Short Note on Bacteriology & Mycology (1).pdf

Bacteria Characteristics Disease Processes Staphylococcus - Bi ocontainment l evel 2 (in general) - Gram positive cocci cl usters - Whi te/creamy on blood agar - Found on skin, mucous membranes, phar...

Bacteria Characteristics Disease Processes Staphylococcus - Bi ocontainment l evel 2 (in general) - Gram positive cocci cl usters - Whi te/creamy on blood agar - Found on skin, mucous membranes, pharynx, GIT. Lecture 6 - Ca ta l ase + (bubble when H2O2 a dded) - Suceptibility testing is a MUST Virulence Factors:  toxi c-s hock syndrome toxin  enterotoxins (food poisoning)  exfol iatins (skin irritants)  va ri ous l eucocidins S. a ureus - Pi nk on CHROMa gar Ruminants/pigs/horses – MASTITIS Bovine Mastitis - Yel l ow on Ma nnitol salt a gar  Conta gious (ma nnitol fermenter)  Udder i s reservoir  Adheres to a nd invades ma mmary epithelial cells - Coa gulase +  Pera cute (ra pidly progressing) or s ubclinical ( milk production)  Trea tment: improve hygiene, i ntra-mammary a ntibiotics - -hemolysis (2-zones)  Col l ect milk sample (cl ean teat) - produces toxic-shock Poultry – BUMBLEFOOT s yndrome toxin, enterotoxins,  common colonizer of poultry, but opportunistic when host defenses breached. exfol iatins, va rious l eucocidins Bumblefoot  ba cteria infect bones, tendon sheaths, a nd joints - Resistant to polymyxins and  s wollen joints, reluctance to s tand, gangrenous dermatitis of feet ALL  -lactam drugs  Col l ect joint/stab swabs (methlicillins and penicillin Septic Arthritis resistant)  purul ent material in joints Trea tment: improve management practices,  s tress/injury, base treatment on s us ceptibility testing. Dogs/cats – opportunistic and skin/ear infections MRSA ST398 (pi gs/cattle) MRSA ST5 (hors es) S. ps eudintermedius - Whi te/grey on blood a gar Dogs/cats – opportunistic and skin infections - Coa gulase +  col onizes 90% of dogs - -hemolysis (2-zones)  s ki n/ear infections - col onizes pharynx  2nd mos t common cause of UTIs  necroti zing fasciitis, nosocomial infections (surgical site, orthopedic i mplants).  often s econdary i nfections to underlying disease (opportunistic) Trea tment: address the primary ca use of the disease. S. epi dermidis - Pi nk on ma nnitol salt agar (not a ma nnitol fermenter) - coa gulase negative - hemolysis (non-hemolyti c) S. hyi cus - hemolysis (non-hemolyti c) Pigs – GREASY PIG DISEASE (exudative epidermidis)  a ffects suckling and newly weaned piglets  hi gh mortality  s poradic occurrence  cl i nical disease following damage to skin (fighting, unclipped teeth, rough bedding) Bacteria Characteristics Disease Process Streptococcus - Bi ocontainment l evel 2 (in general) - Gram positive cocci cha ins - Fa s tidious (require blood/serum in media to grow) - Ca ta l ase negative Lecture 7 - Col onizes mucous membranes and intestinal tra ct - s end samples i n tra nsport media (susceptible to desiccation) - Tx s hould be guided by s usceptibility testing Virulence Factors:  Exotoxi ns (superantigen – S.pyogenes)  Pha ge mediated s uperantigen (s. ca nis)  Ca ps ule (prevents phagocytosis)  Hemolysins (cytotoxic to eukaryotes)  CAMP fa ctor (cytotoxic) S. a ga lactiae - -hemolysis Bovine chronic mastitis (2-zones)  Conta gious mastitis  Res ervoir is i nfected cows (usually s ubclinical)  Ca us ed by poor biosecurity/hygiene Trea tment: improve management/cleanliness, i ntramammary penicillin S. dys ga lactiae - -hemolysis Bovine acute mastitis (1-zone)  Envi ronmental mastitis (contamination of teats)  Often s ubclinical Trea tment: improve management/cleanliness, teat sealer, intramammary a ntibiotics S. equi - -hemolysis S. equi equi – Horses - STRANGLES (pharyngeal abscesses in lymphnode) (2-zones)  Norma l resident of upper respiratory tra ct.  Abs cess of s ubmandibular/retropharyngeal lymphnodes - zoonotic  Hi ghly contagious (high morbidity, l ow mortality) (zooepidemicus)  Tra ns mission by contact w/ discharge from lymphnode/nose/contaminate fomites.  Longterm sequelae possible – metastatic a bscesses (Bastard s trangles), purpura hemorrhagica (vasculitis s econdary to deposition of immune complexes), guttural pouch empyema  75% of hors es will be immune to future i nfections, protection tra nsfers to foals Trea tment: penicillin S. equi zooepidemicus  Hors es (joint infections)  Ca ttl e (mastitis)  Pi gs /Poultry (septicemia)  Ca ts /Dogs (respiratory i nfections)  Huma n (from dogs/horses, drinking unpasteurized milk) S. ca ni s -hemolysis Cats/Dogs – Septicemia, wound infections, abscesses, respiratory infections. (2-zones)  Infection a t any particular anatomical site  Ki ttens (skin/soft tissue i nfections, abscesses, respiratory i nfections) - zoonotic  Dogs (opportunistic – wounds, urinary, mammary)  Severe cases: necrotizing fasciitis and toxic shock syndrome – ca used by phage antigens expressed due to fluroquinolone exposure Trea tment: penicillin DO NOT treat w/ fluroquinolones (sulfonamides) – ca us es expression of Phage superantigens  cytoki ne & s ensitizing host to G- endotoxin  ca pillary l eakage, hypotension, s hock, coagulation a nd complement activa tion  DIC  death S. s ui s - -hemolysis Pigs – MENINGITIS, arthritis, septicemia, sudden death (1-zone)  As s ociated w tra nsport/overcrowding/poor ventilation  Pi gl ets a cquire from sow/environment at ti me of farrowing - zoonotic  Enters body vi a tonsils. Humans – meningitis, HEARING LOSS, sepsis (HUGE RISK TO HUMANS)  Infected with serotype 2  Enters vi a cuts/scratches – pig handling S. pyogenes Humans – strep throat, necrotizing fasciitis Enterococcus - bl ue/grey colonies Cattle – Chronic mastitis spp. on bl ood a gar - not s usceptible to Chickens – mortality in chicks des iccation  Feca l egg contamination - col onizes i ntestinal  Acute (s epticemia, depression, dead birds) tra ct  Chroni c (depression, pyrexia, loss of condition) - di fferentiate from Trea tment: prevent stress, antibiotics based on s usceptibility testing, i mprove hygiene. s trep by a bility to grow i n Na Cl Dogs/Cats – nosocomial infections. - intrinsically  Sys temic: bacteremia, endocarditis resistant to  Loca l ized: abdominal cavity, genitourinary tra ct, resp tra ct. cephalosporins  Di a rrhea (E. hirae) - Trea tment should be gui ded by s us ceptibility testing Bacteria Characteristics Disease Process Corynebacterium - Bi ocontainment l evel 2 - Gram positive cl ub s haped rods (Chinese l etters) (in general) - s urvi ve i n environment - col onize skin, mm, i ntestinal tract normally Lecture 8 - oxi da tive fermentative Dogs/Cats – Skin and urinary tract infections  Ski n – C. a uriscanis (polymicrobial infections)  UTI – C. urea lyticum (ra re) All are intrinsically resistant to fosfomycin C. rena le - CAMP tes t + Cattle – cystitis (bladder infection), pyelonephritis (kidney infection) C. pi l osum - l ow zoonotic risk  UTI C. cys ti ti dis  Cys ti ti s (hematuria/proteinuria s een, not generally ‘s ick’) Sa mple Collection:  Pyel onephritis (fever, depression, reduced feed i ntake) mi d-stream urine  Ma i ntained i n subclinical ca rries and diseased animals (difficult to eradicate)  Tra ns mission by s plashing urine droplets onto vulva of susceptible cow Virulence factors: Tx: penicillin, urinary a cidification (inhibits attachment a nd i nvasion) - Pi l l i – a ttachment - Urea s e – produces Sheep – PIZZLE ROT (inflammation of penis/prepuce) a mmonia  ma kes  Ca us ed by di ets too high i n protein  urea i ncrease in urine  conversion to uri ne more a lkaline a mmonia  i rritation  i nflammation/ulceration  bacteria enter ti ssue  scarring fa ci litates a ttachment  prevents breeding/extrusion. Tx: remove dead tissue/wool, use antimicrobials (penicillin), no breeding. Pigs – kidney abscesses C. ps eudotuberculosis - CAMP tes t negative Goats/sheep – CASEOUS LYMPHADENITIS  Pyogra nulomatous abscess of lymphnodes/internal organs Sa mple Collection:  Conta i ns dried out/cheesy material pus or exudates  Hi ghly contagious, persists i n environment (difficult to eradicate)  Not ea sily treatable (antimicrobials do not penetrate abscesses well) Virulence factor: - Phos pholipase D – Cattle - mastitis neutrophil i nhibitor, Zoonotic: causes abscesses in humans, risk higher with sheep/goat handling. i na ctivates compl ement Di a gnosis: ELISA immunological tests Tx: a nti microbials ca nt access intracellular organisms , control depends on prevalence. C. di ptheriae Virulence factor: Humans – diphtheria - Di phtheria toxin   Infections often tra vel related i nhibits protein  Res piratory (pharyngeal) form most common (pseudomembrane of orga nisms, fibrin, s ynthesis a nd i nflammatory cells forms over pharynx)  Cuta neous form also common Preventi on: DPT va cci ne (diphtheria, pertussis, tetanus). Rhodococcus - Gra m + cocco-ba cilli (in general) - Non-oxi dative fermentative - Generally, like to grow i n l ower temperatures 1 yr in soil)   Clinical signs: might not be seen 2-5 years from initial infection, slow progressive emaciation, weakness/debilitation, increasingly severe diarrhea. Chronic granulomatous enteritis. Diagnosis: 1. Culture MAP from fecal/tissue/environmental sample – look for acid-fast bacteria 2. Molecular methods (PCR) 3. Antibody-based test (look for MAP antibodies). Control: separate young from infected animals/MAP contaminated feces, test/cull program, disinfection. Listeria – Lecture 11 Characteristics  biocontainment level 2  short gram positive rods  facultative anaerobes, growth enhanced with CO2.  small colonies on blood agar -  hemolytic  grows under wide range of conditions o T = 3-45 degrees Celsius  can easily grow in your fridge. o pH = 5.6-9.6  L. monocytogenes is a facultative intracellular parasite and displays tumbling motility in broth. Virulence Factors:  Internalin A (attachment to host cells)  Listerolysin O (lysis of phagosome, allows bacteria to escape into cytoplasm)  Phospholipase C (involved in organism spreading from cell to cell)  Actin polymerizing protein (highjacks host cell actin push organisms into adjacent cells) Sample Collection  Septicemic form – viscera sample  CNS form – CSF, brain stem  Abortions – placenta/fetus  Silage – aseptically collect 100 g in sterile container  Culture ASAP or store at -20 C to prevent growth of contaminants. Zoonosis - pregnant women should avoid contact with ruminants at lambing/kidding Treatment  Ruminants – high dose penicillin  Cats/Dogs – ampicillin + gentamicin  AVOID – cephalosporins and fluroquinolones Control – identify source of infection, remove poor quality silage from feeding. Listeria monocytogenes – ruminants, humans, birds Ruminants – Encephalitis, abortion  common in the environment - feces/plant material, in feed to be ensiled, silage not acidic enough (should be less then pH 5)  cattle ingest contaminated feed  organism enters via compromised mucosal barriers  migrates via trigeminal nerve to the brain  acute meningoencephalitis, microabscesses, Circling Disease  Predilection for uterus and fetal tissues of ruminants (biohazardous) Humans – septicemia, abortion, gastroenteritis, (endopthalmitis – inflammation in anterior chamber of eye - rarely)  Food borne pathogen  uncooked meat/vegetables, raw dairy products, processed foods – ready to eat meats  Risk Factor o Pregnant women – 10x more likely o Older adults and immunocompromised individuals  Syndromes o No clinical signs – transient carrier in GIT o Acute Illness  While pregnant – flu like symptoms. Mother recovers following birth, fetal survival depends on gestational age (newborns can be severely ill) o Non-pregnant adults  Sepsis, meningoencephalitis, abscesses at variety of sites. Birds – septicemia  Sporadic in poultry/waterfowl   Young birds most susceptible  Septicemic form – emaciation and diarrhea  Encephalitic form – depression, ataxia, neuro signs  Common in cold/wet conditions  Should try to identify the source of listeria Dogs/Cats  Uncommon in these species – need >1 billion organisms to cause infection  Similar pathogenesis as people  infection via ingestion of contaminated food, gastrointestinal or neuro/systemic.  GIT disease characterized by fever and V/D  If systemic spread, localization in placenta/CNS Listeria ivanovii Ruminants – abortion  Occurs 2-3 weeks after ingestion of contaminated feed Erysipelothrix – Lecture 12 Characteristics  Biocontainment level 2  Non-spore forming gram-positive rods  Facultative anaerobe  Grows better with 5-10% CO2 White creamy colonies on blood agar -  and  hemolytic  Catalase negative  On agar there are 2 colony forms: o Smooth colonies  slender chains of rods (no-branching) o Rough colonies  irregular cell morphology  Found in many species  Shed in feces o In pigs, healthy carriers may be the primary source of infection  Persistent in the environment, found in soils Virulence Factors  Capsule – layer of polysaccharides o Resistant to phagocytosis – allows survival of oxidative burst within macrophages  Neuraminidase o Promotes attachment, aids in invasion of tissues  SpaA protein o Encourages cell-mediated immunity in the host o Antibodies directed towards this surface protein are protective. Sample Collection  On necropsy – liver, spleen, kidney, heart, long bones  Hard to recover organisms from skin lesions  Blood cultures – for dogs with suspected vegetative valvular endocarditis – also hard to culture  DO NOT FREEZE samples Diagnosis  Blood agar  Selective media – sodium azide, crystal violet  MALDI-TOF for pure cultures Zoonosis  E. rhusiopathiae  occupational hazard – fish handler’s disease, butchers/slaughter house workers. Treatment  Penicillin  Avoid – sulfonamides, aminoglycosides, glycopeptides (vancomycins). Erysipelothrix rhusiopathiae Pigs – eryspieles (diamond skin disease)  Maintained in population by healthy carries that shed pathogen in feces Di a mond Skin Disease –  Affects pigs >3 months old – waning maternal immunity thrombosis i n terminal ca pi llary beds  congestion  Exposure via mouth – food/water  redness.  Enters body via palatine tonsils then systemic spread  Syndromes: o Acute – sudden onset, pyrexia, sudden death, depression, inappetance, diamond skin lesions 2-3 days after exposure. o Subacute – less severe than acute o Chronic – long term sequelae following acute disease, arthritis, stiffness, possibly cardiac insufficiency if serious damage to heart valves. Poultry (turkeys) – sepsis, endocarditis   Likely oral route of infection  Onset of disease is peracute-acute o Begins with death of several birds, others are “droopy” o Toms have congested purple snoods o Death peracute often due to endocarditis, lesions may be absent. o Mortality = 1-50% Wild ungulates – die-offs  Recovered from long bones of dead animals  New phenomenon – first encounter with naïve population? Secondary to stress due to warming temperatures?  Die offs in northern muskox and caribou in Canada Humans – erysipeloid, systemic infections, endocarditis  Occupational exposure  Erysipeloid (mild form) – skin lesions typically on fingers 2-7 days after exposure  Systemic (severe) – L-side endocarditis, high mortality rate, typically in debilitated patient Erysipelothrix tonsillarum Dogs – endocarditis  Clinical signs – fever, recent onset murmur  Treat with high doses of penicillin Pigs – non-pathogenic Eryspielothrix spp Ornamental fish – sepsis and necrosis  Recent cause of mortality in fish in USA  Clinical signs – lethargy, hovering in water, hemorrhage of fins/skin Bacillus – Lecture 13 Characteristics  Large, spore-forming, gram-positive rods  Aerobic, facultative anaerobe  Large, irregular mucoid colonies  Found in water and soil, spores survive for decades – highly resistant to everything. Sample Collection – milk, tissues from aborted fetuses. Do not freeze samples. Lab Diagnosis  B. anthracis - look for encapsulated organisms from tissues under mic roscope, culture on blood agar (non- hemolytic colonies)  Non-anthracis spp – culture on agar Control  Remove 20 cm of top soil  Disinfect soil/equipment  Burn/bury contaminated carcasses  Destroy spores in environment – do not perform necropsies  PPE critical Bacillus cereus  Biocontainment level 2  -hemolytic on blood agar  Food born pathogen  Exotoxins cause gastroenteritis (acute V/D)  Use motility test and MALDI-TOF to identify to the species level. Humans – gastroenteritis  Acute, self limiting  Emetic form – ingestion of cereulide toxin o C/S 1-6 hours after ingestion o Associated with rice, cream, milk products, pasta, infant formula  Long incubation food poisoning – ingestion of hemolysins o Watery diarrhea, nausea, straining to defecate o Association with meat, veggies, cake sauces, dairy  Some strains grow at low temperatures = 4-7 C Bacillus subtilis  Biocontainment level 1  Largely non-pathogenic - opportunistic pathogen Cattle – mastitis Sheep – abortion Bacillus anthracis  Biocontainment level 3  Grey, non-hemolytic colonies on blood agar  “medusa head” morphology on gram stain - long stringy chains of rods  carnivores are most resistant to these infections – they are adapted to be able to eat dead animals. Cattle/sheep/goats – herbivores are most susceptible.  If you suspect anthrax - DO NOT PERFORM NECROPSY & call CFIA (don’t expose bacteria to air because they sporulate and become very hard to get rid of).  Sample collection – collect blood from the ear, respiratory protection essential in a dusty environment  Treatment – high doses of penicilins/tetracyclines, vaccination, antimicrobial prophylaxis, control the area, dispose carcasses properly, prevent additional environmental contamination. Virulence Factors   Protective antigen – forms heptameric pores in cell wall  Edema toxin and lethal toxin o Lethal toxin – affects macrophages, stimulates apoptosis o Edematoxin – stimulates increased cAMP in the cell, affects water homeostasis  Genes encoding these toxins on pXO1 plasmid.  Virulent strains also encapsulated – genes for this found on pXO2 plasmid. Cattle and Sheep – Sepsis  Ingestion of endospores  Seen with drought followed by heavy rainfall  Peracute disease - sudden death – failure to clot, incomplete rigor mortis, splenomegaly Horses – Sepsis, colitis  Colic, diarrhea, fever, depression  Localized cutaneous lesions  Dependent edema – ventral parts of the body (prepuce, brisket, belly)  Fatal septicemia Humans – 4 forms 1. Cutaneous – most common  Direct contact with infected tissues  Lesion develops 2-5 days after exposure  Mortality = 10-20% if untreated 2. Pulmonary – fatal  Inhalation of endospores  Phagocytosis in lungs, lethal toxin kills macrophages, get massive inflammatory reaction  Hemorrhagic necrosis of mediastinum  Incubation period = 1-3 days  Mortality rate = 80-90% if untreated 3. Oropharyngeal – ingestion  Cervical and oral pain and edema  Sepsis and death if untreated 4. Gastrointestinal – when bacteria move distal in GIT  2-7 days incubation  Fever, nausea, bloody vomiting  Sepsis and death if untreated Bacillus thuringiensis – insect pathogen  Crystal toxins – disruption of gut, digestion of crystal liberates toxin, used as larvacide in mosquito control  Resistant to penicillin Non-Spore Forming Anaerobes – Lecture 14 Common Characteristics  Gram negative  Obligate anaerobe  Involved in necrotic and suppurative conditions – stinky  Often polymicrobial  Hard to culture  Opportunistic pathogens  Problematic – on entry into normally sterile sites or when tissue becomes ischemic.  Sample Collection - anaerobic culturette – sterile swab with an oxygen scavenging sachet Lab Dx  Smears of affected tissue  Anaerobic culture – blood agar with special supplements, media pre-reduced (exposed to anaerobic env)  PCR  Antimicrobial susceptibility testing of anaerobes is poorly standardized. Zoonosis – none known Tx/Control  Depends on site of infection rather than the exact species ID o Foot rot – systemic antimicrobials & topical anesthetic  Management practices important o Dietary management – prevent rumen acidosis o Paddock/pasture management – keep feed dry/clean **3 below classes – fuso, dichelo, prevo bacteria all are synergistic. Fuso creates tissue damage that facilitates invasion by the other bacteria. Dichelo and prevo produce growth factors for fuso. Fusobacterium necrophorum  Long stippled slender gram negative rods  Lives in GIT  Common in liver abscesses  Normal members of respiratory tract, GIT and genitourinary systems in people.  Susceptible to penicillin Virulence Factor  Leukotoxin – lysis of bovine leukocytes and toxic for hepatocytes Cattle – calf diphtheria (necrotic laryngitis), liver abscesses  Often associated with Truperella pyogenes  Necrotic foci on larynx, trachea, buccal cavity  Abrasions of pharynx due to rough feed  Fever, depression, excessive salivation  Foul smell  Procession to fatal pneumonia if untreated  Liver abscesses in feedlot cattle – septic embolism following rumenitis Sheep – foot abscesses Dichelobacter nodosus  Straight or slightly curved short rods  Swellings at both ends = “bar bells”  Primary resident of ruminant foot Virulence Factor  Type IV fimbriae – motility and adherence  Serine proteases – degradation of hoof proteins, allows bacteria to get in and cause foot fot. Sheep – contagious foot rot   Lameness  Doesn’t readily survive in environment  Primary reservoir is infected sheep  Associated with warm wet conditions – transmission via transiently contaminated environments (trucks) Goats, cattle, pigs – interdigital infections Prevotella melaninogenica  Short Coccobacilli  Rounded ends  Resident of the mouth of variety of species including people Cattle – interdigital necrobacillosis Capnocytophago canimorsus – Humans  Gram negative rods  Found in mouths of up to 74% of healthy dogs  Infections occur in people bitten by dogs/cats o More common in older/immunocompromised individuals, alcoholics (hepatic cirrhosis), splenectomised people. o No known risk factor  Mortality up to 30%  due to meningitis, endocarditis, sepsis  Other clinical signs – necrosis, cyanosis, skin sloughing  When bacteria is phagocytized it continues to replicate and kills host cell causing a massive inflammatory reaction.  Tx – vancomycin, clindamycin – penicillin.  Avoid sulfonamides and aminoglycosides Clostridium – Lecture 15 Characteristics  Biocontainment level 2, or 3 when it aerosolizes.   Spore forming gram positive rod  Anaerobes – variably tolerant of O2  Wide distribution, found in the environment (water, soil).  Spores germinate in anaerobic environment  Part of normal microbiota, found in feces. Clostridium perfringens  Boxcar morphology  2 zones of hemolysis on blood agar  Positive litmus milk test  Part of normal intestinal microbiota  Many toxins: o Enterotoxin – pore forming toxin o A-toxin – attacks cell membranes results in necrosis o B – toxin – pore forming toxin, lethal and necrotizing – binds endothelial cells o I-toxin – pro-toxin, activated by proteolytic enzymes, cytotoxic  Sample collection/Lab diagnostics: o Culture feces (diarrhea), renal tissue (pulpy kidney disease) o Gram stain for box car cells o Identify toxin via PCR o Tissues for histopath Pulpy Kidney Disease – type D “over eating disease"  From gorging on grain/lush pasture  High starch content stimulates overgrowth  Excess -toxin production leads to toxemia  Acute disease – in healthy lambs, you often find them dead  Autolysis – pulpy soft renal cortex  Control – managing diet Lamb Dysentery – caused by type B  high morbidity/mortality – may have sudden death, predisposed by abrupt change in diet Hemorrhagic enteritis in piglets – type C  high mortality – outbreaks of entire litters, acute onset and death within 24 hours Necrotic enteritis in chickens – type A  acute enterotoxemia, sudden death, necrosis of small intestine. Dogs – type A  netF (pore forming toxin), hemorrhagic gastroenteritis, acute, often fatal disease Horses – type A  net F (pore forming toxin) enterocolitis in young foals Humans – food/water borne, causes necrotizing intestinal disease “fire bowels”  Associated with trypsin inhibitors (prevents toxin degradation)  Associated with contaminated meat products Clostridium tetani  drumstick morphology due to terminal spores Many species – Tetanus (spasms)  soil is natural habitat  organisms enter body via breach in skin  organisms multiply in necrotic tissue  production of toxins o tetanolysins – enhances tissue invasion o tetanospasmin – neurotoxin which causes spasms of both flexor and extensor muscles.  Clinical Signs o Muscle spasms/stiffness o Opisthotonus o Lock jaw – sardonic smile   Tx: high dose penicillin + tetanus anti-toxin  Sample collection/Lab Diagnostics: o Gram stain to see drumstick organisms Clostridium botulinum - Many species – botulism (flaccid)  Soils/aquatic environments  Spores extremely resistant – survive boiling (beware during home canning)  Exposure via ingestion  Botulism toxin – prevents release of ACh at NMJ  flaccid paralysis o 7 toxin types  source varied o forage botulism – spoiled feed becomes anaerobic and supports type B o carrion – animals that die have toxin that contaminate feed o waterfowl – type C  Tx: antibiotics, antitoxin, supportive therapy, vaccination possible (horses)  Sample collection/Lab diagnostics: o Toxicity studies, inject mice with serum/filtrate of rumen contents Humans  5 forms: 1. Food-borne – eating food containing toxin 2. Wound botulism – infection at wound, most common in IV drug users 3. Infant botulism – like shaker foals, C. botulinum replicates in gut and releases toxin (don’t feed babies honey) 4. Adult intestinal toxemia – colonization of the gut 5. Iatrogenic botulism – from people that get too much botox or injection into vein. Clostridium chauvoei – Cattle, sheep – Blackleg  Organism in environment/feces  Ingested endospores usually just pass through the body, occasionally getting lodged into the tissues (hindquarters, cardiac muscle).  Disease occurs when the spore germinates, not sure of the inciting factor – perhaps injury, resulting in a locally anaerobic environment?  Clinical Signs o Usually find a dead cow with affected limb up, often bloated. o Acute febrile disease – lameness, sudden death, necrotizing myositis & systemic toxemia  Necropsy – crepitation due to gas production, muscle dark red/black and rancid  Tx: not practical/possible, try penicillin, surgical debridement of affected tissues  Control – vaccination  Sample collection/Lab diagnostics: o Collect large chunk of tissue (maintain the anaerobic centre) o Histology o Fluorescent antibody test Clostridium septicum Cattle, sheep, pigs – malignant edema  Affects all ages  Organisms from soil, infection via deep puncture + trauma  Outbreaks occur following group procedures  Acute fatal toxemia – produces necrotoxins that cause edema and gangrene  Lesion at site of infection, edema at other body sites  Tx: high dose penicillin systemically and injected locally at the lesion, antitoxin  Control – hygiene during invasive procedures, vaccination  Sample collection/Lab diagnostics: o Collect large chunk of tissue (maintain the anaerobic centre) and do histology Clostridium novyi type B – Sheep (&cattle)– black disease  In environment, fecal contamination of pasture important for transmission   Acute necrotic hepatitis – animals usually found dead  Occurs in well-nourished adult sheep  Spores reach the liver via the blood, germinate with necrotic insult and release alpha toxin  Often associated with liver flukes trauma to the liver  Tx: none  Control – vaccination, control possible inciting cause (liver flukes)  Sample collection/Lab diagnostics: o Collect large chunk of tissue (maintain the anaerobic centre) and do histology Clostridium difficile Many species – “CDAD” – antimicrobial associated diarrhea Humans  Debilitating disease – treatment can be challenging and unrewarding  Tx: vancomycin, metronidazole, fecal transplants  Sample collection/Lab diagnostics: o Culture feces o Identify toxin by PCR  Zoonotic acquisition from pigs Enterobacteriaceae – Lecture 16 & 17 Characteristics  Gram negative rods  Biocontainment level 1-3  Commonly divided based on lactose fermenting ability  On blood agar colonies are typically grey  Widely disseminated – in environment, intestinal and respiratory tracts Escherichia coli  On blood agar is pleomorphic, non-hemolytic mucoid colonies  Pink colour reflects acid production from lactose fermentation  Positive indole test 2 Classes: 1. ETEC – Enterotoxigenic E. coli  Causes neonatal colibacillosis in ruminants/pigs  Species specific pathogenicity  related to presence of receptors for bacterial fimbriae in the intestine (pigs have receptors for F4, calves for F5)  Associated with weanling diarrhea and travelers diarrhea in people  Toxins: o LT – similar to heat labile toxin in V. cholera  increase cAMP levels, increases fluid and electrolyte excretion  diarrhea o ST – interferes with enteric nervous system Attaching and Effacing Ecoli  Eae is a key virulence factor – allows bacteria to attach  Produce characteristic mucosal lesion  Bacteria adhere to enterocytes, and may even colonize them intracellularly Enterohemorrhagic Ecoli  Shiga toxin (stx) – interferes with protein synthesis, causes edema and hemorrhage  May also have eae  O157:H7 = 157th somatic O antigen and 7th flagellar H antigen  Hemorrhagic colitis, hemolytic uremic syndrome (hemolytic anemia, kidney failure + thrombocytopenia)  Fluoroquinolones & TMS may increase toxin expression Piglet Diarrhea  Treat with antimicrobials based on antimicrobial susceptibility testing, fluid therapy  Keep barn clean, and free of pathogens in environment  Keep piglets warm and dry 2. ExPEC – Extraintestinal pathogenic E. coli - causes UTIs, sepsis, mastitis, endometrial pathogenesis Septicemic Ecoli  Wide variety of virulence factors: o Fimbriae – adherence and avoidance of phagocytosis o Capsule – prevents phagocytosis o Aerobactin – iron scavenging o Endotoxin – component of gram negative cell wall (LPS) o Colicin V – serum resistance, avoids complement membrane attack Uropathogenic Ecoli  #1 cause of UTI in people and companion animals  infections opportunistic, ascending from the urethra  Virulence Factors o Fimbriae – protects from phagocytosis o Flagella – swimming up to kidneys from bladder o Siderophores – acquisition of iron o Alpha hemolysin – pore forming  Intracellular infections UTIs – Dogs  Affects 14% of dogs – common in spayed females, less common in cats than dogs  Classified by anatomical site o Lower UTI = bladder + urethra o Upper UTI = ureter and kidney – need more powerful drugs   Complexity o Simple – first time, no underlying abnormality identified o Complicated – repeat infection, associated with underlying condition  Tx - must be based on susceptibility testing and culture o Therapy depends on complexity and anatomical site, need to address underlying disease  Management – get a diagnosis, addressing underlying disease Coliform Mastitis – Cattle  Common even in well managed herds  Shed in feces and then enters teat via environment  Presentation varies from mild to severe  Some cows respond to invasion early and clear infection naturally  Bacteria multiply in the teat, endotoxin released from dead cells  cytokine storm  systemic inflammation  30-40% of cows become bacteremic  Treatment – systemic and intramammary antibiotics (cephalosporins)  Management – remove organic bedding that supports Ecoli growth. Colibacillosis – Poultry - #1 infections seen in chickens  Causes many syndromes: o Omphalitis  Dead embryos, swelling and edema of navel, distended abdomen, mushy chick disease (body wall over yolk sac degenerates)  Tx – antimicrobials  Management – keep things clean, discard floor eggs/exploders, disinfect eggs, vaccination o colisepticemia, swollen head syndrome, air sacculitis  Ecoli can make their way into the egg  Found in the environment from hen feces and exploding eggs. Lab Diagnostics for Ecoli  Diarrhea – fresh feces, colonic tissue for histopath  Mastitis – milk sample  Omphalitis – samples taken from dead chicks  UTIs – aseptically collected urine (cystocentesis)  DO NOT FREEZE samples Ecoli Zoonosis  Foodborne illness – enterohemorrhagic, possible source of antimicrobial resistance  Animal  human  animal  human  Standard precautions – handwashing, PPE Ecoli Treatment Options  Guided by susceptibility testing  Intrinsically resistant to: o Benzylpenicillin, Glycopeptides, Macrolides (azithromycin is exception), Linosamides, Rifampin Klebsiella pneumoniae  Mucoid appears on blood again  Is a lactose fermenter  Differentiated from E.coli by a positive urase and citrate test. Proteus mirabilis  Swarm over the entire plate, stink.  Not a lactose fermenter  Can produce H2S and black colonies on XLT4 agar Salmonella  There are 3 species S. bongori, S. enterica, S. subterranean   S. enterica has 6 subspecies  There are serovars – grouped on presence of surface antigens o O-antigen – based on oligosaccharide associated with LPS o H-antigen – based on flagellar proteins  Normal members of intestinal tract of many animals  Virulence Factors o Salmonella pathogenicity islands – gene clusters of virulence genes  Type 3 Secretion Systems o Detects cells, acts as needle/syringe to inject effector molecule, involved with invasion  Fimbriae o Adherence and colonization Salmonella Dublin – Cattle  Adapted to cattle  Causes severe disease in endemic herds o Septicemia in calves 6 months  Doesn’t spread from individual to individual, usually environmentally or laboratory required  Emerging problem in people in Sub Saharan Africa Crytococcus gattii – Humans/Koala   Found on trees (eucalyptus)  Common along West Coast  Respiratory infections Malassezia  Bottle shaped cells  First isolated from Indian Rhino with exfoliative dermatitis  Sample collection – cytological examination of exudates, tape strip methods, biopsies Malassezia pachydermatitis  Found on skin of mammals and birds  Localized to anatomical sites with lots of sebaceous glands (ear, skin fold dermatitis, between toes)  Lab Diagnosis – microscopy, culture  Not a common human pathogen at all (may cause dandruff) Dogs – Otitis and dermatitis  Superficial infections in warm moist anatomic sites (ear canal, groin, skin folds)  See erythema (reddening), greasy exudate, malodorous exudate  With extensive lesions – lichenification, hyperpigmentation, seborrhea  Seen more commonly in warmer months  Treatment – topical therapy very important, o Pyoderma – 2% miconazole, 2% chlorhexidine o Azole containing shampoos (nizarol) o Burrows solution – changes ear environment, acidifies, dries and makes it an inhospitable environment. Doesn’t select for resistance – not an antibiotic  ID and control underlying disease (atopy, food allergy, endocrinopathy). Lecture 33 – Dimorphic Fungi  2 forms: mycelial (25-30C), Yeast (37C)  Environmental organisms  B. dermatitidis, C. immitis, H. capsulatum are biocontainment level 3 when in mycelial form, biocontainment level 2 when not in yeast form. o Sample Collection = urine for antigen test – very sensitive, very specific – takes a while to get back.  Body, Heat, Changes, Shape Blastomyces dematitidis  Can see large round oval cells and budding organisms  Found in acidic soil, particularly soil near water  Cases often associated with excavation or construction  Found in Saskatchewan and east, NOT in Western Canada  Pathogenesis: spores grow in dirt, inhaled, develop in lungs as yeast phase, move to other body sites  Dogs, Cats, Humans – respiratory infections, opportunistic infections in other body sites (bones)  Sample Collection:  o Urine for antigen test o Fluid from draining lesions o Lymphnode aspirate o Transtracheal wash or bronchio-alveolar lavage Dogs  Low grade signs for days – months  Anorexia, weight loss, cough, dyspnea, ocular disease, lameness, skin lesions o Pyogranulomatous lesions!! o If you see skin lesions – avoid the temptation to bandage them o Covering the draining tract will cause the fungi to grow in mycelial phase  Fever unresponsive to antibiotics  Risk Factors: o Young, large breed dogs o Sporting breeds or hounds o Proximity to waterways, exposures to excavation o Dogs 10x more susceptible than people – maybe because they sniff dirt more than humans  Potential for dog to serve as a sentinel – can transmit to owners Humans  Starts as a respiratory infection – dry cough, fever, weight loss  Bone is most common site of extra-pulmonary involvement  Most common in Mississippi, also found in Manitoba. Coccidioides immitis  Spherules and endospore forms  Found in dry soils in low elevation deserts (South Western USA)  Dogs, horses, cats, humans – Respiratory infections, Bone infections Dogs – “Valley Fever”  Clinical Signs: lameness, chronic illness, respiratory signs, lymphadenopathy, non-healing cutaneous lesions o Subclinical infections common ~70%  Risk Factors: animals with potential exposure in past 3 years (did animal visit Tucson?)  Epidemics most commonly following a heavy rainfall followed by a dust storm  Treatment – amphotericin B, fluconazole, itraconazole Cats  Most commonly a cutaneous disease, may also see sy stemic signs (fever, inappetance, weight loss) Histoplasma capsulatum  Large capsules around them  Found in nitrogenous soils – highly contaminated soils with bird/bat feces  Not in Canada, found along Mississippi river and southern Great Lakes  Presentation depends on the species of histo you get  Pathogenesis: spores are inhaled from areas contaminated with bat or pigeon feces  Dogs, cats, horses, humans – Respiratory and intestinal infections  Most infected animals have disseminated disease  Wide range of non-specific signs: depression, wt loss, fever, dyspnea, diarrhea.  In addition - in dogs due to Histoplasma enteritis: o Diarrhea – large bowel diarrhea, hepatomegaly, splenomegaly, icterus. Dogs  Get primary pulmonary histoplasmosis – may be self-limiting  Therapy is always recommended to prevent dissemination  Antifungals: Amphotericin B, Itraconazole, Fluconazole Sporothrix schenckii  Conidia grow all along the hyphae and in big fruiting structures   Found in old wood, rose thorns, moss – humans get it from gardening  Often found in soil  More of a tropical disease  Biocontainment level 2  Horses, dogs, cats, humans – subcutaneous nodules  Sample Collection: tissue biopsies or exudate from nodules/lesions Horses  Lymphocutaneous disease o Nodules develop at site of infection o Eventually nodules and vutaneous lymphatics ulcerated o Exudation of yellowish exudate from ulcers  Disseminated disease can develop if not treated  Disease develops after damage to skin from contaiminated plant material  Treatment – systemic iodine preparations, itraconazole o $$$$ - owners gotta love their horse to do this Laboratory Diagnosis  DO NOT CULTURE IT, tell the lab what is on your differential list – keeps them safe  Best option = serology (antigen detection in urine) Zoonotic  Coccidioides, Blastomyces, Histoplasma are dangerous when cultured  Can get sporothrix via scratches or bites Lecture 34 – Moraxella and Chlamydiaceae Moraxella  Biocontainment level 2  C. pneumoniae, C. suis, Chlamydophila abortus  Biocontainment level 3  Chlamydia trachomatis, Chlamydophila psittaci  Gram negative rods  Strict anaerobes  Found on mucous membranes of mammals  Don’t survive well outside of the host  Transmission: insects  Virulence Factors: o Type IV pili o Cytotoxin o Transferrin and lactoferrin binding proteins  Avoid – trimethoprim Moraxella bovis – Cattle – BOVINE KERATOCONJUNCTIVITIS (PINK EYE)  Biochemical ID: -hemolytic, catalase positive, gelatinase positive  Incubation of 2 days – 3 weeks  Clinical Signs: o Copious watery lacrimations  o Blephrospasma, phototobia (lots of blinking, light sensitive) o Opacity may develop in centre of cornea which may ulcerate o Most casese recover, but in severe cases eye ruptures causing blindness  Cattle are the reservoir – important point of control  Transmission via mechanical vectors (flies)  Treatment: early infections respond to topical antimicrobials – can also give them parenterally. Adjunctive therapy includes protecting animals from light (housing indoors, eye patches)  Control – no vaccinations, fly control and basic management  Sample Collection – swabs of lacrimal secretions  Laboratory Diagnosis – culture on blood agar  No standard for determining or interpreting antimicrobial susceptibility Chlamydia  Biocontainment level 2  Obligate intracellular parasites  Genome reduction – relies on host metabolic machinery rather than having their own  Biphasic development  Lifecycle: o Elementary bodies bind to cell surface o Endocystosis occurs, formation of inclusion bodies o Organisms becomes metabolically active o Reticulocyte bodies divide o RB then differentiate back into EB o EB escape by lysis or extrustion and infect other cells  Elementary bodies somewhat resistant to environmental conditions  Can survive for several days outside hose  GIT is natural site for C. psittaci (affects psitticine parrots)  Asymptomatic infections are common  Virulence Factors: o Virulence genes make up 10% of their genome o Various secretion systems (Type II, III, V) – secretion of effector molecules involved in cellular invasion o Cytotoxin – slows down cell cycle, organism wants to control when the host cell dies/ruptures.  ALL should be considered as potentially zoonotic and has a broad host range  IMPOSSIBLE to determine antimicrobial susceptibility Chlamydophila psittaci Birds – Pneumonia, air sacculitis, conjunctivitis, pericarditis, encephalitis  Clinical Signs: o Nasal/ocular discharges, conjunctivitis o Green-yellow feces o Inactivity, weight loss  In acute disease – more profound gross and histological lesions o Hepatomegaly, serofibrinous polyserositis, petechial hemorrhages on liver/spleen  Transmission is fecal oral or vertical transmission  Resistant to drying, can remain infectious for several months – this is typically how people get infected  Treatment – antimicrobials, no vaccines for humans or animals  Not reportable, not sure of disease incidence in Canada. Humans – Psittacosis  Infection through exposure to aerosolized organisms – sweeping/vacuuming up dry bird feces  One of the 10 most common laboratory acquired infections – if you suspect this, warn the lab  Clinical Signs o Pneumonia o Mild to sever acute to fulminant infection o Also a cause of culture negative endocarditis  Persons at risk: own pet birds, Veterinarians, zoo keepers, Farmers, poultry industry. Chlamydophila abortus - Sheep/Ruminants/Pigs – enzootic abortion  Abortions typically occur without prior clinical signs in last month of pregnancy  Animals are infected, infection latent until 3-4 months into pregnancy for ewes  See vaginal discharge 3 weeks following the abortion  Common in UK and USA – 45% abortions  Can affect 60% of animals in naïve flock  Control – isolate aborting animals and clean up abortuses  Potential zoonosis – abortion in women, pregnant women should avoid lambing ewes and aborted fetuses Chlamydophila pneumoniae - Humans, Horses, Koalas – Respiratory tract infections Causes respiratory tract infections (laryngitis, pharyngitis, fever, headache) This organism has been linked to many other disease – not proven (MS, asthma, etc) Affects people of all ages Risk Factor: crowded settings are at high risk Quite common ~300,000 cases/year in USA Chlamydia suis – Pigs (only host)– Intestinal Tract Infections  Associated with infections of the reproductive and respiratory tract o Conjunctivitis, rhinitis, pneumoniae o Return to estrus, inferior semen quality  Can survive 30 d in environment  Treatment – antimicrobials (tetracyclines) – make sure you use a drug that reaches high concentration within the cell  Control – no vaccines available, cleaning and good management is important and reducing the environmental reservoir. Chlamydia trachomatis – Humans – Trachoma, inclusion, conjunctivitis in infants, urethritis, proctitis  Sexually transmitted  Clinical Signs: o No overt clinical signs – can damage reproductive system damage and lead to infertility o May experience burning on urination or discharge o Can lead to pelvic inflammatory disease  Transmission from mothers to newborns: conjunctivitis, pneumonia  Treatment – antimicrobials (azithromycin and doxycycline) Sample Collection for Chlamydiaceae  Culture in specialized transport media  Can keep at +4 or -70, freeze thaw cycles kill  Abortions – smears from cotyledons, placenta, vagina  Polyarthritis – joint fluid  Conjunctivitis – conjunctival swab  Systemic Infection – samples of lung/abdominal viscera  Blood for serology Laboratory Diagnosis  Culture – only grows in embryonated eggs, in cell cultures  Microscopic exam of tissues – MZN stains  ELISA  Serology  PCR Lecture 35 – Rickettsiales  Obligate intracellular parasites  Rickettsiaceae are gram negative rods  Anaplasmataceae – lack cell wall components of other gram negatives  Biocontainment level depends on what you aree doing o Level 3 while working with infectious tissues, infected vectors, cell lines or embryonated eggs o Level 2 when performing non-propagative lab procedures (blood smears, PCR)  Generally not possible to culture using traditional bacteriological methods  Arthropod vector – replication of organism occurs in the tick (gut, ovaries, salivary, glands)  Sylvatic Cycle – b/w the vector and reservoir  Tick to tick transmission – transstadial, vertical (female  eggs), horizontal (venereal)  Ticks tend to be colonized with one species of Rickettsia  Identification by PCR or serology (cannot use culture/biochemical tests) Rickettsia - Tends to infect vascular endothelium Rickettsia rickettsia – Humans/Dogs – Rocky Mountain Spotted Fever  First described in 1980s – found in pioneers travelling west “trail fever”  Found all over North and South America  Vector is Hard Ticks = Dermacentor or Rhipicephalus o West = D. andersoni  o East = D. variabilis  Incidence of this disease is unknown in Canada, it is common in people in the USA  Dogs o Clinical Signs  Fever (most common)  Edema or extremities – attacks endothelium  Petechial or ecchymotic hemorrhages = spots  Joint pain and swellings  Myalgia  Neurological signs  Can get necrosis associated with vasculitis o Seasonality – common in March/October  Humans o Clinical Signs:  Rash (most common)  Headache, nausea, vomiting, injected conjunctiva  Long term consequences related to vascular inflammation and thrombosis – may see hemorrhage or thrombosis of organs or brain. Rickettsia prowezakii – Humans – Epidemic typhus  Clinical Signs: o Flu like symptoms o Rash, neuro signs (headache to coma) o Untreated takes 2-3 months to recover o Mortality rate is 40% in untreated people  Spread by Pediculus humanus corporis (human body louse)  Human is reservoir – infected lice die within weeks  Associated with flying squirrels in Southern USA  Happens when people live in dense, awful conditions (filthy conditions, high human density) Rickettsia typhi – Humans – Murine typhus Anaplasma - Tends to infect RBCs, platelets, leukocytes Anaplasma marginale – Cattle – Bovine anaplasmosis  Occurs in souther latitudes  In young animals infection usually subclinical  Disease more severe the older the animal is (>2 years = severe disease)  Clinical Signs: in severely affected animals o Icterus, anemia (extravascular hemolysis) o Fever o Decreased milk production  Severe infections can be rapidly fatal  Bos inducus (tropical cattle) might be more resistance  Treatment – tetracyclines, supportive therapy  Vaccination is possible Anaplasma phagocytophilum – Dogs – Canine granulocytotropic anaplasmosis “Tick Fever:  Vectored by Ixodes ticks  Mirrors distribution of Lyme disease  Clinical signs are non specific o Pyrexia, lethargy, depression, reluctance to move, joint pain  Also reported to affect cats, small mammals, horses, mountain lions, coyotes  Diagnosis – morulae seen in granulocyte in a peripheral blood smear  Treatment – doxycycline  Control – avoid exposure to ticks, ascaricides, no vaccine available Anaplasma bovis – Cattle – Bovine ehrlichiosis Erlichia - tends to infect leukocytes Erlichia canis – Dogs – Canine monocytic erlichiosis  Multisystemic disease – depression, lethargy, bleeding/petechiation, lymphadenopathy and splenomegaly in 20-25% of dogs  Ocular Signs: change in eye colour, blindness, anterior uveitis, retinal disease, neuromuscular disease  Polyarthritis - lameness  Vector: Dermacentor variabilis, Rhipicephalus  Treatment – doxycycline, chloramphenicol Erlichia chaffeensis – Humans – Human erlichiosis Neorickettsia - Tends to infect leukocytes Neorickettsia helminthoeca – Canids – Salmon Poisoning  Highly fatal disease of dogs found in California or BC  Clinical Signs: o Sudden febrile illness 5-7 days after eating fish o Gradually become hypothermic o Marked anorexia and wasting o Develop diarrhea and vomiting 14 days after signs begin  Adult flukes (Nanphyetus salminocola) in dog intestine  eggs pass in feces  cercaria infect fish  metacercariae in fish muscle  as fluke matures it inoculates dog with Neorickettsia  Treatment – tetracyclines, praziquantal, supportive therapy (fluids, anti-emetics)  Prevention – vaccines not effective, prevent exposure (organism survives in rotting fish for months) Neorickettsia risticii – Horses – Potomac horse fever  Clinical Signs: o Milk colic o Fever o Diarrhea – watery o Abortion in pregnant mares  Thought to involve a trematode vector – infection by ingestion of insects infected with trematode metacercaria, also been isolated from freshwater snails  Case fatality rate is 5-30%  Treatment: oxytetracycline, supportive care (NSAIDs, fluids)  Control – inactivated vaccines are available, shown to be marginally protective in field trieals Sample Collection  Blood  Blood smears  Acute and convalescent serum  Feces  Biopsies of lesions (R. rickettsia)  Unless sending to special lab, culture not a concern  Freezing samples is OK Laboratory Diagnostics  Anaplasma – ID morulae in blood, PCR blood  Neorickettsia helminthoeca – fecal flotation, seroconversion (acute vs convalescent)  Neorickettsia risticii – seroconversion, PCR on feces or blood  Erlichia – ID of morulae on smears of buffy coat, PCR on blood  R. rickettsia – serological testing, direct immunofluorescence, PCR Zoonosis  Transmission to people via vectors (ticks), possible through contact with infectious material in the hemolymph  DO NOT squish, burn, scratch or rip off ticks  Avoid exposure to hemolymph, wear gloves, use forceps, disinfect wound.  Client communication is important   Sick dogs does not equal a sick owner  If you have signs, seek treatment immediately Bioterrorism  Potential  Non-specific initial presentations  High morbidity and mortality rate  Ability to aerosolize  Not notifiable in Canada Treatment Options - General  Cannot do susceptibility testing  Tetracyclines  In people macrolides, penicillin’s and aminoglycosides not effective – does not reach high enough concentrations extracellularly Lecture 36 – Coxiella and Borellia Coxiella burnetii  Need MZN stain to identify  Obligate intracellular parasite  Biocontainment level 3  Found worldwide except New Zealand  Need special conditions to cultivate  inoculation of embryonated eggs  Shed in milk, urine, feces and amniotic fluids and can survive in environment for 150 d  Virulence Factors: LPS involved in phase variation (change surface Ag to evade immune system)  Incredibly broad host range  Life Cycle o Small cell variant eaten by macrophage o Vacuole acidifies, stimulates development of large cell variants o Day 2 – parasitophorous vacuole containing lots of replicating LCV o Day 6 – SCV reappear o Day 12 – host cell lyses and SCV release  Control – segregation of parturient ruminants, careful disposal of abortuses and placentas  Vaccination – inactivated vaccines available  Zoonotic – see fever, lethargy, anorexia 2 days after exposure  Sample Collection – blood, serum, placental tissues, milk  Lab Diagnosis – serology or PCR, susceptibility testing is impossible  Capable of causing lab acquired infections – sometimes fatal  Potential biological weapon – can be aerosolized Goats, Sheep, Dogs, Cats – Usually clinically silent, sometimes abortion  Most often clinical signs are mild or not apparent  Clinical signs, if present affect reproductive/mammary tract – causes abortions and shedding in milk  Causes sporadic abortions, placentitis, and fetal pathology related to liver, heart and interstitial pneumonia = systemic infection affecting all body systems   In affected dogs and cats also usually subclinical, but if signs are present dogs will have splenomegaly and cats will have abortion Humans – Q Fever  Reaches high concentrations in placenta and fetal tissues. Animals shed these tissues into environment and bacteria is aerosolized and inhaled. Also passes through gut and excreted in feces  Very low infectious dose with aerosol transmission  enters lungs, replicates in pulmonary macrophages, disseminates throughout the body  50% of people are asymptomatic  Acute febrile flu like illness, usually mild but serious complications can occur: o Pneumonia, granulomatous hepatitis, myocarditis, abortion o Case fatality rate