Micro (Gram +) Flashcards by Meghan May

Which Staphylococci are Novobiocin resistant? Which are sensitive?

What Streptoocci are Opticin sensitive and resistant? What about Bacitracin?

” On the office’s “staph” retreat, there was NO StRESs. : NOvobiocin—Saprophyticus is Resistant; Epidermidis is Sensitive.

OVRPS (overpass). Optochin—Viridans is Resistant; Pneumoniae is Sensitive

B-BRAS: Bacitracin—group B strep are Resistant; group A strep are Sensitive.

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What organisms are α-hemolytic bacteria

Form green ring around colonies on blood agar A . Include the following organisms: Streptococcus pneumoniae (catalase ⊝ and optochin sensitive)
Viridans streptococci (catalase ⊝ and optochin resistant)

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What bugs are B hemolytic

Staphylococcus aureus (catalase and coagulase ⊕)
Streptococcus pyogenes—group A strep (catalase ⊝ and bacitracin sensitive)
Streptococcus agalactiae—group B strep (catalase ⊝ and bacitracin resistant)
Listeria monocytogenes (tumbling motility, meningitis in newborns, unpasteurized milk)

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Gram + bacteria. Has a Protein A virulence factor taht binds Fc-IgG and inhibits complementa activation. Lives in Nose

What diseases does it cause?

Staph. Aureus

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You and your roomate come back from a lunch hosted by school and both start vomitting profusely. Ingestion of what preformed toxin would cuase that rapid of onset?

S. aureus food poisoning due to ingestion of preformed toxin–>short incubation period (2–6 hr) followed by nonbloody diarrhea and emesis. Enterotoxin is heat stable not destroyed by cooking.

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A teamate of yours was playing soccer and got elbowed right in the nose. The trainer packed his nose and has him ice to help with the swelling. The next day at school your buddy wasn’t there and you were told he was taken to the ER last night- he has a fever of 101 and was vomitting and covered in a rash. What bug is responsible and what is the mechanism responsible for the pts symptoms

TSST is a superantigen that binds to MHC II and T-cell receptor, resulting in polyclonal T-cell activation. Staphylococcal toxic shock syndrome (TSS) presents as fever, vomiting, rash, desquamation, shock, end-organ failure. Associated with prolonged use of vaginal tampons or nasal packing. Compare with Streptococcus pyogenes TSS (a toxic shock– like syndrome associated with painful skin infection).

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Infects prosthetic devices (e.g., hip implant, heart valve) and intravenous catheters by producing adherent biofilms. Component of normal skin flora; contaminates blood cultures. Novobiocin sensitive.

Staph. Epidermidis: Gram +, Catalase +, Coag - and Novobiocin resistant

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Second most common cause of uncomplicated UTI in young women (first is E. coli). Novobiocin resistant.

Staphy. Saphrophiticus

Gram +, Coag +, Cat -, Novo resistant (Cow don’t get UTIs)

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Strep. Pneumo is implicated in many common disesase: which are they?

What does this bug look like?

S. pneumoniae MOPS are Most OPtochin Sensitive.

Meningitis, Otitis Media, Pneumonaie, Sinusitis

Lancet-shaped, gram-positive diplococci: Encapsulated. IgA protease.

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You are treating a little boy that is in the office becaues his mother says his H.influenza virus “is back”. He was in the week before and tested + for H.flu, was given antiB and sent home. Your PE is significant for diffuse lobar consolidation on both sides as well as rusty sputum which he coughed on your face.

What is the Dx?

What’s the key virulence factor?

Streptococcus pneumoniae

pneumococcus is associated with “rusty” sputum, sepsis in sickle cell disease and splenectomy.

No virulence without capsule.

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α-hemolytic. They are normal flora of the oropharynx that cause dental caries (Streptococcus mutans) and subacute bacterial endocarditis at damaged heart valves (S. sanguinis). Resistant to optochin, differentiating them from

S. pneumoniae, which is α-hemolytic but is optochin sensitive

Viridans group streptococci

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Pneumonics to remember the Viridians group streptococci

Sanguinis = blood. Think, “there is lots of blood in the heart” (endocarditis).

S. sanguinis makes dextrans, which bind to fibrin-platelet aggregates on damaged heart valves.

Viridans group strep live in the mouth because they are not afraid of-the-chin (op-to-chin resistant).

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Group A Strep.Pyogenes causes many diseases, name as many as you can:

Pyogenic—pharyngitis, cellulitis, impetigo, erysipelas
Toxigenic—scarlet fever, toxic shock–like syndrome, necrotizing fasciitis
Immunologic— rheumatic fever, acute glomerulonephritis

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Bacitracin sensitive, β-hemolytic, pyrrolidonyl arylamidase (PYR) ⊕.

What bacteria does this describe

Streptococcus pyogenes (group A streptococci)

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Antibodies to ________ enhance host defenses against S. pyogenes but can give rise to rheumatic fever.

_______detects recent S. pyogenes infection.

M protein

ASO titer

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Little boy comes to the office with a diffuse rash on his face as seen below

What bacteria is responsible for this?

What other skin associations are associated?

Streptococcus pyogenes (group A streptococci)

pharyngitis, cellulitis, impetigo, erysipelas

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Little girls comes to the office with her mother who is very concerned as she said her daughter has been recently peeing blood. Her daughter has a bad sore throat a few days before. What bacteria is involved?

titers would be elevated in this patient?

Streptococcus pyogenes (group A streptococci)

ASO titer detects recent S. pyogenes infection.

Pharyngitis can result in rheumatic “phever” and glomerulonephritis.

Impetigo more commonly precedes glomerulonephritis than pharyngitis.

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Little boy comes in with a rash all over his body, rough texture. On PE you see a strawberry tongue. What bacteria is responsible? What other body systems may become involved?

Streptococcus pyogenes (group A streptococci)

may see subsequent desquamation and glomerulonephritis

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What are the Jones criteria?

Is be bactiera Bacitracin resistant or sensitive?

J♥NES (major criteria for acute rheumatic fever):

Joints—polyarthritis ♥—carditis–Nodules (subcutaneous) Erythema marginatum Sydenham chorea

Streptococcus pyogenes (group A streptococci)

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Screen pregnant women at 35–37 weeks of gestation. Patients with ⊕ culture receive intrapartum penicillin prophylaxis

Streptococcus agalactiae (group B streptococci)

–Group B for Babies!

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Bacitracin resistant, β-hemolytic, colonizes vagina; causes pneumonia, meningitis, and sepsis, mainly in babies.

Streptococcus agalactiae (group B streptococci)

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What is the mechanism of action of infection of Group B strep?

Produces CAMP factor, which enlarges the area of hemolysis formed by S. aureus. (Note: CAMP stands for the authors of the test, not cyclic AMP.) Hippurate test ⊕.

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are normal colonic flora that are penicillin G resistant and cause UTI, biliary tract infections, and subacute endocarditis (following GI/GU procedures).

Enterococci (E. faecalis and E. faecium)

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________ is based on differences in the C carbohydrate on the bacterial cell wall. Variable hemolysis.

VRE (vancomycin-resistant enterococci) are an important cause of _______

Lancefield grouping

nosocomial infection.

hardier than nonenterococcal group D, **can grow in 6.5% NaCl and bile** (lab test). Entero = intestine, faecalis = feces, strepto = twisted (chains), coccus = berry.

Enterococci

Colonizes the gut and can cause bacteremia and subacute endocarditis and is associated with colon cancer.

**S. gallolyticus** (S. bovis biotype 1) *_Bovis in the blood = cancer in the colon_*.

Symptoms include pseudomembranous pharyngitis (grayish-white membrane A ) with lymphadenopathy, myocarditis, and arrhythmias. Dx and method of disease

Causes _diphtheria via exotoxin_ encoded **by β-prophage**. Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2.

Lab diagnosis based on **gram-positive rods** with metachromatic (blue and red) granules and **⊕ Elek test for toxin.**

Corynebacterium diphtheriae

What are the ABCDEFG of Corynebacterium diphtheriae

**A**DP-ribosylation **β**-prophage **C**orynebacterium **D**iphtheriae **E**longation **F**actor 2 **G**ranules

What are the benefits to spores and

Some bacteria can form spores at the end of the stationary phase when nutrients are limited. Spores are **highly resistant to heat and chemicals**. Have **_dipicolinic acid_** in their core. Have no metabolic activity. Must autoclave to potentially kill spores (as is done to surgical equipment) by steaming at 121°C for 15 minutes.

What disease is associated with the following bacteria that produce spores? Bacillus anthracis Bacillus cereus Clostridium botulinum Clostridium difficile

Bacillus anthracis: Anthrax Bacillus cereus: Food Poisoning Clostridium botulinum : Botulism Clostridium difficile : Antibiotic-associated colitis

What disease is associated with the following diseases Clostridium perfringens Clostridium tetani Coxiella burnetii

Clostriudium Perfringen : Gas Gangrene Clostridium tetani: Tetanus Coxiella burnetii: Q fever

Produces **_tetanospasmin_**, an exotoxin causing tetanus. Tetanus toxin (and botulinum toxin) are proteases that cleave SNARE proteins for neurotransmitters. Blocks release of inhibitory neurotransmitters, GABA and glycine, from Renshaw cells in spinal cord. Causes spastic paralysis, trismus (lockjaw), risus sardonicus (raised eyebrows and open grin). How do we treat this?

_Prevent_ with *tetanus vaccine*. Treat with _antitoxin +/− vaccine booster_, **diazepam** (for muscle spasms). \*Gram-positive, spore-forming, obligate anaerobic bacilli.

Gram-positive, spore-forming, obligate _anaerobic bacilli._

C. difficile , C. perfringens ,C. botulinum

Produces a preformed, heat-labile toxin that _inhibits ACh release_ at the neuromuscular junction, causing botulism. In adults, disease is caused by ingestion of \_\_\_\_\_\_\_\_\_\_. In babies, ingestion of spores in honey causes disease (floppy baby syndrome). Treat with \_\_\_\_\_\_

preformed toxin antitoxin (Botulinum is from bad bottles of food and honey (causes a flaccid paralysis)

**Produces α toxin** (lecithinase, a phospholipase) that can c_ause myonecrosis_ (gas gangrene and hemolysis.

**C. perfringens**: Perfringens perforates a gangrenous leg.

Produces 2 toxins. Toxin A, enterotoxin, binds to the brush border of the gut. Toxin B, cytotoxin, causes cytoskeletal disruption via actin depolymerization--\> pseudomembranous colitis --\> diarrhea.

C. difficile

Often 2° to antibiotic use, especially _clindamycin or ampicillin_. Diagnosed by detection one or both toxins in stool by PCR.

C. difficile

Caused by Bacillus anthracis, a gram-positive, spore-forming rod that produces anthrax toxin. The only bacterium with a

polypeptide capsule (contains d-glutamate).

What happens when you inhale antrax?

Inhalation of spores flu-like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis, and shock.

Causes food poisoning. Spores survive cooking rice. Keeping rice warm results in germination of spores and enterotoxin formation. Emetic type usually seen with rice and pasta. Nausea and vomiting **within 1–5 hr.** Caused by cereulide, a preformed toxin. Diarrheal type causes watery, nonbloody diarrhea and GI pain **within 8–18 hr.**

**Bacillus cereus**

_Facultative intracellular microbe_; acquired by *ingestion of unpasteurized dairy* products and *cold deli meats*, via *transplacental transmission*, or by vaginal transmission during birth.

Listeria monocytogenes

How does Listeria avoid antibodies?

Forms “rocket tails” (via actin polymerization) that allow intracellular movement and cell-to-cell spread across cell membranes, thereby avoiding antibody.

Can cause amnionitis, septicemia, and spontaneous abortion in pregnant women; granulomatosis infantiseptica; neonatal meningitis; meningitis in immunocompromised patients; mild gastroenteritis in healthy individuals.

Listeria monocytogenes

Both are Gram Positive anf form long, branching filaments resembing fungi 1. Gram positive **Anaerobe** and not acid fast 2. Gram positive **Aerobe** and acid fast (weak)

1. Actinomyces 2. Nocardia

Gram + anaerobes, not acid fast and are found in normal oral flora. Causes oral/facial abscesses that drain through sinus trats and forms yellow "sulfur granules"

Actinomyces

Gram + Aerobe, Acid Fast (weakly) and found in soil Causes pulmonary infections in immunocompromised and cutaneous infections after trauma in immcucompetent. Tx with **Sulfonomides**

Nocardia

Viral particles isolated from the nasal exudate of a 10 yr male shown to lose their inefectivity once exposed to ether. It can be concluded that the viral particles are most likely:

Enveloped Ether and organic solvents dissolve lipid bilayer that makes up outer viral envelope

1. TB often resistant to drugs 2. pulmonary TB-like symptoms 3. causes disseminated non-TB disease in AIDS; often resistant to mult drugs

Mycobacterium TB M.Kansasii M.Avium-intercellulare (prophy tx with azithromycin)

\_\_\_\_\_ in virulent strains of TB inhibits macrophage maturation and induces release of TNF-alhpa.

Cord factor

What three situations would yield a PPD + test?

current infection with TB Past exposure BCG vaccination

When would individuals test - for PPD? What test is more *specific* then PPD for TB?

If no infection or anergic (steroids, malnutrition, immunocompromised) and in sarcoidosis Interferon Gamma release assay (IGRA) is more specific; has fewer false + from BCG vaccination

Compare and Contrast Primary and Secondary Tuberculosis

**Primary tuberculosis**: seen as an i_nitial infection_, usually in children. The initial focus of infection is a _small subpleural granuloma_ accompanied by _granulomatous hilar lymph_ node infection. Together, these make up the **_Ghon complex_**. In nearly all cases, these granulomas resolve and there is no further spread of the infection. **Secondary tuberculosis**: seen _mostly in adults_ as a _reactivation of previous infectio_n (or reinfection), particularly when health status declines. The granulomatous inflammation is much more _florid and widespread_. Typically, the _upper lung lobes_ are most affected, and **cavitation** can occur.

What two things make up a Ghon complex? What does this represent?

a parenchymal subpleural lesion, often just above or just below the interlobar fissure between the upper and the lower lobes, and enlarged caseous lymph nodes draining the parenchymal focus. THis is seen in primary TB

Pt comes into clinic after recently visiting friends down south. They were hunting exotic animals, like armidillos, obviously. Months later his wife notices several plaques on his back. What immune response is going on? What's the disease? What do you tx the pt with?

Pt has Tuberculoid Leprosy This is High-Cell mediated immunity with mostly TH1 type immune response Tx: multidrug: Dapsone and Rifampin for 6 months

You and your friend volunteered to go to Brazil and work at a free clinic for a month. You are working with a pt that rough rasied lesions over his face and complains of tingling in his fingers and toes. What part of the immune system is most active in this diesase? What is the tx recommended?

Leprosy: often diffuse over skin, **lion like** facies and communicable Low cell mediated but **HUMORAL Th2 response** (lions are Humorous 2) Tx: _Dapsone, Rifampin and Clofazimine_ for 2-5 yrs

12 yo boy comes to docotr with fever, chills and rash that started in the AM. Two days prior he had a sore throat and his temp is 101. You note a diffuse erythematous rash on chest and abdomen that blanches with pressure as well as 1-2 mm papules. The throat is erythemaotus with gray-white tonsilar exudate and the tongue is bright red. Dx and bug responsible? What may this pt look like in a week? What complications do we worry about?

Scarlet fever from Group A Strep Pyogenes Dt pyrogenic exotoxins Can see desquemation of the rash towards the end of the first week, often starts at armpits, groin and tips of fingers Can predispose you to Acute rheumatic fever and Glomerulonephritis

What is the bacteria responsible for causing black ulcers and Hemorrhagic mediastinis? What is special about it's capsule?

Bacillus anthracis: on culture it forms long chains and looks serpintine produces antiphagocytic capsule that is unique; **has D-glutamate** instread of polysaccaride