folliculitis, mastitis, myositis, pyoderma
Virulence factor: Adhesions
Pathogenic effect: Tissue colonization
Virulence factor: Hemolysins
Pathogenic effect: Tissue destruction- cytolytic
Virulence factor: Enterotoxins
Pathogenic effect: Tissue destruction- heat stable toxins- food poisoning
Virulence factor: Toxic shock syndrom toxins
Pathogenic effect: Tissue destruction- superantigen leading to excessive cytokine release- toxic shock
Virulence factor: Protein A
Pathogenic effect: Immune evasion- binds Fc portion of IgG and inhibits opsonization
Virulence factor: Leukocidin
Pathogenic effect: Immune evasion- leucocidal
Virulence factor: Coagulase
Pathogenic effect: Immune evasion- hide bacteria from polymorphonuclear leukocytes
Fibrinogen to fibrin. S aureus can coat its coat with fibrin and this fibrin clot may protect bacteria from phagocytosis and make bacteria more virulent
Coagulase test
To detect most virulent staphylococci
Positive= fibrinogen in rabbit plasma is converted to fibrin by coagulase and visible clot formation in tube
Negative= coagulase- negative staph- less virulent
Bovine Staphylococcal Mastitis
Contagious mastitis in cattle cause by S aureus
Chronic subclinical disease with periodic clinical episodes during lactation
Majority is not cleared by immune system- chronic, low-grade or subclinical-> production losses
Source of infection: infected mammary gland of another cow
predisposition: impaired phagocyte function-> ability of pathogen to survive within mammary gland
Bovine Staphylococcal Mastitis- transmission
Milking through contaminated hands of milker
Teat cup liners and udder cloths
Bovine Staphylococcal Mastitis- Peracute gangrenous masitis
Venous thrombosis and local edema
Tissue necrosis, udder discoloration
Swollen quarters, sore on palpation
Fever, depression, anorexia
Bovine Staphylococcal Mastitis- acute mastitis
Sever swelling of affected gland
Purulent secretion with clots
Extensive fibrosis
Bovine Staphylococcal Mastitis- chronic subclinical mastitis
Most common
Elevated somatic cell counts
Episodes of bacterial shedding
Inflammatory response-> blockage of ducts and atrophy of alveoli
Bovine Staphylococcal Mastitis- Tx and prevention
Proper milking technique and good hygiene when milking -single use paper towels to dry teats -milker wears gloves -teat dip in iodine Dry cow therapy after drying off Detect subclinical inections -segregating infected -antimicrobial tx -cull chronic cows prevent into of positive cows to heard
Botryomycosis
rare
Chronic granulomatous suppurative disorder with formation of micro-abscessation
Cutaneous form with small subdermal granulomas
Tx: long term AB tc and surgical removal of affected tissue
Prevention: hygiene during surgical procedures, proper would care
Bumblefoot
Local chronic pododermatitis (and tenosynovitis) of the foot of all types of birds
Entry of bacteria through weakened area or scratches in birds foot (injury from nail trimming, rough roosts etc) sometimes leading to staph arthritis and septicemia in turkeys
Prevention: good husbandry practice (splinter free bedding and roosts, balanced diet, regular check up)
Pyoderma, otits externa and other suppurative conditions
local skin diseases in dogs and cats (pyodermas: folliculitis), otitis externa, infected wounds, UTI, conjunctivitis, abscesses
S. pseudintermedius is most common opportunistic path in dogs
Primary cause for otitis externa often parasites, food allergies, foreign bodies, accumulation of hair, autoimmune diseases– bacterial infections usually secondary- triggered by overgrowth of normal resident or transient skin microbiota (skin disease that changes from dry to humid can predispose to overcolonization)
Colonization is not infection- not much zoonotic concern
Pyoderma: tx
ID of underlying problems
Cleansing shampoo followed by antimicrobial shampoo
Judiciously choose topical vs systemic antibiotics
Use narrow-spectrum antibiotics
2% mupirocin ointment
Grooming and clipping of hair coat
Greasy pig disease
Highly contagious exudative epidermitis in suckling and weaned pigs
up to 3 months old
Excessive sebaceous secretion and exfoliation, anorexia, depression, fever
Morbidity 20-100%
Mortality up to 90% in severely affected litters
S. hyicus can be isolated from vag mucosa and skin of healthy sows and preputial diverticulum of boars
Entry of skin through minor abrasions (bite wounds)
Greasy pig disease- tx and prevention
Early systemic AB therapy with topical tx with antiseptic or AB suspensions
Strict isolation of infected pigs
cleaning and disinfection of contaminated buildings
clipping needle teeth of newborn
Soft bedding, good hygiene in weaner accomidation
TSS
Caused by effect of superantigens entering bloodstream
Fever, headache, vomiting, diarrhea
Conjunctival reddening, hypotension, skin rashes, kidney failure
Food poisoning
Caused by eating food where S aureus has multiplied and produced enterotoxins
Nausea, vomiting, severe abdominal cramp
Diarrhea, sweating, etc
Lab diagnosis
Specimens: exudates, pus from abscesses. mastitic milk, skin scrapings, urine, affected tissues
Direct microscopy: gram staining. Gram+ clusters and evidence of inflammation with adundance of neutrophils
Isolation: culturing on blood agar and macconkey agar
Molecular typing with PCR
Tx
With antimicrobial agents and elimination of primary cause
Choice of therapy depends on infection site, severity and staph strain
-amoxicillin, clavulanic acid, etc
-penicillinase-resistance B lactams
-quinolones not recommended
Antimicrobial susceptibility testing always recommended
Always look for primary cause- staph is opportunistic
Antimicrobial resistance
B lactimase-mediated resistance common in staph spp
Methicillin resistance in S aureus (MRSA) and S pseudintermedius (MRSP)- mediated by medA gene- altered penicillin binding proteins
Resistance to B-lactam antibiotics often coincides with resistance to other antibacterial drugs (multidrug resistance)
Antimicrobial resistance- infection control
Nares are common site of colonization and hands common source
Contact precautions
awareness of increased risk
isolation of animals if possible
counseling the owners about risk
immunocompetent old clients consult with their docs
Streptococcus
Gram+ cocci in chains Facultative anerobes non motile non spore forming Catalase - Fastidious commensals on mucus membranes -upper respiratory tract -lower urogenital tract Host humans and animals Species specific primary and opportunistic pathogens don't survive well in environment
Streptococcus continued
Type of hemolysis: -B hemolytic: clear complete hemolysis -a hemolytic: green, partial hemolysis -gamma: no hemolysis Biochemical testing Lancefield classification -based on cell wall polysaccharide Ag -Groups A-H -ring precipitation test and latex agglutination
Virulence factors and pathogenesis
Entry in upper respiratory tract via purulent exudates or discharging abscesses
Multiplication in tonsillar tissue and/or lymph nodes and guttural pouch-> carries
Overcome innate immune response, M-protein, Hyaluronic acid capsule
Inflammation, large numbers of neutrophils, abscess formation
Systemic dissemination
Septesemia
Pneumonia, arthritis, meningitis
Virulence factor: Streptokinase
Pathogenic effect: invasion
Virulence factor: Hyaluronidase
Pathogenic effect: invasion
Virulence factor: Protein F
Pathogenic effect: adhesion
Virulence factor: M protein
Pathogenic effect: evasion
Virulence factor: Hyaluronan
Pathogenic effect: evasion
Virulence factor: streptolysins
Pathogenic effect: evasion
Virulence factor: Streptococcal pyrogenic exotoxins
Pathogenic effect: toxins
Virulence factor: Lipoteichoic acid
Pathogenic effect: toxins
Strangles, Equine distemper
Highly contagious febrile disease involving upper respiratory tract with abscessation of regional LNs
Swollen LNs can cause airway obstruction leading to death
Enzootic in domesticated horses worldwide- not commensal
Transmission via purulent exudates from respiratory tract or discharging abscesses form carrier or diseased animal
Strangles, Equine distemper-more
Morbidity up to 100% mortality less than 5%
all ages- most common in yearlings
Incubation period 3-6 days
CS: High fever, depression, anorexia, purulent oculonasal discharge
Submandibular LNs affected and eventually rupture discharging purulent highly infectious material
Strangles, Equine distemper- Guttural pouch empyema
Usually secondary to upper respiratory tract infection
Accumulation of purulent exudate in guttural pouch
Stiff head carriage, painful swelling in parotid area, difficult breathing
Strangles, Equine distemper- bastard strangles
Disseminated infection with abscessation in many organs
1% of cases
Strangles, Equine distemper- Purpura haemorrhagica
Immune complex mediated vaculitis
Strangles, Equine distemper: dx and tx
> 75% recover spontaneously after abscesses mature and rupture and develop strong immunity
Dx: CS,
-culturing from abscess swab, nasal swab, lavage fluid
-serology- ELISA for anti M protein Ab
-PCR targeting M protein
Tx: Symptomatic- relieve pain, drainage of mature abscesses
AB only effective given soon after exposure and before abscess formation (also for bastard strangles)
Strangles, Equine distemper- prevention
Vx: not 100% effective inactive vaccines (M protein enriched) for pregnant mares and foals to maintain high levels of anti M protien opsonizing Ab Live intranasal vx to stimulate mucosal immunity and serum opsonizing Abs
Prevention: stop movement of animals upon suspected infection
Quarantine, hygiene, disinfection
Notifiable disease in many states
Strangles, Equine distemper-Carriers
ID and tx of carriers eliminated possible infectious horses - reduces outbreaks
Newly acquired horses, non affected in contact horses after outbreak, affected in contact horses after outbreak
3 neg cultures 1/wk- release from quarantine
Incubatory: nasal shedding 4-7d after exposure with or without nasal discharge
Clinical: shedding from affected sites
Convalescent: nasal shedding for up to 6 wk after recovery
Long term chronic shedding
Streptococcus suis
In pigs
Recognized worldwide as cause of sig losses in pig industry
Associated with meningitis, arthritis, septicemis, bronchopneumonia
Sporadic cases of endocarditis, neonatal deaths and abortion
Carrier rate near 100%
Disease incidence <5%
without tx mortality=20%
pigs natural carriers in tonsillar tissue
Streptococcus suis- dx
Serotyping- routine infection dx
- 35 serotypes described
- pigs can cary different ones
- # 2 is predominant
Streptococcus suis- predisposing factors
Environment co-infection closeness stress etc
Streptococcus suis-tx and control
Tx: penicillin or ampicillin
Prophylaxis in heard with neonatal death or meningitis at weaning
-long acting penicillin given by inj to sows 1w before farrowing
-long acting penicillin given by inj to piglets during first 2w of life
Eradication impossible
Improved husbandry and hygiene
Streptococcus suis- emerging zoonotic pathogen
Underreported and underdiganosed in many countries
Most common cause of adult meningitis in Asia
Risk: employment in swine industry
consumption of raw pork meat
Bovine Streptococcal Mastitis- contagious
S. agalactiae colonizes milk ducts (obligate parasite of mammary glands)
persistent infection with intermittent bouts of acute mastitis (chronic)
Bovine Streptococcal Mastitis- environmental
S. dysgalactiae colonizes buccal cavity and geitalia, skin of mammary gland-> acute mastitis
S. uberis colonized skin, tonsils, vaginal mucosa -> subclinical mastitis
Bovine Streptococcal Mastitis- tx, control, and prevention
Prepare cows properly for milking
- pre and post milking teat dipping
-use separate paper towels and dry teats before machine application
Have good milking system and apply properly
-reduce teat end injury and other trauma
-segregate chronic mastitis cows, milk last
Dry cow treat all
Well-balanced nutrition and hygiene management
Screen cows before intro to heard
Monitor somatic cell counts in milk
Etiopathology of cattle mastitis is multifaceted with 3 factors involved
- exposure to microorganisms
- host defense mech
- environmental conditions
Pyogenic strepticocci infections-S. equi subsp zooepidemicus
S. equi subsp zooepidemicus
Opportunistic pathogen of broad range of animals- causing purulent infections
Usual habitat in mucus membranes
Upper respiratory tract infections, pneumonia, mastitis, navel infections, foal septicemia
Emerging zoonotic pathogen-> necrotizing myositis and meningitis in humans
Pyogenic strepticocci infections- Streptococcus canis
Streptococcus canis
Streptococcal toxic shock syndrome and necrotizing fasciitis in dogs and cats (esp kittens and puppies)
Commensal on skin and mucus membranes in cats and dogs
Infection from vagina or umbilical vein-> peritoneal cavity-> liver -> bacteremia
Septicemia and embolic lesions in heart and lungs
Pyogenic strepticocci infections- Streptococcus pyogenes
Streptococcus pyogenes
Causes mild superficial skin diseases to life threatening system disease
Impetigo (localized skin infections), pharyngitis with abscesses on throat
Bacterial infection-> toxin production-> destruction of skin, fat, and muscles -> streptococcal toxic shock
Flesh eating bacterium- causing rare but serious to deadly infection known as necrotizing fasciitis
Non-pyogenic diseases: rheumatic fever, glomerulonephritis
Enterococcus
Gram+ ovoids, often in pairs (diplococci) or short chains
Facultative anaerobes
Some strains motile
Non spore forming
Catalase -
Commensals of GI tract of humans and animals
Low grade pathogens ->opportunists
Opportunistic infections
Enterococcus faecalis, Enterococcus faecium Wound infections Mastitis in cattle Urinary tract and ear infections in dogs Nosocomial infections
Antimicrobial resistance VRE
Naturally resistance to many antimicrobial agents
Acquired resistance to vancomycin and beyond
Enterococci are commensals of GI tract. May be the cause of different opportunistic infections
Some are of emerging importance because of their innate resistance to antimicrobial drugs and ability to acquire resistance
Listeria
Gram + coccobacillary rods
Facultative anaerobes
Tumbling motility (1-4 flagella) at 25C
Catalase +, oxidase -
Tolerate pH between 5.5 and 9.6
Grow on non-enriched media over a wide temp range (0-50C)
Psychrophilic-> growth in fridge
Ubiquitous in environment (soil) and carried in mammalian GI
Resistant to harsh environmental conditions
Hosts: humans and animals
Recovered from herbage, feces, sewage effluent and water
often asymptomatic carriers
Septicemia, abortion, encephalitis
Listeria- virulence factors and pathogenesis
Contaminated silage Inhaled -travel along trigeminal n to brain -encephalitis, neuro symptoms Ingested -blood stream -Encephalitis -Septicemia -abortion
Pathogenicity- intracellular replication -> cell death and focal microbabscess formation
Facultative intracellular bacteria: persist in macrophages
Invasion of both phagocytic and non-phagocytic cells
Survive and replicate intracellularly: escape from phagosome before its maturation to phagolysosome
Cell-to-cell transfer without exposure to humoral defense mechanisms
Virulence factor: Internalin A and B (InlA, InlB)
Pathogenic effect: adhesion
Virulence factor: Listeriolysin O
Pathogenic effect: Pore-forming cytolytic toxin: destroys membranes of phagosomes
Virulence factor: ActA protein
Pathogenic effect: Actin-polymerizing protien
Virulence factor: Phospholipase C enzymes (PLCs)
Pathogenic effect: Degradation of cytoplasmic and endocytic membranes
Circling disease, silage disease
Encephalitis is most readily recognized from of listeriosis in ruminants, affecting all ages and both sexes
Winter-spring disease of feedlot or house ruminants: less acidic pH of spoiled silage enhances multiplication of L. monocytogenes. Outbreaks occur about 10 days after feeding poor-quality silage
Economically important disease with seasonal occurrence
Ingestion, inhalation, or entry via breaks in oral and nasal mucosa
Circling disease, silage disease- CS
Anorexia, depression, disorientation (seen first)
Dullness, turning or twisting of head to one side, walking in circles towards affected side
Unilateral trigeminal and facial nerve paralysis with drooping ear, deviated muzzle, lowered eyelid, strabismus, nystagmus, head pressing
Purulent unilateral endophthalmitis
Circling disease, silage disease- Dx
Ketosis in cattle Pregnancy toxemia in ewes BSE (bovine spongiform encephalopathy) Thrombotic meningoencephalitis Rabies Lead poisoning Parasitic infections Ante-mortem: History and symptoms, season, incubation time, silage quality
Circling disease, silage disease- Dx- Lesions in brain stem
Prominent lesions in brain stem
- microabscesses and glial nodules infiltrated by neutrophils and macrophages that may contain bacteria
- Meningitis, perivascular cuffs composed of lymphocytes, neutrophils and histiocytes
- acute vascular fibrinoid necrosis
- neuronal necrosis, neuritis and perineuritis of cranial nerves
Circling disease, silage disease- Dx- culture of brain stem
In case of septicemia
-culture of liver, spleen, and blood
-potentially gross lesions (focal hepatic necrosis and hemorrhagic gastroenteritis)
In case of abortion
-foetal abomasal content and uterine discharges
Circling disease, silage disease- Tx
Early stages of septicemic listeriosis:
-systemic therapy with penicillin, tetracycline, erythromycin and trimethoprim/sulfonamide
Neural listeriosis:
-Response to antibiotic therapy may be poor, usually not attempted in ruminants
-prolonged high doses of ampicillin and gentamicin
Prevention is key
Poor quality silage ph>5.5 not fed
Optimize forage quality through proper harvesting, ensiling and feed out practices. Silage feeding should be discontinued if outbreak confirmed
Zoonosis and food-borne disease
About 1600 people in us get sick from listeria each year
Listeria is 3rd leading cause of death from food poisoning
At least 90% of people who get is are in YOPI group
Intracellular localization and tolerance to heat- survives pasteurization
Direct infection from infected animals rare in healthy non pregnant individuals
Erysipelothrix
Gram + small rods or filaments (morphological variation)
Facultative anaerobes
Non motile
Catalase -, oxidase -
Widespread in tonsils and intestines of many species
Present in slime layer of fish -> source of human infection
Up to 50% of healthy pigs harbor E. rhusiopathiae in tonsillar tissues
Carrier pigs excrete the organism in feces and in oronasal secretions
Resistant to harsh environmental conditions (even isolated from salted and smoked pork)
Swine most important reservoir: Septicemia, dermatopathy, arthritis, endocarditis
Erysipelothrix- virulence factors and pathogenesis
Pathogenicity- production of neuraminidase
-cleaves sialic acid on endothelial cell surfaces-> vascular damage -> hyaline thrombus formation
E. rhusiopathiae includes 26 serotypes of which 1a, 1b, and 2 are common in pigs
Excretion in feces and oronasal secretions
Transmission by ingestion of contaminated material
Virulence factor: Polysaccharide capsule
Pathogenic effect: protection against phagocytosis and allows intracellular replication
Virulence factor: Neuraminidase
Pathogenic effect: Adherence and invasion of endothelial cells
Virulence factor: Hyaluronidase
Pathogenic effect: Dissemination of bacteria within tissues
Virulence factor: spaA surface protein
Pathogenic effect: Adhesion
Swine erysipelas, diamond skin disease
Acute form: sudden death or fever, stiff gait (walking on toes), separate from group, anorexia, skin lesions
Subacute form: inappetence, mild fever, skin lesions
Chronic form: may follow (sub)acute form- arthritis, heart problems after exertion
Diamond shaped skin lesions are pathognomonic for swine erysipelas
Swine erysipelas, diamond skin disease- chronic form
Endocarditis, polyarthritis, skin lesions
Most susceptible: pigs 3 months to 1 year of age
- less than 3 months: protected by maternally derived anibodies
-over 3 years: protective active immunity through exposure to strains of low virulence
Stress factors can trigger clinical erysipelas: transport, weather, mixing etc)
Swine erysipelas, diamond skin disease- Dx
Skin lesions
Isolation of E rhusiopathiae (but rarely recovered from skin lesions or chronically affected joints)
PCR based methods
Swine erysipelas, diamond skin disease-Tx
Acute form: isolate and treat with antimicrobials (penicillin or tetracycline)
Intrinsic resistance to vancomycin, aminoglycosides and sulfonamides
Cull chronically affected animals
Swine erysipelas, diamond skin disease- control
Good hygiene practices and management
Vaccination before entering breeding herd, boars every 6 mo and sows 3-4 w prior to farrowing
Erysipelas in Turkeys
Important disease worldwide and birds of all ages susceptible
Acute form: septicemia, sudden death
Chronic form: endocarditis and gradual weight loss
Non-suppurative polyarthritis in lambs
Organisms enter through umbilicus or castration wounds
Post dipping lameness is due to cellulitis and laminitis in older lambs
Erysipeloid in humans: zoonosis
Occupational hazard- vets and peopl working in fish, poultry, swine
E. rhusiopathiae enter through minor skin abrasions in contact with infectious animal organs and secretions
-localized cellulitis in fingers
-diffuse skin infections
-septicemia
Human erysipelas is an infectious skin disease caused by group A beta-hemolytic streptococci
Bacillus
Large square end Gram + rods and chains
Aerobes or facultative anaerobes
Endospore-forming
Catalase +, oxidase -
Motile EXCEPT bacillus anthracis
Medusa head colonies on microscopic observation
Ubiquitous in soil (soil saprophytes)
Majority are non-pathogenic environmental organisms
Most important pathogen B anthracis is an obligate mammalian pathogen
Cases of anthrax occur sporadically- mostly in cattle
Source is usually soil with spores
Bacillus endospores
Proven to be most durable type of cell in nature
Cryptobiotic state of dormancy-> viable for extremely long periods of time (millions of years)
Resistant to extremely adverse conditions (desiccation, high temps, irradiation etc)
Typically one endospore formed per vegetative cell as response to nutrient depletion
Endo=formed intracellularly (although eventually released as free spores)
Koch described developmental cycle of spore formation in B anthracis and used anthrax bacteria in on fo the most historical experiments leading to koch’s postulates
Bacillus- virulence and pathogenesis
Susceptibility of animals for replication
Survival endospores in soil- exposure of carcass to O2
Ecological cycles of infection
Bacillus Predisposing soil factors
History of precious anthrax deaths and buried carcasses
soil conditions: alkaline (pH >6), rich in Ca and N, high moisture content
Warm temps
Repeated cycles of flooding and evaporation: soil rearrangements brings endospores to surface; endospore concentration increases in standing surface water
Drought conditions: animals forage closer to ground -> soil ingestion and mechanical injuries
Bacillus anthracis capsule
Polymers of D-glutamic acid Encoded on plasmid pXO2 Only produced in vivo Anti-phagocytotic Virulence derived from capsule and extracell factor (tripartite anthrax toxin)
Anthrax toxin
A tripatite lethal combination
Three separate proteins encoding plasmis pXO1
Protective antigen (PA): cell binding factor
-translocation into cell
Edema factor (EF): calmoduline-dependent adenylate cyclase
-enters the cell following binding to PA
-Increase in levels of cyclic AMP-> disturbance of water homeostasis -> edema
-Neutrophils are primary target
Lethal factor (LF): zinc metalloprotease
-cell death and hypoxia-induced tissue injury and shock -> necrosis and hemorrhage
Anthrax
Incubation period ranges from hours to days
Clinical presentation varies with species affected, challenge dose and rout of infection
-peracute septicemia: ruminants
-acute septicemia: horses
-Pharyngeal: pigs, dogs
-intestinal: pigs, dogs, humans
-pulmonary: humans (wool sorters disease)
-cutaneous: humans (malignant carbuncle)
Peracute septicemia
Ruminants
Rapidly fatal disease with respiratory distress and shock
Bleeding from orfices
Postmortem: dark unclotted blood, incomplete rigor mortis
Splenomegaly
Anthrax: Dx
Do not conduct a field necropsy if you have anthrax in your differential diagnosis list
call state/federal officials
Anthrax is a obligatory reportable disease
It is responsibility of health care provider (vet) not the patient or client to report cause of disease
BSL-3 agent
Select agent
ID only in reference labs
Anthrax: Dx- direct examination of samples
Collection of peripheral blood from tail vein
Blood and organ smears stained with polychromatic methylene blue (mcfadyeans methylene blue) -> blue staining organisms with pick capsule
Gram stain: chains of encapsulated, G+, non-spore forming rods, non-motile, rectangular with square ends
Aerobic culture on blood agar
PCR for detection of B anthracis DNA in deteriorating or stored samples
Anthrax: tx and control
Endemic regions: annual vax; long acting penicillin when outbreaks threaten valuable livestock
Nonendemic regions:
-quarantine herd (for at least 30d following last death)
-Use PPE when handling animals and contaminated materials
-Tx of all animals with long acting antimicrobials
-keep in contact animals under close observation for at least 2 weeks
-Vaccinate 8-12 days after AB tx
-Incinerate carcasses or deep burial (more than 6.5’) under layer of quicklime
-Disinfect contaminated materials
Woolsorter’s disease
Anthrax in humans Cutaneous, intestinal (rare), pulmonary, injection People at risk: -people who handle animal products -vets -livestock producers -travelers -lab professionals -mail handlers, military personnel, response workers
Woolsorter’s disease: tx and control
Early tx required
Penicillin, tetracycline, doxycycline, ciprofloxacin
Resistance or reduced susceptibility has been shown for erythromycin, trimethoprim, and azithromycin
Antimicrobial susceptibility testing should only be done by approved reference labs
Vaccination for humans exposed to infection in the course of their work in endemic regions
Acid fast (-partial) bacteria
Mycobacterium= acid fast Acid fast-partial: Corynebacterium Rhodococcus Nocardia
Genus Cornebacterium
Gram-positive, pleomorphic bacteria- angular clusters
Aerobes or facultative anaerobes
Short mycolic acids in cell wall
Non-spore forming
Pathogenic corynebacteria are non motile
Commensals on mucus membranes
Many spp also found in soil and other environmental sources
Largely host specific
Opportunistic pathogens causing mostly pyogenic infections
Tissue trauma usually precedes establishment of pathogenic corynebacteria
Gram+ aerobes with an unusual lipid rich outer layer which tend to survive in macrophages (facultative intracellular pathogens) and cause chronic granulomatous diseases
Cornebacterium: Virulence factors and pathogenesis
Purulent material
Inhalation or ingestion of bacteria- skin injuries etc
Replication within phagocytes (facultative intracellular pathogen)
Inflammation. Formation of abscesses
Virulence Factor: External lipid coat (mycolic acids)
Pathogenic effect: Protection from hydrolytic enzymes in host phagocytes
Virulence Factor: Exotoxin Phospholipase D (PLD)
Pathogenic effect: Hydrolyze cell membranes -> damage endothelial cells -> increased vascular permeability
Virulence Factor: Diphtheria toxin
Pathogenic effect: Infers with protein synthesis in cells
Caseous lymphadenitis (pseudotuberculosis)
Sheep and goats
Chronic pyogranulomatous infection of lymph nodes
Abscessation and enlargement of superficial or internal lymph nodes
Infection spread by puss from ruptured abscesses, and from nasal and oral secretions
Organism can survive in the environment for several months
Internal abscesses lead to chronic weight loss (thin ewe syndrome)
Caused by non-nitrate-reducing biotype C. pseudotuberculosis
Curse of the goat industry- not hot or painful
Incubation period ~3m
Caseous lymphadenitis (pseudotuberculosis)
Caseous necrosis of lymph nodes
Initial lesions begin as lymphadenitis with the formation of multiple microscopic abscesses in the cortex -> coalesce of microabscesses -> area of caseation
Encapsulation of abscesses by fibrous connective tissue -> enlargement of lymph nodes
In goats: exudate is less dry and not concentrically laminated or mineralized
Caseous lymphadenitis (pseudotuberculosis): Economic losses
death, condemnation of infected carcasses, hide and wool loss, devaluation of hides, loss of sales for breeding and premature culling of infected animals
Caseous lymphadenitis (pseudotuberculosis): diagnosis
Clinical signs: abscess, chronic weight loss
Culture of purulent material
Radiography and ultrasonography to detect internal abscesses (challenging!)
Serology
Caseous lymphadenitis (pseudotuberculosis): diagnosis by serology
Synergistic hemolysin inhibition (SHI) test: detects antibodies to phospholipase D exotoxin
Positive titers indicate past resolved infections, recent exposure, recent vxn or active lesions
If doubt- repeat titer in 2-4 wks to see if titer is rising
False-neg titer when testing is done early in infection <2wks or animals with chronic walled off abscesses
Interpretation in young animals is difficult due to presence of maternal antibodies -> results from lambs (<6m) should be interpreted with caution
Low or no titer doesnt rule out disease
Caseous lymphadenitis (pseudotuberculosis): control
Not considered curable- owner education stressing the persistent recurrent nature of the disease
Only animals with genetic or emotional value are treated
-isolate animals in area that can be disinfected
-lancing and draining, surgical excision of abscesses
-Iodine, bleach, and chlorhexidine to disinfect area
-Systemic antibiotics and intralesional antibiotics (penicillin, rifampin, tulathromycin)
Ideally, infected animals should immediately be culled
Commercial CL vxns, species specific for use in sheep and goats respectively
-not recommended for clean herds without history
Good biosecurity, hygiene and management practices
Caseous lymphadenitis (pseudotuberculosis): control- countries free of disease
Only import from countries free of disease or with low incidence
Pre-importation testing with ELISA
Quarantine for several months and infected animals slaughtered
Caseous lymphadenitis (pseudotuberculosis): control- countries with low prevalence
Animals with lesions should be culled
Regular testing of flocks/herds with ELISA -> culling of positive or doubtful animals
Removal of lambs from seropositive dams at birth and reared artificially
Disinfection contaminated buildings and equipment
Caseous lymphadenitis (pseudotuberculosis): control- countries with high prevalence
Strict hygenic measures in shearing sheds and disinfection regularly of docking equipment
Vaccines
Ulcerative Lymphangitis in horses
Pigeon fever, dry-land distemper
Infectious, inflammatory condition of the cutaneous lymphatic system of lower limbs and chronic abscesses in the pectoral and ventral region
Caused by nitrate-reducing biotype C. pseudotuberculosis
Swelling of chest or abdomen, fever, loss of appetite, lameness, deep subcutaneous external abscesses
One of the most common and economically important infectious diseases of horses in cali and TX with increasing prevalence in other western and mid western states of USA
Common in dry areas
Seasonal incidence: more prevalent in autumn and early winter
Stable flies, horn flies, and house flies: roll in dissemination of the organism
Bacteria enter through skin abrasions
Ulcerative Lymphangitis in horses: Tx
Long-term systemic antibiotic therapy with topical treatment
Ulcerative Lymphangitis in horses: Prevention
Isolation of infected horses, fly control and good sanitation
Contagious bovine pyelonephritis
Inflammation of urinary bladder (cystitis) that may ascend the ureters to cause infection of kidneys (pyelonephritis)
Caused by C. renale, C cystiditis, C pilosum
Reservoir: vulva and vagina of clinically normal carrier cows
Contributing factors: stress of parturition, peak lactation, high protein diet, trauma to bladder and urethra (catheterization)
Contagious bovine pyelonephritis: clinical symptoms
Fever, loss of appetite, painful urination, ammoniac odor of urine, acute abdominal pain (kicking at the abdomen), decreased rumen contractions and milk production
Murine pseudotuberculosis
Lungs: suppurative pneumonia
Kidney, liver, heart: nodular lesions
Joints: arthritic lesions of pedal extremities
Lymph nodes: lymphoid hyperplasia of regional nodes
Rhodococcus
Gram-positive bacteria occurring as cocci or rods
Aerobic soil saprophyte
Non-motile
Characteristic, mucoid salmon-pink colonies
Weakly acid-fast (envelope structure rich in mycolic acid)
Opportunistic pathogens of young foals (<6m of age)
Facultative intracellular pathogen
Survival in macrophages with granuloma formation
Main respiratory pathogen of foals under 6m of age causing suppurative bronchopneumonia. Reason for susceptibility of foals is unclear but appears to be the result of a bacterial-directed inappropriate th2- rather than th1 based immune response
Rhodococcus: virulence factors and pathogenesis
Healthy foals <3m or foals with clinical disease (poop)
Contamination of dust
Inhalation
Bronchopneumonia
Increase in dry weather
high foal density
Poor grass cover on paddocks
Large number of horses on farm
Virulence is maintained in horses (isolates from non-equine hosts usually lack virulence-associated proteins)
Particular susceptibility of foals <6m, attributed to impaired cellular immunity in lungs
Virulence factor: vapA protein
Pathogenic effect: Promote survival in non activated macrophages
Encoded by a large plasmid
Virulence factor: Capsular polysaccharides
Pathogenic effect: retard phagocytosis
Virulence factor: Mycolic acids
Pathogenic effect: retard phagocytosis
Suppurative bronchopneumonia in foals
Bronchopneumonia and lung abscession in foals, 1-4 m of age
Infection occurs mostly within the first 2 wks of life
Signs of acute disease in 1m old foals: fever, anorexia, (diarrhea), cough and dyspnoea
Mostly slowly progressive: CS often difficult to detect until pulmonary infection reaches critical mass-> decompensation of foals
Polysynovitis, intestinal and mesenteric abscesses, ulvcerative enterocolitis
Suppurative bronchopneumonia in foals: economic impact
Mortality, prolonged tx, surveillance programs for early detection, relatively expensive prophylactic strategies
Suppurative bronchopneumonia in foals: diagnosis
Thoracic auscultation and percussion: crackles and wheezes with asymmetric/regional distribution, dull resonance
Ultrasonography of the thorax: nodular long lesions
Cytological examination of respiratory secretions: neutrophilic leukocytosis
Culture of transtracheal or broncheoalveolar wash samples
Suppurative bronchopneumonia in foals: treatment
Prolonged tx (4-10 wks): combination therapy of macrolide antibiotic and rifampicin Supportive therapy including rehydration and bronchodilatory agents Survival rate is ~70-90% with appropriate therapy. The case fatality rate without therapy is ~80% Response to therapy is variable and severely affected foals may not recover
Suppurative bronchopneumonia in foals: prevention and control
Administration of hyperimmune serum from the dam to the foal in first month of life
Colostrum
Dust control
No commercial vxns available
Combo of early detection, tx, and environmental management is needed
Nocardia
Gram +, pleomorphic bacteria- long chains
Cocci or rods with characteristic long or branching filaments
Aerobes
Facultative intracellular bacterium
Non motile, non spore forming
Acid fast partial (mycolic acid in cell wall)
Ubiquitous in soil and water
usually non pathogenic for immunocompetent individuals
Pathogenic nocardia are saprophytes found in soil and decaying vegetation. Infections are often nosocomial or through skin wounds
Opportunistic, non contagious, pyogranulomatous to suppurative disease of domestic animals, wildlife, and people.
Thoracic (pneumonia, pyothorax), cutaneous (abscesses) and dissemination forms are recognized in dogs, mastitis in cattle
Canine nocardiosis: thoracic form
Fibrovascular proliferative reaction on pleura and accumulation of sanguinopurulent fluid in thoracic cavity
Peritoneal empyema
Canine nocardiosis: Cutaneous form
Ulcers or granulomatous swelling
Canine nocardiosis: Disseminated form
Non-specific clinical signs- organ system affected
Canine nocardiosis:
Mostly caused by N astroides and infection by inhalation, through skin wounds, or ingestion
Sulphur granules in exudate
Bovine Nocardial Mastitis
Chronic mastitis with multifocal fibrosis in affected glands
White clots intermittently in milk
Out-breaks associated with the use of dry cow therapy
Control is difficult but nocardial mastitis is usually sporadic
Occasionally systemic reaction with fever, depression and anorexia
Actinomyces
Gram+ club-shaped rods and filamentous branching bacteria
Facultative or strict anaerobic and capnophilic
Non spore forming and non motile
Characteristic microcolonies growing in the center of lesions, surrounded by macrophages (sulphur granules)
Outer zone of lesions has granulomatous characteristics (chronic infection)
Commensals of the oral cavity
Colonize nasopharyngeal and oral mucosae
Virulence factors are not well describes for species impt in vetmed
Part of the normal microbiota of the oral mucus membranes or tooth surfaces of mammals, including humans
Most infections are endogenous (into of a commensal organism to susceptible tissue of host)
When causing disease it is a chronic progressive, pyogranulomatous disease
Actinomyces: virulence factors and pathogensis
Pathogenesis of chronic progressive pyogranulomatous disease
Polymicrobial infection with oropharyngeal microbiota
Common in active outdoor animals (hunting dogs)
Disruption of oral mucosal barrier
Spread by direct extension to bones (lymphogenous and hematogenous spread also possible)
Chronic infection with bone lysis
Lumpy jaw in cattle
Pyogranulomatous osteomyelitis
Localized, chronic and progressive granulomatous abscess involving the mandible, the maxillae and other bony tissues of the head
Introduction of bacteria via penetrating wounds of the oral mucosa (course hay etc)
Bone infections result in facial distortion, loose teeth and dyspnea from swelling into nasal cavity
Predisposition: trauma in oral cavity
Lumpy jaw in cattle: diagosis
CS: swelling of jaw with fistulous tracts discharging purulent exudate
Microscopic examination of crushed granules from aspirates or preferably unopened lesions
Culture of purulent material (capnophilic)
Radiography can be used to determine degree of bone destruction
Lumpy jaw in cattle: tx
Susceptible to penicillin G and iodine
Long term tx (3-12 m) with high dose penicillin
If lesions are small and circumscribed -> surgery with excision of foreign bodies and lesions
Lesions are chronic, walled off microcolonies -> even prolonged antimicrobial therapy may fail
Lumpy jaw in cattle: control
Minimize risk of mechanical injury
Remove foreign bodies
Dermatophilus
Gram +, filimentous branching bact
Aerobic
Motile asexual zoospores form which filamentous hyphae germinate
Divides into two planes to give tram-track appearache and produce coccoid fragments which become motile zoospores
Zoospores germinate to produce hyphae, which penetrate into the living epidermis and subsequently spread in all directions from the initial focus -> inflammation
Normal protective skin barriers have to be educed or deficient
Dermatophilus- other characteristics
Cause severe infections of traumatized and persistently wet skin with formation of scabs and crusts
-acute infection: 2-3wk, lesions heal spontaneously
-chronic infection: cornification of invaded epithelium -> scabs -> moisture enhances proliferation and release zoospores from hyphae
Cattle sheep goats and horses less frequently pigs, dogs, cats
Worldwide but more in tropics
Can be transmitted from infected animals to humans through skin contact- rare tho
Factors such as high humifity, temp, and carious ectoparasites that reduce barrier of skin influence incidence, seasonal prevalence and transmission
Epidermal abscesses with hyperkeratosis and scab formation
Spread by direct or indirect through arthropod contact
Obligate pathogenic skin bacterium
Dermatophilus
Exudative epidermitis with scab formation
1. filaments colonize hair follicles and penetrate skin layers
2. Inflammatory cell layer is formed under infected epidermis and keratinizes-> scab and crust formation
3. accumulations of cutaneous keratinized material forming wart-like lesions and hair matted together
Some parts of the world: sig morbidity and mortality, loss of body condition, decreased milk production and increases somatic cell counts in milk
Dermatophilus: diagnosis
Clinical appearance of lesions
Detection of D. congolensis in stained smears or histologic sections from scabs
Cytological examination of fresh crusts stains with Giemsa stain
Dermatophilus: Tx
Parenterally administered antibiotics
Topical treatments are less effective but may include 0.5% chlorohexidine and 4% iodine tincture
Dermatophilus: control
Isolate and treat clinically affected animals
Provide shelter during prolonged rainfall periods
Clear grazing areas of thorny scrub
Reduce tick infestation
Prophylactic use of long-acting tetracyclines in endemic regions
Control of intercurrent diseases
Resistance through modification of skin microbiota
Trueperella
Gram+ pleomorphic
Facultative anerobic and capnophilic
Non motile, non spore forming and non capsulated
Found on mucosal membranes of GI tract, resp and urogenital tract of cattle and swine- survives in environment
Opportunistic pathogens of cattle (and sheep and swine)
Suppurative infections
Disease prevalence is sporadic and governed by precipitating stress or trauma
Pyolysin: haemolytic toxin, cytotoxic for neutrophiles and macrophages, dermatonecrotic and lethal for lab animals
Important opportunistic path of cattle. causing multiple purulent infections (often chronic) with a tendancy to cause bacteremia
Pathogenic synergy with Fusobacterium necrophorum
Truperella pyogenes
Clinical infections: purulent wounds Abscesses mastitis endocarditis arthritis abortion metritis Navel infection footrot, foot wounds chronic pneumonia
Summer mastitis
Mastitis of non-lactating cows and heifers during summer months
Synergistic action of Trueperella pyogenes, Peptostreptococcus indolicu and Streptococcus dysgalactiae
Transmission of infection by head fly
Affected quarter is swollen, hard, painful, hot, grossly enlarged teat
Udder secretion thick and clotted like grains of rice
Yellow/green pus
Truperella infections: diagnosis
Smear and gram stain of purulent material
Necropsy and isolation of bacteria
Truperella infections: Tx
Penicillin G
Reports of resistance
Truperella infections: Prevention
Prevent primary cause
No efficient vxn
Actinobaculum
Actinobaculum suis Gram+ rods Anaerobes Non motile, no spore forming Commensal organism in preputial diverticulum of boars NOT in urogenital tract of healthy sows Transmitted at coitus Porcine cystitis and pyelonephritis 3-4 wks post coitusL anorexia, arching of back, dysuria, haematuria Potentially fatal due to renal failure
