Block 2 Flashcards

Question

Staphylococcus aureus Staphylococcal Toxic Shock Syndrome (TSS) what is it who gets it what causes it CS

Answer 1

* TSS of HUMANS * Caused by **superantigens** entering the bloodstream -improper blinding of MHC II molecules--extreme T cell proliferation an drelaeast of cycotine--nausia, vomiting, fever, shock and posibly death * CS: * Fever, headache, vomiting, diarrhea * Reddening of the conjunctiva, hypotension (low blood pressure), skin rashes, kidney failure * Can ultimately result in death

Answer 2

Food poisoning * Caused by eating food that Staphylococcus aures has multiplied and produced enterotoxins in *** Enterotoxins:** type of heat stable exotoxin, destroys cells and tissue (food poisoning) * CS: Nausea, vomiting, abdominal cramps, diarrhea, sweating

Answer 3

Dogs and Cats * Most common opportunistic pathogen in dogs that is involved in a wide range of purulent diseases * This bacteria is always “hanging out” on dogs and cats * Pyodermas, otitis externa, wound infections, UTI, vaginitis, balanitis, conjunctivitis, bacteremia, abscesses * Otitis externa: bacterial infection is secondary * Primary causes: food allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases * Fix/treat the primary cause first and then treat for the bacteria! * Pyoderma: usually due to overgrowth of the normal skin microbiota -most always growth negative * Can be other bacteria involved, but usually S. pseudintermedius * Primary causes: allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases * Fix/treat the primary cause first and then treat for the bacteria! * Tx: antimicrobial shampoo, topical antibiotics, use narrow-spectrum, 2% Mupirocin ointment * Prevention: grooming and maintaining the hair coat * S. pseudointermedius can be carried on human skin, but is is **NOT zoonotic** * MRSP: Methicillin resistance in S. pseudintermedis at.geeapersonisuersinterdermalnsimiartoAncylostoma d opportunistic

Answer 4

*you have a note on the slide, I cannot read it. slide 7 * Otitis externa: bacterial infection is secondary * Primary causes: food allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases * Fix/treat the primary cause first and then treat for the bacteria!

Answer 5

* Pyoderma: usually due to overgrowth of the normal skin microbiota -most always growth negative * Can be other bacteria involved, but usually S. pseudintermedius * Primary causes: allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases * Fix/treat the primary cause first and then treat for the bacteria! * Tx: antimicrobial shampoo, topical antibiotics, use narrow-spectrum, 2% Mupirocin ointment * Prevention: grooming and maintaining the hair coat

Answer 6

S. pseudointermedius can be carried on human skin, but is is **NOT zoonotic**

Answer 7

* MRSP: Methicillin resistance in S. pseudintermedis

Answer 8

GREASY PIG DISEASE * **Highly contagious** exudative epidermitis affecting **pigs up to 3 mo**. of age (suckling and weaning aged) adult pigs are carriers but not affected. * Excessive sebaceous secretion from skin (greasy looking), anorexia, depression, fever *no pus * **High morbidity (up to 100%) and high mortality (up to 90%)** * N**ormal commensal of adult pigs in the vaginal mucosa and skin of sows or preputial diverticulum of boars** * Does NOT cause disease in adult pigs because they develop immunity with age * The bacteria enters the via **skin lesions** like bite wounds from piglets nipping at each other * Tx: isolate infected pigs and treat with antibiotics, clean and disinfect contaminated building * Prevention: clip needle teeth, hygiene and management (soft bedding)

Answer 9

* Gram pos., cocci in chains, catalase neg., **facultative anaerobe**, non-motile, fastidious growth

Answer 10

Catalase can be used to tell the different between Staphylococcus and Streptococcus

Answer 11

Commensals (normal residents) of the **mucous membranes** and does not survive well in the environment * Upper respiratory tract and lower urogenital tract * Exception: Streptococcus equi subsp. equi is NOT a commensal

Answer 12

Primary pathogenic (usually species specific) or opportunistic infections, in humans and animals * Suppurative or pus filled lesions, systemic infection (septicemia), infections in the adjacent throat/LN, chronic mastitis, or pneumonia

Answer 13

Types of hemolysis: **BAG** * Beta-hemolytic (complete lysis) , Alpha-hemolytic (partial hemolysis), Gamma-hemolytic (no hemolysis) * **Lancefield classification: ONLY FOR STREPTOCOCCUS SPP.** * Latex bead test or ring precipitation test based on cell wall polysaccharide antigen (**groups A-H)**

Answer 14

Virulence factors: **FAME** * Streptokinase and hyaluronidase: invasion of skin (eat away at tissue) * Protein F: adhesion/attachment * M protein: evasion * Exotoxins and lipoteichoic acid *you have a note on this I can't read slide 10

Answer 15

Pathogenesis: bacteria enters into the respiratory tract, multiplication in tonsils/LNs, causes inflammation and abscess formation, and septicemia

Answer 16

substances used to treat a wide variety of infectious diseases in humans and animals. They: kill micro organisms stop micro-organisms from growing and multiplying ex. antibiotics such as ciproflaxacin

Answer 17

the ability of micro-organisms to withstand antimicrobial treatments ex. MRSA commonly presenton human skin and mucous membranes

Answer 18

overuse and misuse of antibiotics. spread through various routes treatment may become ineffective serious risks to public health

Answer 19

b lactamase-mediated resistance common in staphylococcal species

Answer 20

§ Methicillin resistance in S. aureus (MRSA) and S. pseudintermedius (MRSP)

Answer 21

Resistance to b-lactam antibiotics often coincides with resistance to other antibacterial drugs (“multidrug resistance”) e.g. macrolides, aminoglycosides, tetracycline, potentiated sulfa drugs

Answer 22

Methicillin resistance is mediated by mecA gene resulting in altered penicillin binding proteins

Answer 23

Hospital-acquired (HA) infections (nosocomial) and increasing circulation of community acquired (CA) infections by MRSA

Answer 24

Equine Distemper AKA Strangles * **Reportable,** highly contagious febrile disease involving the upper respiratory tract and causes abscessation of the regional LNs **ISOLATE** * Called strangles due to the swelling of the LN causing obstruction of the airway that can result in death * **Enzootic in domestic horses worldwide and all ages are susceptible, but tends to affect yearlings and weanlings (foals are protected by the mares antibodies)** * **High morbidity (up to 100%), low mortality (less than 5%)** * After an infection, most animals **recover spontaneousl**y (about 75%) and have immunity * **NOT a commensal** and is transmitted by carriers or currently infected animals * Via purulent exudate from the respiratory tract or by pus from the abscesses * Direct contact or indirect by contaminated buckets, troughs, stables, flies, grass * Incubation period: 3-6 days * CS: high fever, depression, anorexia, purulent discharge from the nose and eyes * LN lesions: **submandibular (1st affected) and retropharyngeal** LN’s are affected and will eventually rupture/release purulent material that is highly infectious (this pus is what you send to the lab for testing) *WHAT LN's are affected?

Answer 25

COMMON, CONTAGIOUS, CONTROLABLE 4 potential complications of Stranlges * **Guttural pouch empyema:** **abscess ruptures in/towards the guttural pouch,** secondary to upper respiratory tract infection * Stiff head carriage, painful swelling around parotid gland, difficult breathing, BAL is necessary, can result in a carrier * **Bastard strangles: **disseminates or spreads causing **abscesses in other organs**, very rare *** Purpura hemorrhagica**: immune complex mediated vasculitis, very rare *** Asymptomatic carriers**: ID and treat ASAP, there can be long term chronic shedders, testing is important (new horses or horses that were in contact with infected ones)

Answer 26

When an animal is infected, **3 negative cultures** taken at weekly intervals is required to be released from quarantine * Dx: clinical symptoms and culture of pus, ELISA or PCR for **M proteins** * Tx: **drain abscesses** (put Penicillin inside) and relieve pain, can give **antibiotics** but they are **only effective if given before abscess formation** * Vaccination: not completely effective, give inactive vaccine to pregnant mares and foals to keep high levels of anti-M antibodies, live intranasal vaccine * Prevention: stop movement of animals if an infection is suspected, quarantine, hygiene and disinfection

Answer 27

* Causes significant economical losses in the pig industry due to the high fatality rates * **Meningitis, arthritis, septicemia, bronchpneumonia, and possibly endocarditis, neonatal death, or abortion BAMS** * **Nursery disease**: affecting pigs 2-5 weeks post weaning (roughly 5-8 weeks of age) so they are under a high level of stress * **Nearly all pigs are CARRIERS of the bacterial in their tonsils!** * Doesn’t often cause disease, but when it does, the mortality rate is high (around 20%) * There are 35 different serotypes and their antigenicity is based on the capsular polysaccharide * Pigs can carry different serotypes but **serotype 2 **is predominant worldwide (and it has different sequence types) * Predisposing factors: STRESS due to changes in housing, temp. changes, poor ventilation * Tx: penicillin or ampicillin * Prophylaxis: long acting penicillin can be given by injection to sows (1 week before farrowing) and piglets (during the first 2 weeks of life) * Prevention: hygiene and husbandry, decrease stressful predisposing factors * **Emerging zoonotic pathogen:** underreported and underdiagnosed * Most common cause of adult meningitis in Asia and humans are usually infected by consuming raw pork meat or because of occupational hazard On DIRECT CONTACT

Answer 28

Streptococcus agalacticae * CONTAGIOUS MASTITS * Bacteria will colonize in the milk ducts (obligate pathogen), which leads to a persistent infection with intermittent episodes of acute mastitis * Chronic mastitis -IDK what this says "resovict mammary quarter"

Answer 29

Streptococcus dysgalacticae * ENVIRONMENTAL MASTITIS * Bacteria will colonize in the buccal cavity, genitalia, and **skin of the mammary gland (so not inside the gland!)** * Acute mastitis

Answer 30

Streptococcus uberis * ENVIRONMENTAL MASTITS *** Linked to straw bedding** * After a night out, “Uber” home and get in “bed" * Bacteria will colonize on the skin, tonsils, and vaginal mucosa * Subclincal mastitis

Answer 31

teat dip,clean towel, nutrition, reduce teat trauma Reduce teat injury and trauma * Mastitis is multifactorial: exposure to microorganisms, host defense mechanisms, environmental conditions

Answer 32

Streptococcus euqi subsp. zooepidemicus * **Opportunistic pathogen of many species (horses, cattle, dogs, lambs, pigs)** * Commensal of mucous membranes * Purulent infections: respiratory tract infections, pneumonia, mastitis, navel infections, foal septicemia * **Emerging zoonotic pathogen** causing necrotizing myositis and meningitis (in humans)

Answer 33

Streptococcal toxic shock syndrome and necrotizing fasciitis in dogs and cats * Puppies and kittens are the most susceptible * Don’t confuse with TSS of humans from Staphylococcus aereus * Commensal on the skin and mucous membranes * Can get an infection from vagina or umbilical vein which will lead to bacteremia * Septicemia and embolic lesions in heart and lungs

Answer 34

* Affects many species, but is mostly associated with **humans** * **Can cause anything from a mild superficial skin disease to a life- threatening systemic infection** * Localized skin infection with sores/blisters (impetigo), pharyngitis with abscesses on the throat * Can cause streptococcal toxic shock: bacterial infection with toxin production, destruction of skin/fat/muscles * **Flesh eating bacteria:** necrotizing fasciitis * Rare but serious and potentially deadly * Rheumatic fever or glomerulonephritis are examples of non-pyogenic diseases

Answer 35

Overview * Gram pos., **diploccoci (PAIRS)** facultative anaerobes, catalase neg., can be motile (but not many) * Enterococcus is tested for in water: drinking, beaches, pools * Commensals of the GI tract in animals and humans so they are opportunistic! **ENTEROCYTES=CELLS OF SI** * Low grade pathogens found in general wound infections and UTI’s * **Fecal transmission** is the key for spreading * Antimicrobial resistance: * Naturally resistant to many antimicrobials like cephalosporins for examples * **VRE: Vancomycin resistant enterococcus** * Acquired resistance

Answer 36

Wound infections * Secondary mastitis in cattle * **UTI** and ear infections in dogs * Nosocomial infections *-faecalis/faecium-like fecal b/c fecal transition*

Answer 37

Gram pos., coccobacillary rods (short/thick rods), catalase pos., oxidase neg., facultative anaerobe

Answer 38

Psychrophilic (grows in cold), most species have **tumbling motility at 25oC**, tolerate a pH between 5.5-9.6 (acid, neutral, or basic) *-what psycho likes the cold*

Answer 39

no, animal is too warm

Answer 40

**Commensals **(normal residents) of the the mammalian **GI tract **in low numbers and found throughout the **environment** (especially soil) * Resistant to harsh environments due to the wide temp. range; can be found in herbage, feces, sewage and water

Answer 41

Pathogenesis: ruminants are the most susceptible * Uptake via inhalation: goes to trigeminal n. and causes encephalitis (most common presentation in ruminants) * Uptake via ingestion: absorbed through the intestinal wall and into the blood stream, hematogenous spread

Answer 42

rarely overlap **Encephalitis**-seen in very young rumenants **Septicemia** (common with monogastrics), multifocal miliary abscesses, can affect multiple organs but we commonly see lesions in the liver or kidney **Most common in rumenants** *** Abortion:** fetal hepatic necrosis

Answer 43

Virulence factors: * Internalin A: adhesion to enterocytes * Internalin B: adhesion to hepatocytes * Listeriolysin O (LLO): pore formation to break the membrane of the phagosome for escape * ActA protein: actin-polymerizing protein, pushes bacteria to the side of the cell wall * Phospholipase C enzymes: helps degrade membranes so Listeria can progress through cells *can invade phagocytes and non-phagocytes

Answer 44

Pathogenicity: * The bacteria can replicate inside **ANY** cell causing cell death and micro- abscesses to form *** Facultative intracellular** persisting in macrophages which allows for the bacteria to move from one host cell to the next * The bacteria is up taken by a phagocyte, formation of a **phagosome**, bacteria will escape *(LLO*), multiplication, then the Actin tail pushes the bacteria to the side of the cell and helps propel it into the adjacent cell via pseudopod * **This process allows the bacteria to travel without being exposed to the humoral defense mechanisms** *escapes phagasome... something about lysome fusion slide 20*

Answer 45

yes -d*rinking lysterine makes your heart spin* ?

Answer 46

Circling disease or Silage disease * Economically important disease causing **encephalitis in ruminants** due to poor silage quality * Mostly seen from **winter-spring** and is associated with **decreased acidic pH of soiled silage** which allows for high multiplication of bacteria- **outbreak and clinical signs usually seen around 10 days after ingestion** * Transmission: ingestion, inhalation, or through breaks in the oral or nasal mucosa * CS due to CNS lesions: anorexia, depression, disorientation, dullness, **turning/twisting of the head to one side, walking in circles TORWARDS the affected side, UNILATERAL trigeminal and facial n. paralysis** (drooping ear, deviated muzzle, droopy eyelid), nystagmus, head pressing, purulent unilateral endophthalmitis * Dx: anti-mortem vs. post-mortem * Anti-mortem: symptoms and history (new batch of silage?),season, silage quality * Post-mortem: look for lesions in **the brainstem like** micro-abscesses, meningitis, vascular and/or neuronal necrosis * Have to use an enrichment culture and histology is important! * Q. Will a blood sample be helpful? **NO IT IS SHORT LIVED IN THE BLOOD** * Can potentially see necrosis or inflammation in the liver and spleen, test abomasal content if there was an abortion *-ONCE ? CAN'T TREAT NO VALL*

Answer 47

* Gram pos., small rods or filaments, facultative anaerobes, non-motile, **catalase neg.,** oxidase neg. * Commensals (normal residents) of the tonsils and intestines of many animal species * **Even present in the slime-layer of fish which is a common source for human infection** *-Ares is all talk (tonsils) and a slimeball (fish slime) -same as strep suis*

Answer 48

Pigs: most important reservoir, up to 50% of all healthy pigs will harbor E. rhusiopathiae in their tonsils * Carrier pigs will excrete bacteria in the feces and/or the oronasal secretions * Very resistant in the environment and under harsh conditions * There are 26 serotypes with 1a, 1b, and 2 being common in pigs * Transmitted: ingestion (fecal-oral route) * Virulence factors: * Polysaccharide capsule: allows for intracellular replication and protection against phagocytosis * **Neuraminidase: adhesion and invasion of endothelial cells by cleaving sialic acid** * Leads to vascular damage which leads to thrombus formation * Hyaluronidase: dissemination or spread of bacteria within tissues * spaA surface protein: adhesion * Can cause septicemia, dermatopathy, arthritis, and valvular endocarditis,

Answer 49

Commensal of the tonsils, **pigs between 3 months and 1 year of age are the most susceptible** * Under 3 months: protected by maternal antibodies * 1-3 years: building protective active immunity by being exposed to low virulent strains * STRESS can trigger clinical erysipelas (infection of the top layers of skin) * 3 forms: * Acute form: sudden death (within 48 hours), fever, stiff gait/walking on toes, seclusion from the group, anorexia, skin lesions * Subacute form: inappetence, mild fever, skin lesions * Chronic form: may follow the subacute form, **arthritis, endocarditis, polyarthritis, and skin lesions** * **Diamond-shaped skin lesions are pathognomonic for swine erysipelas, so these lesions are diagnostic!** * Dx: skin lesions, culture (difficult to recover bacteria), PCR * Tx: can treat the acute form if the pig survives by isolation and antimicrobials, cull animals with chronic infection * **Resistance to vancomycin, aminoglycosides, sulfonamides** * Prevention: hygiene and management, vaccination before breeding * Vaccinate boars every 6 months and sows 3-4 weeks before farrowing

Answer 50

Erysipelothrix rhusiopathiae in turkeys * Economically important disease worldwide that affects turkey of all ages * 2 forms: * Acute form: septicemia, sudden death * Chronic form: endocarditis, gradual weight loss

Answer 51

* Non-suppurative polyarthritis (no pus, arthritis in multiple joints) * Bacteria enters through umbilicus, castration wounds, or skin abrasions * Post-dipping lameness is due to cellulitis and laminitis in older lambs

Answer 52

Erysipelothrix rhusiopathiae in humans *** Occupational hazard** by working with fish, poultry, and swine * Commensal of the slime layer of fish *not eaten * **Enters through skin abrasions** and causes localized cellulitis on fingers, diffuse skin infection, septicemia