1/11
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
Tuberculosis and paratuberculosis (+ activation of disinfectants)
Etiology
TB: M. bovis (mammals, man), M. tuberculosis (man, car, su), M. avium complex (birds, pigs)
ParaTB (Johne’s disease): M. avium subsp. paratuberculosis
Acid-fast, aerobic, very resistant in environment, chronic granulomatous diseases.
Tuberculosis (TB)
Epizootology
Worldwide, zoonotic, WOAH-listed.
Controlled in many countries, but wildlife reservoirs persist.
Reservoirs: badgers, deer, wild boar, possums.
Slovakia TB-free; Norway had M. bovis reappearance in 2022.
Transmission
Mainly aerogenic (inhalation).
Also milk/feed, vertical transmission, contact with tissues.
Pathogenesis
Inhalation/ingestion → granulomas/tubercles → caseous necrosis ± calcification → chronic systemic disease.
Clinical signs
Cattle (M.bovis): Chronic cough, Weight loss, Dyspnoea, Fever, Enlarged LN, Often asymptomatic
Birds (M. avium): Often asymptomatic, Weight loss, ↓ egg production, Bone lesions
Pigs: Usually alimentary form, Intestinal lesions/LN lesions, Often asymptomatic
Humans: Pulmonary TB with Productive cough, Hemoptysis, Chest pain, Fever, fatigue
Diagnosis
Tuberculin skin test (main test), IFN-γ test, PM inspection, Histology (granulomas), Ziehl-Neelsen staining, Culture, PCR. (Serology is NOT used for tuberculosis)
Public health risk
Zoonotic - Infection from raw milk, meat, aerosols. Risk groups: vets, farmers, slaughterhouse workers. M. bovis is resistant to pyrazinamide.
Paratuberculosis (Johne’s disease)
Epizootology
Worldwide, chronic wasting disease of ruminants. High economic losses. Not officially zoonotic.
Transmission
Ingestion of contaminated milk, colostrum, faeces. Vertical transmission possible. Faecal shedding before clinical signs.
Pathogenesis
MAP in ileum/Peyer’s patches → granulomatous enteritis → malabsorption/protein loss.
Clinical signs
Adult ruminants: Chronic watery diarrhoea, Progressive weight loss despite appetite, ↓ milk production, Bottle jaw, Cachexia
Young animals: Usually infected young, Clinical disease appears in adulthood (long incubation).
Diagnosis
History + CS, ELISA (important screening test), PCR, Faecal culture, Histology, Tuberculin test with avian tuberculin
a) Prevention, control, outbreak measures, legislation
Legislation: Regulation (EU) 2016/429, Commission Delegated Regulation (EU) 2020/689, Commission Implementing Regulation (EU) 2020/200
Prevention & control
Veterinary supervision of animal movement, Quarantine of healthy animals, Tuberculin testing (TB), Surveillance/screening, PM meat inspection, Pasteurisation of milk, Biosecurity & hygiene, Identification & traceability, Movement restrictions
Outbreak/suspicion
Mandatory reporting, Isolation of suspect animals, Testing, Test & slaughter / depopulation, Rendering plant disposal, Epidemiological investigation, Final disinfection, Observation period (~110 d)
b) Sanitation, focal disinfection, activation of disinfectants
Environmental resistance
TB: Soil: 4 y, Pasture: 2 y, Water: 2 y, Slurry: 100–200 d
ParaTB: Soil: 11 mo, Faeces: 240 d
Focal disinfection: Chloramine T 6–10%, Peracetic acid 1%, Alkaline formalin 3%,
Environmental disinfection; Glutaraldehyde 2%, Formaldehyde, lime powder
Disinfection of objects: Sodium hypochlorite 2%
Excrements/slurry: 0.3% peracetic acid, 3% lime, Slurry storage >6 months
Activation of disinfectants:
Activation of disinfectants means increasing disinfectant efficacy by heating, adding alkalis/detergents, and removing organic material before disinfection!
Heating: Chloramine T: 50–60°C, NaOH: 70–80°C
Addition of detergents: sodium carbonate added to water (Detergents help disinfectants penetrate fat-rich mycobacterial cell walls)
Alkaline formaldehyde = NaOH + formaldehyde
Factors decreasing efficacy: Organic matter, Low temperature

Brucellosis (+ biothermic treatment of manure)
WOAH-listed, Contagious + zoonotic (except B. ovis)
Causes: Abortion, placentitis in females, Epididymitis/orchitis in males, and intracellular bacteria surviving in macrophages. Virulence factor: LPS endotoxin.
Etiology + Main hosts
Brucella abortus → cattle
Brucella melitensis → sheep/goats (Malta fever in humans)
Brucella suis → pigs
Brucella canis → dogs
Brucella ovis → rams (NOT zoonotic)
Epizootology
Worldwide. Endemic mainly in Africa, Asia, Middle East, eastern Europe. Wildlife reservoirs complicate eradication.
Norway & Slovakia: Free from: B. abortus, B. melitensis, B. suis, B. canis
Recent situation: B. melitensis: France & Italy, B. suis: wild boar in Finland; domestic France
Transmission
Horizontal: Ingestion of aborted material/milk, Direct contact with placenta, foetus, birth fluids
Venereal transmission
Vertical - Especially B. abortus* and B. canis
Important: Brucella survives for months in cool, moist environments.
Pathogenesis
Entry → survival in macrophages → spread to reproductive organs → placentitis/abortion.
Clinical signs
Cattle (B. abortus): Late abortion (5–7 month), Retained placenta, Infertility, Weak calves
Rams (B. ovis): Epididymitis, Orchitis, Infertility
Males generally: Testicular swelling, Arthritis/lameness possible
Horses: Fistulous withers, Poll evil
Humans: Malta fever/Undulating fever, Sweating, Weakness, Weight loss, Arthralgia
Differential diagnosis of abortions
Cattle: Tritrichomonas foetus (2–4 mo), Campylobacter foetus (4–6 mo), Leptospira (6–7 mo), Listeria (6–8 mo), Herpesvirus, Aspergillus
Sheep/goats: Campylobacter, Chlamydia psittaci, Listeria, Salmonella, Coxiella burnetii, Toxoplasma gondii, Pestivirus
Pigs: Leptospira, Parvovirus, Pestivirus, Herpesvirus
Diagnosis
Samples: Placenta, Aborted foetus, Vaginal swab, Milk, Semen, Blood
Tests: Serology (Rose-Bengal test, Complement fixation test, Serum agglutination, Milk ring test (cattle)
Other: Culture + modified Ziehl-Neelsen stain, PCR, Brucellin skin test, Guinea pig bioassay
Public health risk assessment
Important zoonosis. Risk groups are Veterinarians, Farmers, Slaughterhouse workers. Infection via: Raw milk, Contact with aborted material, Aerosols
Prevention in humans: Pasteurisation, PPE (gloves, masks, goggles)
a) Prevention, control, outbreak measures, legislation
Prevention & control
Surveillance + serology, Milk ring test/Rose-Bengal, Test breeding animals, Quarantine + testing (>12 mo), Movement control, Pasteurisation, Rodent/insect control, Use Brucella-free breeding animals, Vaccination (Only in endemic areas, mainly ruminants), No human vaccine!
Outbreak/suspicion
Mandatory reporting, Isolation/quarantine, Test & slaughter, Selective or radical depopulation, Disposal at rendering plant, Epidemiological investigation, Final disinfection, disposal at rendering plant: 133°C for 20 min
b) Sanitation, focal disinfection, biothermic manure treatment
Resistance: Brucella survives months in Manure, Slurry, Cool/moist environment. But easily destroyed by common disinfectants
and at 50–60°C heat
Focal disinfection
Housing: Chloramine T 4%, Peracetic acid 0.3–0.9%
Surfaces: Formalin 2%, NaOH 2–3%, Sodium hypochlorite 2.5%
Skin: Ethanol, Iodophores
Equipment: Autoclave (121°C/15 min), Dry heat (160–170°C/1 h)
Manure: composting with lime
Slurry: 3% lime, 0.3% peracetic acid (Slurry storage: 6 months storage with lime )
Biothermic treatment of manure (composting)
= Thermophilic aerobic composting producing heat that kills pathogens.
Contaminated manture is placed on a surface layer of non-infected manure, straw and dry leaves, and covered with non infected manure.
Conditions:
Temperature: 55–70°C
minimum for 4 weeks
Aeration: O2 for the composting process
Moisture: 40–60%
C:N ratio: 25:1
pH: 5.5–8
Important:
Improves soil quality
Kills vegetative bacteria, larvae, eggs
Spores may survive → combine with disinfectants (3% lime for 4 weeks)

Anthrax, tetanus, botulism, and other anaerobic infections (+ conditions for the use of formaldehyde for disinfection with regard to protection of human and animal health)
Anthrax
WOAH-listed | Zoonotic
Etiology:
Bacillus anthracis
Spore-forming bacterium, produces: lethal toxin + oedema toxin
Epizootology
Worldwide except Antarctica, Endemic: Africa, Asia, southern/eastern Europe
Spores survive in soil for decades. Rain/flooding may expose spores
Norway: no reported cases
Transmission
1. Inhalation (most fatal), 2. Ingestion, 3. Cutaneous inoculation
Pathogenesis
Spores → macrophages → lymphatics → septicaemia → sudden death → sporulation after death.
Clinical signs
Peracute: Sudden death, No rigor mortis, Cherry-red unclotted blood from orifices, Rapid bloating
Acute/subacute: Fever, Dyspnoea, Convulsions, Depression
Human forms
Cutaneous: black ulcer
Pulmonary: severe pneumonia
Intestinal: bloody diarrhoea
Pathology
Splenomegaly (“blackberry jam spleen”), Haemorrhages, Congested organs, DO NOT OPEN CARCASS
Diagnosis
Report immediately! Blood from a live animal, Ear tissue from a dead animal
PCR, ELISA, Culture (“Medusa head” colonies), Ascoli precipitation test, Giemsa/McFadden stain
Treatment/prevention
Penicillin, oxytetracycline
Annual vaccination in endemic areas
Never necropsy!! Incineration preferred
Tetanus (“lockjaw”)
Zoonotic
Etiology:
Clostridium tetani → Neurotoxins: tetanospasmin + tetanolysin
Transmission
Contaminated wounds, Soil/manure contamination
Pathogenesis
Toxin blocks inhibitory neurotransmitters (GABA/glycine) → spastic paralysis
Clinical signs
Horse: Sawhorse stance, Third eyelid prolapse, Tail elevated
Dog: Muscle rigidity, Retracted lips, Often localised form
Humans: Lockjaw, Risus sardonicus, Opisthotonus
Cause of death: Respiratory paralysis
Diagnosis
History + wounds, Toxin serology, Culture (“drumstick” appearance)
Treatment/prevention
Antitoxin, Metronidazole/penicillin, Wound cleaning + oxygenation, Vaccination (tetanus toxoid)
Botulism (“limber neck”)
WOAH-listed | Zoonotic
Etiology
Clostridium botulinum, Toxins A–G, Animals mainly C & D, Humans mainly A, B, E
Epizootology
Worldwide, Toxin in decaying food/carcasses, Birds infected through maggots
Norway: rakfisk, cured meats (spekemat), contaminated needles
Transmission
Ingestion of toxin/spores, Improper canned food, Honey in infants, Iatrogenic injections
Pathogenesis
Blocks acetylcholine release → flaccid paralysis.
Clinical signs
Birds: Limber neck, Paralysis, Cannot fly/walk
Mammals: Dysphagia, Weakness, Drooling, Progressive paralysis
Horse: Colic, Ileus, Shaker foal syndrome
Diagnosis
Feed history, Toxin ELISA/neutralisation, Serum/GIT samples
Treatment/prevention
Antitoxin, Gastric lavage, Remove contaminated feed, Proper food preservation
Other important anaerobic infections
Clostridium perfringens → Enterotoxaemia (Diarrhoea, Bloody faeces, Malabsorption)
Clostridium chauvoei → Blackleg (Young cattle, Gas-producing myonecrosis, Lameness + dark muscle)
Clostridium septicum → Malignant edema (Wound contamination, Necrosis + gangrene, Fatal septicaemia)
Clostridium haemolyticum → Bacillary haemoglobinuria (Intravascular haemolysis, Haemoglobinuria)
Fusobacterium necrophorum → Necrobacillosis (Calf diphtheria, Hepatic necrosis, Foot rot)
Public health risk
Anthrax: inhalation spores = most dangerous
Botulism: food poisoning
Tetanus: wound contamination
PPE + hygiene important
a) Prevention, control, outbreak measures
Anthrax: Do NOT open carcass, Incineration, Vaccination in endemic areas, Rodent/insect control, Disinfection before restocking, Prophylactic ATB for exposed workers
NB! If the carcass accidentally opens → ATB to exposed people, Vaccinate the herd, Soil disinfection
Tetanus: Early wound treatment, Vaccination, Antitoxin therapy
Botulism: Proper canning/storage, Remove dead birds/carcasses, Rodent control, Antiserum
b) Sanitation & focal disinfection, conditions for use of formaldehyde
Anthrax
Resistance: Spores survive: heat, UV, desiccation, survives for decades in soil
Housing: 10% Chloramine T, 10% chlorinated lime, 10% NaOH, 10% formalin, 4% glutaraldehyde, 1% peracetic acid
Soil: Lime, Phosphoric acid, Peracetic acid
Manure: Incineration, Composting + formaldehyde/glutaraldehyde
Slurry: 3% phosphoric acid, 1% peracetic acid
Spores destroyed by Autoclaving
Tetanus: 10% chlorinated lime, 3% formaldehyde, Autoclaving
Botulism: Autoclaving, Gamma radiation, Heating:100°C/10 min or 80°C/30 min
Formaldehyde — conditions of use
Properties
Effective against: bacteria, fungi, viruses, mycobacteria, spores (it is not stable)
Usage
30% active formalin
Spray: 2% (max10%)
Focal: 3% + 3% NaOH (alkaline formaldehyde)
Vapour: humidity 70–90%, temperature >15°C
Risks
Carcinogenic (Category 1B)
Suspected mutagen (class 2 mutagen)
Irritating/toxic by inhalation/contact
Important
Use only by trained professionals with PPE!!!
approved for animal housing, animal feet, vehicles, and eggs in hatcheries in 2015

Salmonelloses of animals and poultry (+ physical disinfection)
WOAH-listed* | Contagious | Zoonotic
Etiology
Main agent: Salmonella enterica
Important serovars:
S. typhi → enteric fever in humans
S. pullorum* → pullorum disease (septicemic disease in young chicks)
S. gallinarum *→ fowl typhoid (older chickens)
S. typhimurium → fowl paratyphoid, zoonotic, not host specific
S. dublin → cattle
S. abortusovis* → sheep → abortions
S. bongori → reptiles
Epizootology
Worldwide. Common in intensive poultry farming. Associated with poor hygiene and stress/immunosuppression. Wildlife birds maintain infection.
Public health importance: Eggs and egg products = highest-risk foods. Major foodborne zoonosis.
Europe 2022: Kinder chocolate products of S. typhimurium
Europe January 2023-2025: outbreak with 509 confirmed cases inlcuding Norway, Finland and Sweden, traced to sprouts, especially alfalfa and clover from a supplier in Italy, and the investigation is still ongoing
Norway: B-disease. Most human infections are acquired abroad or from imported food, except S. typhimurium 50% of cases contracted in Norway.
Slovakia & Norway: S. abortusovis absent!
Transmission
Horizontal: Faecal–oral route, Contaminated feed/water, Raw diets, Carrier animals, Rodents/insects
Vertical: Through eggs
Human infection: Raw eggs, Meat, Milk, handling exotic pets/reptiles
Pathogenesis
Ingestion → intestinal replication → enteritis → possible septicaemia → possible infection of CNS, bones, uterus etc.
Important: LPS endotoxin released during bacterial lysis causes: endotoxaemia, vascular damage and shock
Clinical signs
General: Many healthy adult animals are asymptomatic.
Young animals: Septicaemia, Sudden death, Fever, Severe diarrhoea
Calves: Acute enteritis, Bloody diarrhoea, Fever
Cattle (S. dublin): Abortion, Septicaemia
Sheep (S. abortusovis): Abortion
Pullorum disease (S. pullorum): Young chicks → White diarrhoea, Weakness, Dehydration, Septicaemia, High mortality
Fowl typhoid (S. gallinarum): Older chickens → Septicaemia, Sudden death, High mortality
Fowl paratyphoid (S. typhimurium): Arthritis, Lameness, Conjunctivitis, Blindness, Enteritis, Sudden death
Diagnosis
Samples: Faeces, Shoe-cover swabs, Serum
Methods: Culture (main) XLD agar: red colonies with black centre (H₂S), PCR
Serovar differentiation: Serology → Rapid slide agglutination, CFT, ELISA
Treatment
Humans: usually self-limiting, fluids, severe cases: ciprofloxacin
Animals: Ampicillin/other ATB, NSAIDs, Fluid therapy
Public health risk assessment
Important foodborne zoonosis. Eggs/poultry major source. Raw foods and reptiles important reservoirs.
Risk groups: Poultry workers, Farmers, Veterinarians, Consumers of raw eggs/meat
a) Prevention, control, outbreak measures, legislation
Prevention & control:
There is legislation that requires monitoring of breeding flocks and hatcheries for S.enteritidis and S.typhymurium + slaughter of positive flocks
Risk management: culture day-old chicks and 4 + 2weeks before laying
Serology: test swabs on 2 pairs of boots in broilers and pooled fecal samples of layers (60 samples)
Take dust samples for annual monitoring and control feed
Biosecurity: Rodent control, Insect/vector control, Hygiene “Black & white system.”
Important: Do NOT brush eggs → removes protective cuticle, bacteria enter pores
Food safety: Pasteurisation of milk, Proper cooking
Outbreak measures
Slaughter/elimination of positive flocks, Movement restriction, Cleaning/disinfection, Vaccination in countries with prevalence >10%
b) Sanitation, focal disinfection, physical disinfection
Resistance: Wet faeces (1 week), Dry faeces (up to 6 years), Dust (1–4 years), Biofilms (months)
Destroyed by: Heat, Sunlight, High pH, Ozone, Disinfectants
Sanitation
Housing: Chloramine T 6%, Peracetic acid
Manure: Composting at 65°C
Slurry: 0.3% peracetic acid, 3% lime, Ammonia
Water: Chlorination
Eggs: 2% formaldehyde vapours
Meat cooking temperatures: Steak: 63°C, Ground beef: 71°C, Poultry: 77°C
Physical disinfection
Moist heat (most effective → coagulation of proteins)
Boiling/hot water: 80C for 10 min (vegetative organisms), or 100C for 5min (C.perfringens spores), 10min (B.anthracis)
Autoclaving (steam): 121°C, 1atm/bar, 15 min → kills spores/endospores
Pasteurisation: 72°C for 15 sec
UHT: Ultra-high temperature treatment (140C for 2sec)
Dry heat (on animal housings like floor, walls, kill MO by oxidation)
140–200°C for 1–2 h
Flame gun/blow lamp for housing/tools
Direct heat by using flame or hot air oven with 170C for 2h (mention this one!)
NB: some organisms like prions may not be killed by dry heat
Desiccation: Removes moisture, variable effect. great for materials contaminated witg urine, pus, mucus
Osmotic pressure: High salt/sugar
Radiation
nonionizing (UV, food industry, surgery), ionizing (Gamma/X-ray)
6. Filtration & freezing

Campylobacterioses, yersinioses (+ disinfection in food production)
Campylobacteriosis
WOAH-listed | Contagious | Zoonotic
Etiology
* Campylobacter fetus venerealis → Ru → bovine genital campylobacteriosis
* Campylobacter fetus fetus→ Ru
* Campylobacter jejuni → poultry, mammals, man
* Campylobacter coli → animals, man
Important: C. jejuni and C. coli are normal intestinal flora in many animals and poultry. Poultry = major reservoir.
Epizootology
Worldwide. Most commonly reported food-borne zoonosis in Europe.
The main human source = undercooked poultry.
Europe: C. fetus venerealis reported in cattle in France and Ireland.
Norway: C. fetus venerealis = B-listed disease.
Transmission
Genital forms (C. fetus): Venereal transmission (Bulls are asymptomatic carriers → Spread during natural breeding/AI)
Enteric forms (C. jejuni, C. coli): Faecal–oral route, Contaminated food/water, Raw poultry, Unpasteurised milk
Pathogenesis
GIT form → Colonisation of jejunum/ileum/colon → enteritis. Toxin: Cytolethal distending toxin → inflammation + villous atrophy.
Genital form → Catarrhal inflammation of the reproductive tract.
Clinical signs
GIT form: Diarrhoea (may be bloody), Enteritis, Abdominal pain, Anorexia, Often asymptomatic adults
Genital form: Bulls → Usually asymptomatic carriers. Cows → Endometritis, Metritis, Infertility, Irregular oestrus, Early embryonic death, Abortion
Diagnosis
GIT: Faecal culture (Skirrow selective agar and blood agar), Oxidase positive (reagent turn purple), PCR, Gram stain
Genital: Vaginal/preputial wash culture (skirrow agar), PCR, ELISA (use on vaginal mucus), VMAT (vaginal mucosal agglutination test, a field test)
Treatment
GIT: ATB, often limited usefulness
Genital: Vaccination, Streptomycin in bulls
Humans: Erythromycin, Gentamicin
Public health risk
Major food-borne zoonosis. Poultry = highest risk. Infection mainly from undercooked chicken/raw milk.
Yersiniosis
Contagious | Zoonotic
Etiology
* Yersinia pestis → black death, pneumonic plague (pest) in man. mammals are PH.
* Yersinia enterocolitica → enteritis in man and pigs.
* Yersinia pseudotuberculosis → birds, rodents, swine, car, cervids
Epizootology
Y. pestis: Historical Black Death pandemic (bubonic plaque pandemic in europe and asia in 1300)
Endemic in East Africa, Asia, South America
Cats are highly susceptible. Rodents = reservoir.
2009 china: pneumonic plague outbreak
2021 madagascar: pneumonic and bubonic plaque
Transmission
Y. pestis: Rat fleas, Aerosols, Skin wounds/contact with infected animal
Y. enterocolitica: Ingestion of contaminated pork
Pathogenesis
Y. pestis: Skin inoculation → buboes (lymph node abscesses) → septicaemia/pneumonia.
Severe forms: Bubonic plague, Septicaemic plague, Pneumonic plague
Y. enterocolitica: Colonises ileum/cecum → enteritis + lymph node enlargement.
Clinical signs
Y. pestis
→ Bubonic: Painful enlarged lymph nodes
→ Pneumonic: Respiratory failure
→ Septicaemic: DIC and tissue necrosis
Y. enterocolitica: Usually self-limiting enteritis
Diagnosis
History + CS, Blood agar culture (Blood/nasal swabs, LN aspirates), PCR, ELISA, Agglutination tests, Gram stain
Treatment
Rodent control, Flea treatment, Gentamicin, Doxycycline
Public health risk assessment
Campylobacter: Major zoonotic foodborne disease. Poultry = main source.
Yersinia: Third most important zoonosis after Campylobacteriosis and Salmonellosis
a) Prevention, control, outbreak measures
Campylobacter:
Prevention: Cook meat properly, Pasteurise milk, Hygiene/biosecurity, Remove faeces, Rodent & insect control, Bull examination, Vaccination before breeding
Outbreak: Treatment or culling/selection
Yersinia:
Prevention: Cook pork properly, Milk hygiene, Rodent control, Flea treatment, Water hygiene
Outbreak: Treatment or selection/culling, No vaccine
b) Sanitation, focal disinfection, food production disinfection
Resistance: Low environmental resistance, Survive best in moist conditions
Campylobacter sanitation
Housing: 4% chloramine T, 0.3% peracetic acid, 2% formalin, 2% NaOH, 20% slaked lime, Cresol-sulphuric mixture
Water: Chlorination
Physical methods: Moist heat, Dry heat, UV, Gamma radiation
Yersinia sanitation
Easily destroyed by: Heat, Drying, Sunlight, Disinfectants
Disinfectants: 2% NaOH, 2% chloramine T, 0.5% formaldehyde, Other: Drying for 2 days, Moist/dry heat
Disinfection in food production
HACCP (Hazard Analysis Critical Control Points)
identifies contamination risks in food production.
Cleaning/disinfection steps:
1. Remove food
2. Mechanical cleaning
3. Pre-rinse: high pressure water
4. Detergent cleaning: remove biofilm (washing soda, Na2CO3).
alkaline cleaning agent: Removes fats/proteins
acid cleaning agent: Removes encrusted residues like milkstone/waterstone
neutral cleaning agent: Smooth surfaces wo dirt/manual cleaning
5. Rinse
6. Drying (to not dilute the disinfectant)
7. Disinfection
Disinfection methods:
Physical: Hot water, Steam, UV, Radiation, Ultrasound
Chemical: Iodonal A, Sodium hypochlorite, Nitric acid, QUACs (Despon). MUST NOT LEAVE TOXIC RESIDUES!

Borreliosis and other tickborne diseases (+life cycle of ticks and their prevention and control)
Borreliosis (Lyme disease) — Vector-borne | Zoonotic | Natural focal disease
Etiology
* Borrelia burgdorferi sensu stricto → Lyme disease
* Borrelia afzelii, Borrelia garinii
* Borrelia anserina → avian spirochaetosis
Important: Borrelia burgdorferi s.l. complex causes Lyme disease in mammals and humans.
Reservoirs = small rodents, birds, and insectivores.
Natural focality
Natural focus includes:
Pathogen (pathoergont), Reservoir host, Vector (blood-sucking arthropod), Recipient host (animal/man) and Suitable environment
Other natural focal diseases: leptospirosis, rabies, TBE, ehrlichiosis, babesiosis.
Epizootology
Worldwide, endemic in Central Europe and Southern Scandinavia
Seasonal: spring–autumn. Professional risk for outdoor workers
Norway: endemic areas in the southern regions
Transmission
Ixodidae hard ticks (Ixodes*)
Transstadial transmission, occasionally transplacental
B. anserina is transmitted by soft ticks (Argas) via transstadial + transovarial transmission
Pathogenesis
Tick bite → skin penetration → bacterial replication → spread via blood/lymph → immune complex formation → kidney/joint damage.
Clinical signs
Animals:
Fever, Lethargy, Enlarged lymph nodes, Arthritis, swollen joints, lameness, Glomerulonephritis, Uveitis, Arrhythmias, Abortion
Humans:
1. Flu-like signs, 2. Erythema migrans, 3. CNS/joint involvement (facial paralysis, headache, neck stiffness)
Birds:
Anaemia, Cyanotic comb, Green diarrhoea
Diagnosis
Culture: Barbour–Stoenner–Kelly II medium at 33C
PCR
Dark-field microscopy
ELISA, indirect IFA
Cross-reactions with Leptospira* and Treponema
Treatment
Doxycycline, Penicillin, Amoxicillin, Erythromycin
Symptomatic + anti-inflammatory therapy
Other vector-borne infections
Tick-borne:
Ehrlichiosis, Rickettsiosis, Babesiosis, Tularaemia, Tick-borne encephalitis (TBE), Crimean–Congo haemorrhagic fever
Mosquito-borne:
West Nile fever, Dengue, Yellow fever, Equine encephalitis
Culicoides-borne:
Bluetongue, African horse sickness
Public health risk assessment
Major zoonotic vector-borne disease. Expanding tick populations and climate change increase risk to animals and humans.
a) Prevention, control, outbreak measures
Tick control with acaricides (Permethrin): Amitraz collar for dogs, Fipronil spot on, Fluralaner (bravecto)
Rodent control (deratization)
Protective clothing, avoid tick habitats
Vaccination in endemic areas
Tick repellents: DEET, Picaridin, IR3535
Outbreak measures
Antibiotic treatment, Tick elimination, Monitoring of exposed animals/humans
b) Sanitation, focal disinfection, tick life cycle & control
Borrelia destroyed by:
Chloramine T, Peracetic acid, Sodium hypochlorite, 70% ethanol
UV light
Heat
Tick life cycle (Ixodidae – hard ticks)
incomplete metamorphosis
Egg → larva (6 legs) → nymph (8 legs) → adult (8 legs)
Types:
One-host ticks, Two-host ticks, Three-host ticks (Ixodes = Borrelia vector)
Ixodes larva and nymphal stage feed on reservoirs (small mammals and birds) and get infected by the pathogen, then they feed on man/animal and spread the pathogen.
Soft ticks (Argasidae)
Multi-host life cycle, Can survive years without feeding
they have several nymphal stages and may feed on several hosts like rodents and birds, and transmit borrelia at anyh developmental stage
Tick/insect control methods
Mechanical: traps, screens
Physical: heat, UV, steam
Biological: natural enemies
Chemical: insecticides/acaricides (permethrin, amitraz, ivermectin)

Mycoplasmosis (+ aerosol disinfection)
WOAH-listed | Contagious | Mostly respiratory diseases | Zoonotic risk low/no in animals
Etiology
Mycoplasma capricolum subsp. capripneumoniae → Contagious caprine pleuropneumonia (CCP)
Mycoplasma mycoides mycoides → Contagious bovine pleuropneumonia (CBP)
Mycoplasma bovis → mastitis, pneumonia, arthritis, vulvovaginitis
Mycoplasma agalactiae → contagious agalactia in sheep/goats
M. gallisepticum → chronic respiratory disease in poultry
M. synoviae → arthritis/synovitis in poultry
M.hyopneumonia, M.hyosynovia, M.hyogenitalia (PIGS)
M.genitalium, M.pneumonia (mild “walking pneumonia” in humans)
Important: Mycoplasma lack a cell wall → fragile in environment but resistant to some antibiotics.
Epizootology
Worldwide: Africa: endemic CBP with high mortality, Europe: CBP eradicated since 1999
Norway: M. bovis free country
Backyard poultry in Nordic countries is commonly affected by avian mycoplasmosis (yearly in Iceland), and in Finland in 2024)
CCP outbreaks associated with stress, transport, cold
Transmission
Horizontal transmission: Inhalation (main route), Milk/dairy products, Venereal transmission
Wind spread possible up to 200 m (M. mycoides*)
Location
Mainly respiratory tract, but also Mammary gland, Joints, Eyes, Urogenital tract
Pathogenesis
Inhalation → pneumonia, pleuritis, hepatization of lungs
Ingestion → spread via blood to mammary gland, joints, eyes
Chronic latent infections are common
Clinical signs
Cattle (CBP / M. bovis):
Fever, Pneumonia, Dyspnoea, chest pain, Mastitis (“sand-like” milk), Vulvovaginitis, Otitis media
Goats/sheep:
Mastitis, Arthritis, Keratoconjunctivitis, Abortion, Septicaemia
Poultry:
Airsacculitis, Tracheitis, Sinusitis, Swollen joints
Diagnosis
Culture on PPLO agar (“fried egg” colonies) and PCR
ELISA, HIT
Samples: Nasal swabs, Pleural fluid, Synovial fluid, Lung lesions, Lymph nodes
Treatment
Often difficult/not recommended due to latent carriers
Culling + quarantine preferred
Vaccination in endemic areas
Antibiotics: Enrofloxacin, Tulathromycin, Gamithromycin
Public health risk assessment
Animal mycoplasmoses are mainly veterinary/economic problems. Human mycoplasmas exist (*M. pneumoniae*, M. genitalium), but animal strains are generally not zoonotic.
a) Prevention, control, outbreak measures
Prevention & control
Quarantine + movement restrictions
Serological screening and Vaccination in endemic areas
Good husbandry and milking hygiene
Test breeding bulls
Expand poultry flocks from seronegative birds
Rodent/insect control
Outbreak measures
Eliminate positive animals, Quarantine affected herds/flocks
Antibiotic treatment is usually not sufficient
b) Sanitation, focal disinfection, aerosol disinfection
Resistance
Poor survival in environment, but can survive for years when frozen
Destroyed by:
Heat: 55–60°C for 30 min or 100°C for 1 min
Extreme pH
Chloramine T, Peracetic acid, NaOH, Formalin, Chlorinated lime, cresol-sulphuric, peracetic and formaldehyde vapours for eggs in hatcheries.
Aerosol disinfection
Common in the poultry industry.
Ultrafine dispersions of solid of solid or liquid disinfectant in gases
not uniform deposition: 75-85% of aerosol particles is captured on horizontal surfaces
Conditions:
Particle size: 0.5–10 µm (max 20)
Humidity: 70–90%
Temperature: >15°C
Exposure: overnight (≥6 h)
Volume: 5-25ml per 1m3. 5ml/m3 in presence of animals.
Methods:
Karcher, Igeba, Formalin lamp, Exothermic reaction
Disinfectants used:
Peracetic acid vapours (non-stable, min.15%. not by thermomechanical reaction → explosion. 12mil Pedox + 4g chlorinated lime is very effective)
Formaldehyde aerosols (non-stable, min 30%. exothermic reaction → inactivate virus, fungi, spore forming. use Formalin + potassium permanganate mixtures or mixed with chlorinated lime)

Q fever & other rickettsioses (+Treatment and disinfection of soil and pastures)
WOAH-listed | Vector-borne | Zoonotic
Etiology
* Coxiella burnetii → Q fever
* Reservoirs: ruminants, birds, various mammals
* Humans are infected mainly through farm animal exposure
Other rickettsioses:
* Rickettsia rickettsii → Rocky Mountain spotted fever
* Ehrlichia canis → canine ehrlichiosis
* Ehrlichia ruminantium → heartwater disease
* Rickettsia prowazekii → epidemic typhus
* Anaplasma phagocytophilum → granulocytic anaplasmosis
Epizootology
Q fever worldwide except New Zealand
Large outbreak: Netherlands 2007–2011 (>4000 human cases)
Norway: 8 human cases in 2019
Slovakia: largest outbreak in 1993 after men handled aborted goat kid. 2011 - goat cheese. 1 human case in 2019.
Spread possibly over long distances by aerosolized spore-like forms
Tick-borne diseases are increasing due to climate change/global warming
Seasonal tick activity mainly spring–autumn
Transmission
Q fever:
Inhalation (main route)
Ingestion of contaminated milk/food
Exposure to birth fluids, placenta, aborted foetuses
Tick transmission possible
Rickettsioses/ehrlichiosis:
Hard ticks (Dermacentor, Amblyomma, Rhipicephalus*)
Transstadial/transovarial transmission
Pathogenesis
Q fever:
Inhalation → replication in macrophages → lymph nodes → bacteraemia → uterus, placenta, mammary gland.
Rickettsioses:
Attack vascular endothelium or WBCs → vasculitis/DIC → multiorgan damage.
Clinical signs
Animals (Q fever):
Often asymptomatic, Abortions, Weak offspring, Endometritis, Agalactia
Humans (Q fever):
Flu-like disease, Chronic endocarditis, Hepatitis, Arthritis, Premature birth
Rocky Mountain spotted fever:
Fever, Rash, CNS signs, Endothelial damage
Ehrlichiosis:
Fever, Lymphadenopathy, Thrombocytopenia, DIC, Seizures/coma in severe cases
Diagnosis
PCR, ELISA / IFA, Blood smears, Cell culture / embryonated eggs, Giemsa or Stamp staining
Samples: Blood, Birth fluids, Placenta/foetus, Milk, Vaginal discharge
Treatment
Doxycycline (main antibiotic), Supportive therapy, Q fever in animals: usually no treatment
Public health risk assessment
Important zoonotic diseases. The highest risk during animal parturition and handling of contaminated birth materials.
Aerosol spread creates major outbreak potential.
a) Prevention, control, outbreak measures
Prevention & control
Proper disposal of birth products/manure
Cleaning and disinfection
Tick control: Permethrin, Amitraz, Fipronil
Pasteurization of milk
Vaccination in endemic areas
Awareness and biosecurity
Remove contaminated birth fluids immediately
Outbreak measures
Treatment where appropriate
Elimination/isolation of positive animals
Movement restrictions
b) Sanitation, focal disinfection, treatment and disinfection of soil/pasture
Resistance
Survive for months in environment. Aerosol spread over large distances
Disinfection
Chloramine T (4%), Peracetic acid (0.5%), NaOH (2%), Formaldehyde (2%), Lime (3%), Moist/dry heat
Manure compost
Slurry: 3% lime, 1.5% phosphoric
Pasture: 3% lime & no grazing for 90 days
Tick bite disinfection: 70% isopropyl alcohol and 2% tincture iodine
Manure/slurry treatment
* Composting (biothermic treatment)
* Lime or phosphoric acid treatment
* Burning/burying if necessary
Storage condition: minimum 15m from milking parlour & 50m from well
Pasture/soil disinfection
3% lime
1–1.5% phosphoric acid
0.3-0.5% peracetic acid
all 10L per 1m2
* No grazing for 90 days

Chlamydiosis (+hygiene measures to reduce airborne diseases)
WOAH-listed: Yes* C: Yes Z: Yes*
Aetiology
* Chlamydia psittaci → birds (avian chlamydiosis), zoonotic
* C. abortus → sheep/goats, enzootic abortion, zoonotic
* C. felis → cats, conjunctivitis
* C. suis → pigs, respiratory/enteric/reproductive disease
* C. trachomatis → humans (STD)
* C. pneumoniae → mild respiratory infection in humans
Unique reproductive cycle
* Elementary body (EB) = infectious, small, metabolically inert
* Reticulate body (RB) = intracellular replicative form
EB enters host cell → RB replicates in inclusion bodies → cell lysis → spread
Epizootiological situation
Worldwide distribution
Avian chlamydiosis common in psittacines & poultry
Reported in Norway in 2019
Enzootic abortion of sheep is endemic in UK, France, Spain, Germany
An important cause of abortion in sheep in Europe
Transmission
Horizontal:
Inhalation of dust/faeces/discharges
Ingestion
Direct contact with afterbirth/vaginal discharge
Venereal transmission
Milk ingestion
Vertical:
Placenta & milk (especially C. abortus)
Pathogenesis
Inhalation/ingestion → EB enters host cell → RB replication → cell lysis → infection of mucosal epithelial cells & macrophages → possible septicaemia
Clinical signs
Birds:
Anorexia, lethargy, weight loss, Yellow droppings, Conjunctivitis, sinusitis, sneezing, Hepatosplenomegaly, airsacculitis, pericarditis
Mammals:
Late-term abortion, Stillborn/weak offspring, Inflamed placenta
Cats: conjunctivitis, rhinitis, bronchopneumonia
Humans:
Flu-like illness to severe pneumonia/encephalitis
Pregnant women at risk from C. abortus
Diagnosis
History + clinical signs
PCR = method of choice
McCoy/BHK cell culture
Giemsa, Ziehl-Neelsen, Macchiavello staining
ELISA, CFT serology
Treatment
Long-course doxycycline/tetracycline
a) Prevention & control
Avian:
No vaccine, Monitoring, All-in/all-out, Remove dead birds
Mammalian:
Vaccination (C. abortus, C. felis), Quarantine & isolation, Disinfection after abortions, Veterinary surveillance, Doxycycline treatment
General:
Pasteurise milk, Control rodents, insects & wild birds, Avoid contact with aborted material
Outbreak measures
Depopulation/slaughter, Incineration of carcasses/material, Vaccination in mammals
b) Sanitation & disinfection
Sensitive to most disinfectants: Sodium hypochlorite, Ethanol, Peracetic acid, Glutaraldehyde, Hydrogen peroxide, Lime, Heat (autoclave 121°C/15 min), chlorination of water, quick lime on pasture, manure composting
Hygiene measures against airborne spread
Max gases in animal housings: CO2 (0,25%), H2S (10ppm), methane, ammonia (25ppm), N2O (nitrous oxide)
Air of animal house differ from atmospheric: No UV (disinfection), high humidity (no dehydration of MO), higher dust (carriers of MO), aerosol droplets (carry MO)
Reduce dust & aerosols
Good ventilation
Proper humidity: Most airborne bacteria survive better at RH either higher or glower than 50-80% RH range
Regular manure/bedding removal
Adequate animal spacing
Biosecurity distances between farms
Public health risk assessment: Important zoonosis. Avoid contact with aborted foetuses, placentas, discharges, contaminated dust, and unpasteurised milk. Pregnant women should not handle suspected cases.

Listeriosis and other bacterial encephalitis (+microbiological control of disinfection)
Listeria:
C: No Z: Yes
Important food-borne zooanthroponosis, especially in immunocompromised individuals.
Etiology
Listeria monocytogenes
Produces Listeriolysin O (LLO)
FH: mammals (ruminants, humans), birds asymptomatic
Listeria ivanovii → Sporadic abortions in sheep & cattle.
Reservoir: rodents → urine contaminates silage, vegetables etc. (tror e ho sa på epizoo eksamen)
Epizootiological situation
Worldwide: soil, water, silage, faeces, plants
Grows at 4–44°C (important food-borne pathogen)
Survives: Soil: up to 5 years, Silage: 12–16 month, Faeces/water: 1–2 years, Winter–spring disease in colder climates
2023: Norway (dogs in Bergen), Italy, Austria, Netherlands
2024: USA
Transmission
Horizontal:
Contaminated silage/feed, Unpasteurised dairy products, Undercooked meat, Direct contact/inhalation
Vertical:
Placenta, milk
Excreted in:
Faeces, urine, milk, uterine discharge, aborted foetuses
Pathogenesis
Entry via alimentary tract/conjunctiva → blood & lymph → CNS, liver, spleen, genital tract
Migrates along peripheral nerves to CNS
Survives in macrophages using *Listeriolysin O**
Pregnancy/immunosuppression predispose disease
Clinical signs
Mammals
Septicaemic form (young):
Fever, diarrhoea, weakness, Nasal/ocular discharge, Death within 24–48 h
Encephalic form (adults):
Circling, Facial paralysis, Torticollis, Opisthotonus, Paralysis/coma
Abortion form:
Late gestation abortion, Retained placenta, Mastitis
Sheep
Rapid encephalitis, Droopy ears, protruding tongue, Excess salivation, Circling
Birds
Septicaemia in young, CNS signs in adults
Humans
Pregnancy infections, Neonatal sepsis/meningitis, Gastroenteritis, Encephalitis/meningitis, Cutaneous listeriosis in veterinarians
Pathology
Liver & spleen necrosis, Brain oedema, Suppurative meningitis, Placental inflammation, Oedematous/mummified foetus
Diagnosis
Clinical signs + necropsy, Blood agar/BHI culture, PCR, IFA, Gram stain, Serology not recommended
Treatment
* Penicillin + gentamicin
* Dexamethasone for CNS inflammation
Other bacterial encephalitis
* Streptococcus suis — pigs
* Streptococcus equi — strangles
* Haemophilus parasuis — Glässer disease
* Histophilus somni — cattle
a) Prevention & control
* Avoid spoiled silage (pH 4.5), Good farm hygiene, Burn aborted material, Pasteurise milk, Cook food properly, Rodent/vector control, Regular disinfection, All-in/all-out, Isolation of affected animals
outbreak: Isolation of affected animals – Tx (if CNS is not involved)
Vaccine: in sheep – but not very effective
b) Sanitation and disinfection
Sensitive to:
* Chloramine T, Formaldehyde, NaOH, Peracetic acid, Heat, Chlorination/ozone
Microbiological control of disinfection efficiency
1. Chemical control – determines concentration of active substance by chemical swabs
2. Microbial control – the most objective test – based on microbial swabs (area – 10cm2)
a. Total no. of bacteria or presence of indicator microbes is established
b. Preventative (quantitative), focal (qualitative), direct or indirect
Before disinfection - Evaluation of effect of disinfectant
Take sterile swabs from 10cm^2
Total no. of Mo on nutritive agar and indicator on endo agar
CFU = colonies grown on plate x 00 (dilution)
- e.g.: 86 colonies x 00= 8.6x10^3CFU/cm^2
After disinfection
Preventive
30 sterile swabs on 10cm^2 area into physiological solution
Measures total no. of MO & indicator MO
Make decimal dilutions 10^1, 10^2, 10^3, 10^4
On nutritive agar
Max 10% positive indicator MO
Focal
30 sterile swabs on 100cm^2 area & into selective liquid broth
Make decimal dilutions
On endo agar
Should be negative!!
CFU: Colonies x 00(dilution) x 0
Total no. can be 1.2x10^3CFU/10cm^2
Public health risk assessment
Major zoonotic food-borne disease.
High risk for:
Pregnant women, Elderly, Immunocompromised people
Avoid contaminated silage, raw milk, undercooked food, unwashed vegetables, and aborted material

Leptospirosis and other spirochetosis (+stages of rodent control)
Spirochaetosis
* Gram-negative, motile, spiral bacteria
* Endocellular flagella
* Mostly anaerobic
Order: *Spirochaetales**
Includes:
* Leptospira → leptospirosis
* Borrelia → Lyme disease
* Borrelia anserina → avian spirochaetosis
* Brachyspira → intestinal spirochaetosis
Leptospirosis
C: No Z: Yes
Aetiology
* Leptospira interrogans
Reservoir: *rodents**
Common serovars:
* Dogs: canicola, icterohaemorrhagiae, grippotyphosa, pomona
* Cattle/horses: grippotyphosa, pomona
* Pigs: pomona, bratislava
FH:
* Dogs, cattle, pigs, horses, humans
Epizootiological situation
Worldwide
Associated with muddy water, lakes, riverbanks
Natural focal disease - More common after rainfall, Seasonal in temperate climates
Europe:
2021: 1246 human cases in Europe (mainly France)
Slovakia: 21 cases (2017–2021)
Norway: B-listed disease, mainly in wild rats/imported cases
Transmission
* Urine-contaminated water (main source)
* Contact through skin or mucous membranes
* Ingestion
* Venereal
* Placental transmission
* Rodent vectors
Dogs:
* Infection often from bites, carcasses, placenta
Pathogenesis
Skin/MM contact → bloodstream → bacteraemia → kidney, liver, uterus
→ intravascular haemolysis & liver injury
Leptospira persist in renal tubules → shedding in urine
Clinical signs
Dogs
Vomiting, Icterus, Renal failure, Severe lung disease, Death
Ruminants
Abortion
Horses
Uveitis, Conjunctivitis, Photophobia
Pigs
Usually mild/subclinical
Humans
Fever, myalgia, Meningitis, Pulmonary haemorrhage, Icterus - Weil disease
Diagnosis
EMJH culture medium, Dark-field microscopy, Levaditi silver stain, PCR
Serology: ELISA, MAT = gold standard
Samples:
Blood, urine, placenta, Kidney, liver, brain, eye
NB:
Intermittent shedding → paired samples after 3–4 weeks
Treatment
Penicillin, Tetracycline, Streptomycin, Supportive therapy
Annual vaccines: Dogs, Cattle, Swine
Other Spirochaetoses
Brachyspira (Swine dysentery → Mucohaemorrhagic diarrhoea)
Borrelia burgdorferi (Lyme disease - Tick-borne → Kidney & joint damage)
Borrelia anserina (Avian spirochaetosis - Soft tick transmission → Septicaemia, liver/spleen necrosis)
Treponema cuniculi (Rabbit syphilis → Papules & erosions)
a) Prevention & control
Rodent control, Tick removal (<12 h), Vaccination, Fence open water sources, Proper sanitation, Quarantine, Black & white system, All-in/all-out
Outbreak: Isolation, Treatment, Vaccination
b) Sanitation, focal disinfection and rodent control stages
Sensitive to:
Chloramine T, NaOH, Formaldehyde, Peracetic acid, Chlorination of water, Heat/pasteurisation
Rodent control stages
1. Assessment of rodent population (number based on feces etc)
2. Choose control method:
Mechanical, Physical, Biological, Chemical
3. Protection of non-target animals (bait box etc)
4. Assess effectiveness
5. Protocol/documentation
Public health risk assessment
Important zoonosis. Humans infected mainly from contaminated water or urine.
High-risk groups: Farmers, Veterinarians, People exposed to floodwater or rodents.

Mycoses (+ use of acids for disinfection)
Mycoses = fungal diseases of humans & animals
Worldwide distribution
Cause:
Dermatomycoses (skin)
Systemic mycoses (internal organs)
Dermatomycosis (Ringworm)
C: Yes Z: Yes*
Key facts
Affect skin, hair, nails, Caused by dermatophytes, Colonise stratum corneum
Hyphae & spores highly resistant in environment
Types of dermatophytes
Anthropophilic: Human hosts, Do not survive in soil. T. rubrum
Zoophilic: Animal → human transmission. Microsporum canis, Trichophyton verrucosum, T. mentagrophytes
Geophilic: Soil fungi. M. gypseum
Aetiology
Family: Arthrodermataceae
Important species:
Trichophyton verrucosum,T. mentagrophytes, T. equinum,T. gallinae
Microsporum canis, M. nanum, M. gypseum
Transmission
Direct contact, Indirect contact with spores, Soil contamination, Animal/vector transmission
Pathogenesis
Spores attach to skin/hair follicles
→ hyphae develop (~2 weeks)
→ invade hair centre
→ circular alopecia/crusts
→ regression after ~2 months
Clinical signs
Red, itchy, scaly circular lesions + Alopecia
Typical locations:
* Dog: head, neck, limbs
* Cat: neck, chest
* Calves: around eyes & ears
Diagnosis
Wood’s lamp, KOH microscopy, Sabouraud agar culture, Serology
Treatment
Usually self-limiting.
Cats: Itraconazole
Dogs: Itraconazole, Ketoconazole (toxic in cats)
Cattle/Horses: Enilconazole, Iodine antiseptics
NB: Remove crusts before topical therapy, Burn removed scabs
Systemic Mycoses
C: Yes Z: Yes*
Aetiology
Histoplasmosis: Histoplasma capsulatum → Dogs, horses, humans
Candidiasis: Candida albicans → Ruminants, birds
Blastomycosis: Blastomyces dermatitidis → Dogs, humans
Aspergillosis: Aspergillus fumigatus, A. flavus, A. niger
Transmission
* Inhalation of spores
* Opportunistic infection
* Egg contamination (Aspergillus)
Clinical signs
Histoplasmosis: Pulmonary/generalised disease, Equine lymphangitis
Candidiasis: White cheesy plaques, Oral/vaginal lesions, Crop stasis in birds
Blastomycosis: Respiratory & skin lesions
Aspergillosis: Respiratory disease, Yellow nodules, Gaping, Voice changes, Embryo death, Mycotic abortion
Diagnosis
Histoplasmin skin test, Smears/culture, Sabouraud agar, ELISA, X-ray
Treatment
Fluconazole, Lime sulphur dips
Other mycoses
Malassezia pachydermatis: Dogs/cats, Opportunistic dermatitis/otitis
Cryptococcus neoformans: Inhaled spores → CNS/respiratory disease
Coccidioides immitis → Valley fever, Inhalation of arthroconidia
a) Prevention & control
Clip hair, 70% ethanol disinfection, Rodent control, Good hygiene, Remove mouldy feed, Good ventilation, Avoid dusty environment, Regular testing
Outbreak: Treat animals and owners (zoonotic)
b) Resistance & sanitation
Fungal spores survive: 12 months–2 years
Disinfection: Sodium hypochlorite, Peracetic acid, NaOH, Formalin, Ethanol
Use of acids for disinfection
Inorganic acids: Hydrochloric acid, Sulphuric acid, Nitric acid, Phosphoric acid
Organic acids: Peracetic acid, Virkon-S
Public health risk assessment
Many mycoses are zoonotic. Transmission mainly through:
Direct animal contact, Spores in environment, Contaminated dust/hair/soil
High risk for:
* Immunocompromised people, Veterinarians, Animal handlers.
