Blastomyces dermatitidis

- Eastern and central US

- natural reservoir in soil

- in dogs and humans, sometimes siamese cats

- inhalation of conidia

- grows in lung in yeast form, spread via hematogenous

- bone can become infected

- chronic cough, shortness of breath

-  Dx by culture

- Tx antifungal agents

- frequently will recur

Histoplasma capsulatum

- midwestern US

- in soil, associated with bird and bat droppings

- conidia are inhaled, yeast form grows in lungs

- granuloma formation, disease similar to blastomyces

Coccidioides immitis

- in hot desert soils of Southwest US

- " Valley Fever"

- inhalation of arthroconidia

- in sheep, cattle, dogs, and humans

- fatal

- lymph nodes- granulomas, can go to liver, brain, spleen, bones and kidneys

Aspergillus

opportunistis mycoses

A. fumigatus

- most common in poultry and caged birds, sheep, calves and horses also involved

- can cause abortions

- inhalation of conidia

- grow in animal as hyphae

- hematogenous spread-inflammation of bld vessel, emboil

- blood stained sputum-frequently observed

-can cause hypersensitivity reactions

- AFLATOXINS--cause necrosis, cirrhosis, carcinomas in liver---don't sniff on a plate!

Candida

opportunistic myocoses

Candida albicans

-yeast form infective and found in animals

-starts as commensal-->overgrowth-->cutaneous mucosal surfaces- GI and genital, can become systemic

- also normal flora of oral cavity, GI, and genital tracts

- immunosuppressed individuals predisposed

- Virulence factors: adhesins, extracellular proteases, lipases/phospholipases

-white stuff on tongue!

Crytpococcus neoformans

- in pigeon droppings

- in soil as mold form, yeast form is in infections, capsule

required for disease

- inhalation of mold form, or direct invasion of skin poss.

- hematogenous spread

- DOGS AND CATS infection in pharynx and paranasal sinuses

- lesion on head and neck

-CNS common site, low MW nitrogen containing compounds needed for growth

- little inflammation, capsule in tissue-inhibits phagocytosis

-produces melanin--protects fungal cells

Streptococcus

-Gram (+), facultative anaerobe, chains of cocci

-catalase (-)

-opportunistic pathogen by commensal microflora and cause suppurative infection

Streptococcus

Pathogenesis:
-Capsule - hyaluronic acid (a polysaccharide polymer)
-Complex, heterogeneous, dynamic cell envelope
-Surface fibrils for host cell attachment (M protein)
-easily spread thru tissues due to Streptokinase which digests fibrin cots and inhibits walling off of bacteria
-produce cytotoxins—streptolysins, form membrane pores and lyse PMN’s
-but doesn’t survive within phagocyte, inhibits uptake via M protein and hyaluronic capsules

Streptococcus

Virulence Factors—Insoluble:adhesins

- F protein and M protein

Streptococcus agalactiae (C)

-common cause of bovine mastitis, colonize milk duct, persistent infection

-Beta hemolytic

-treat with antibiotics parenteral or intrammammary route

Streptococcus zooepidemicus (C)

-commensal in many animal species

-Most common cause of wound infections in horses

-can localize to joints and cause stiffness and pain

-Frequently a 2ndary invader following URI in young foals

Streptococcus equisimilis (C)

-freq cause of suppurative arthritis in young pigs

-transmitted from genital tract of sow thru umbilicus

-Causes: anorexia, fever, swelling of joints, lameness

-important in horses

-suppurative infection of the URT and draining lymph nodes

-very contagious

Transmission: horse to horse via oral/nasal, ingestion, inhalation

Multiplication and spread: attaches to epithelial cells after entry via oropharynx, invades thru mucosa, spread via lymph (submandibular and retropharyngeal) causing abscess formation

-streptolysins kill phagocytes, and Hyaluronic acid capsules and M proteins are antiphagocytic factors

Clinical signs: about 3-14 days post exposure

-loss of appetite, fever, purulent nasal discharge, pharyngeal area is painful, pharyngeal swelling--inflammation is so bad it obstructs the airway it causes noisy, rapid, dyspnea---“Strangles”

Treatment: Penicllin, drain lymph nodes

Streptococcus Suis (D)

* zoonotic in pig farmers—meinigitis, vertigo, permanent hearing loss

-causes meningitis and septicemia in young pigs

-colonize the tonsils, nasal mucosa

-predisposing overcrowding in cold weather and poor ventilation

-Type 1 in baby pigs, more invasive

-Type 2 in older pigs

Treatment: Penicillin

Condidia

(Macro or Micro in Dermatophytosis)

Chlamydia felis

-Gram negative rod

-causes conjunctivitis in cats, pneumonitis in kittens

Chlamydia psittaci

- gram negative rod

- causes anorexia, depression, nasal and ocular discharge, greenish yellow diarrhea in Turkeys!

- Necropsy: lung congestion, air sacculitis, pericarditis, hepatomegaly, spleenomegaly

- # 1 zoonotic problem in Turkeys

- people inhale dust/ aerosol droplets

Chlamydia abortus and Chlamydia pecorum

- enzootic abortion in sheep

- damage of placenta causes late stage abortion in sheep, retained placenta, vaginal discharge, fever, thick and clay colored cotolydons

- can also cause polyarthritis in sheep

-lambs can get pneumonia and CNS disease

R. rickettsia

- Causes Rocky Mountain Spotted Fever

- dogs and humans

- Clinical Signs: high fever, hemorrhagic mm's, painful joints and lymph nodes, CNS sxs, Kidney and heart failure

Coxiella burnetti

- Causes Q fever

- Ruminants and humans

- inhale, ingest, or arthropod (tick bite)

- can be in mammary gland (zoonotic) up to 32 months

- can cause abortions

Rickettsia

pathogenesis

- hematogenous entry

- proliferates in endothelial cells and phagocytes

- escapes the phagolysosome

- causes cell lysis resulting in vascular damage

Coxiella

Pathogenesis

- hematogenous entry

- proliferates in endothelial cells and phagocytes

- proliferates in phagolysosome

- causes cell lysis resulting in vascular damage

Ehrlichia canis

- monocytic ehrlichiosis

- long incubation up to 3 weeks, remain carriers 29 mths

- fever, thrombocytopenia, leukopenia, anemia

Neorickettsia helminthoeca

- salmon poisoning disease

- from liver fluke infestation of nanophytes salmoncola

Anaplasma marginale

- bovine anaplasmosis

- can see anaplasma in RBCs it forms an occlusion along the margin of the cell

Mycoplasm hyopneumoniae

Gram (-)

Sxs: dry hacking cough, few mortality, 25-30% morbidity,  slow growth rate

- lesions are cranioventral in lung—primary infection

- bacteria adhere to tracheal cilia & destroy via oxidases

-stimulates cytokines and draws in immune cells, causes peribronchilymphocytic hyperplasia, the nodules around the bronchi compress the

Sampling: from lung, tracheal/bronchial swabs, nasal swabs

Transmission: spread in the air

Mycoplasm hyopneumoniae

Testing: PCR to check for antigen look for mycoplasm DNA in sample or ELISA shows exposure not if the animal has developed immunity or not.

Treatment: Macrolides (lincomycin) to inhibit protein synthesis, prevent with vaccine or decrease severity of infection.

Brachyspira hyodysentarie

-Gram (-) spirochete, obligate anaerobe but oxygen tolerant

- “Swine Dysentery”

- pig with bloody diarrhea, results in death or chronic form of inflammation of mucosa of LI, cecum, and rectum, stops at the ileocecal junction, edematous colon, petechia in mucosa only affecting the Large intestines---results in malabsorption disease

Transmission: fecal/oral, fomites, mice, flies?

 Brachyspira Hyodysentariae

Sampling: feces, fixed tissue and fresh

Treatment: Macrolides---lincomyci, NO vaccine

-clean swine lagoon pits

Mycobacteria

-Gram aerobic (+) rod shaped bacteria

-acid fast bacillus within macrophages on stain, saprophytic and pathogenic lifestyles

- has outer mycolic acid in their cell wall  with a little peptidogylcan

-outer mycolic acid retains acid fast stain, and give protection and resistance

Mycobacterium bovis *zoonotic

-causes bovine tuberculosis

-natural reservoirs are captive elk, deer, bison

-pasteurization may not kill organism

Transmission: most common-- Inhale, ingest

-Organism disseminates via lymph and lodges in lungs, spleen, liver

-Localized lesions of lymph nodes of the head and lungs are also noted

-Progression is slow and requires 1-5 years before clinical

signs become apparent.

Mycobacterium bovis

Clincal Signs: appear in late stage disease coughing, emaciation, dyspnea, increased respiration, nodules on organs

Mycobacterium bovis

Diagnose: culture or impression smear

Tuberculin skin test—caudal fold test followed by comparative cervical test

-          Type IV hypersensitivity reaction

Treatment: none for cattle because it is zoonotic, depopulate

Mycobacterium avium subspecies paratuberculosis

- Causes Johne’s Disease

- in domestic ruminants, wildlife, and possibly humans (Chron’s disease)

-stimulates growth in the intestines causing malabsorption of nutrients

Mycobacterium avium subspecies paratuberculosis

Transmission: Ingestion of contaminated feces is the highest form of transmission but also shed in milk, urine, and semen

Clinical Signs: Takes 1-3yr progression of disease to see CS

– Thickening of the intestinal wall due to epithelial cell proliferation

–SEVERE WEIGHT LOSS, Emaciation despite normal appetite

– Swelling of regional lymph nodes (org within macrophages)

--Lymph nodes show caseous necrosis in goats

– Coat becomes dry and rough

– “Bottle jaw”, a mandibular edema caused by protein loss

– Chronic or intermittent diarrhea

Mycobacterium avium subspecies paratuberculosis

Diagnosis: Fecal culture, Serum ELISA, DTH test using johnin, but don’t see accuracy until late stage

Treatment: NONE, depopulate due to poss zoonotic

Clostridium perfringens

lamb dysentery

pulpy kidney disease (enterotoxemia/overeating disease)

spore forming Gram (+)

-Causes Gas gangrene

-Yellow Lamb Disease

-depression, pale mucous membranes, anemia, icterus, hemoglobinuria, death 6-12hrs of sxs

-Lamb dysentery

-Pulpy kidney disease—enterotoxemia in sheep and goats, caused by epsilon toxi

-free living in the soil and commensals in GI and oral cavity

In ruminants

-Blackleg (myositis, gas gangrene), muscle necrosis

-in the soil, either thru open wound or ingestion, or as teeth are lost in young cattle

-tissue damage due to alpha toxin

Treatment/control: vaccination and penicillin

Diagnosis: FA of tissue

-Malignant edema in sheep

-tissue invading, tissues are filled with gelatinous exudates (dissolved muscle and connective tissue)

-no gas produced

Diagnosis: FA of tissue

Treatment/control: Vaccine and penicillin

-Red Water Disease—bacillary hemoglobinuria

-associated with liver infarcts from liver flukes

Diagnosis: FA of liver

Treatment: eliminate liver flukes/snails, vaccinate, penicillin

-Gas gangrene in man, cattle, and sheep and “Big head” in rams caused by butting

-Black disease (infectious necrotic hepatitis)

-organism in soil and in the intestinal tract of herbivores

Diagnosis: FA of liver

Treatment: Eliminate flukes, snails, vaccination

-ulcerative enteritis or quail disease

- occurs in birds, quail

-natural infection via oral route

-lodges in liver—diffuse necrosis

- entertoxemia of rabbits and lab rodents

-antibiotic associated

-cecum is massively dilated

-pseudomembranous enterocolitis, due to pseudomembrane plaques on the colonic mucosa

-lab animals –guinea pigs

-Antibiotic associated

Diagnosis: toxins ELISA test

Treatment: Vancomycin

******Gram (-) spore forming*********

-Tyzzer’s disease

- in rodents, due to stress

Diagnosis: Organism in gram stain, liver lesions

Treatment: broad-spectrum antibiotics in the liver

-tetanus—lock jaw

-horse and man

-in horse—infection thru the soil, wound

-toxins: tetamolysin, tetanospasmin--neurotoxin, non-spasminogenic toxin

Diagnosis: spores and clinical signs

Treatment: vaccine or penicillin, active immunization with toxoid

-horse and man esp.

-preformed toxin

Diagnosis: toxin assay

Treatment: antitoxin

 Fusobacterium necrophorum

-Gram (-) anaerobic rod, non spore forming

-foot rot in cattle

-predisoposing factors: warm wet weather, injury to interdigital skin, overgrown hooves

-from intestinal tract or lesion

- Gram (-), anaerobic rod, non-spore forming

-obligate parasite of hooves of ruminants esp sheep

-predisposing factors

Bacteroides (prevotella) melaninogenicus

-normal flora of human oral cavity

-intestinal flora

-in cattle, sheep, dogs, and cats

-causes suppurative lesions

Bacteroides Fragilis

-in humans mostly

-causes abscesses

-resists oxygen

- gram (+), facultative anaerobe, produces capsules

-normal commensals of skin/mucosal surfaces

-catalase (+)

- pus forming, hallmark of clinical manifestation is abscess, invasion into deeper tissue can cause pneumonia, osteomyelitis, meningitis, arthritis, endocariditis

-common cause of mastitis in cattle, TSS in humans and food poisoning

-coagulase allows clotting of blood and protection of organism, hemolysis phenotype used for speciation

-grow/stimulate growth of biofilms—Protein A

Multiplication and spread:

-resistant to phagocytosis, intracellular survival in phagocytes, adhesion to epithelial cells, Protein A and polyuronic acid capsules, Coagulase & hylauronidase production, hydrolases, toxin production-staphylococcal leucocidin kill leukocytes

-abscess formation due to dead neutrophils phagocytes releasing enzymes propagates inflammatory cascade

-gram (+), catalase (+)

-suppurative lesion of mammary glands in cattle

-opportunistic pathogen

Stapylococcus hyicus

-exudative epidermitis in swine “greasy pig disease”

-highly contagious in pigs 1-7wks old

Transmission: via skin lacerations from fighting bite wounds

Clinical signs: skin is covered in moist greasy exudates, skin is thickened and sloughed off

Morbidity and mortality are highly variable

Virulence factors: exfoliatoxin, lipase, hylaurondiase

Treatment: Tylosin

Aerobic Gram Positive Rods

Bacillus

Corynebacterium

Rhodococcus

Listeria

Erysipelothrix

Bacillus anthracis

- Large aerobic gram positive rod

- produces endospores, looks like non staining areas in rods

- has capsule helps ressist phagocytosis

- soil organism, likes alkaline high nitrogen soil

Bacillus Anthracis

Toxins: Holo toxin

-edema factor: increases vascular permeability

- protective antigen: helps binding to host cell

- lethal factor: depresses CNS, causes quick sudden death, go into shock

Corynebacterium psuedotuberculosis

- caseous lymphadenitis in goats (and sheep) ulcerative lymphadenitis in horses

-abscess of jaw of goat and pectoral of horse

- disease via sheering sheep

Transmission:

-via open wound, because normal commensal

Corynebacterium pseudotuberculosis

Toxins:

-phospholipase D: increases vascular permeability

- pyrogenic factor: traps leukocytes

-surface lipid: decreases phagocytosis ( toxic to phagocytes)

- lives in urinary tract, commensal  organism

- cows can handle it but no when pregnant and immunosuppressed

-causes cystitis and pyonephritis

Treatment: NO vaccine, Penicillin

-soil organism, spread by inhalation, causes abscesses, suppurative bronchopneumonia  in lungs of foals

- some maternal protection but foals get sick once this decreases

Sample: via tracheal lavage

-causes meningioencephalitis or “circling disease”

-intracellular parasite of macrophages

- oral ingestion of high alkaline silage with a pH of 5.0 or greater, found in the soil

-systemic diseasesà migrates to cranial nerves up trigeminal ganglion causes CNS sxs—circling

-can cause abortion in ruminants because it collects in placentomes, causes retained placenta

-ingestion of infected milk or Ice cream in people, puppies drank human breast milk from a woman

-in swine mostly—“diamond skin disease”—acute lesions

-causes red, raised lesions (erythematus), high fever, sudden death, spleenomegaly

-causes arthritis and valvular vegetative endocarditis if they survive (chronic form)

Transmission: Nose to Nose contact

Sampling: the organism is found in the tonsils (carriers) and spleen, can sample these

Treatment: penicillin, Antiserum, vaccine