MID: Streptococcus

What is impetigo? What causes it?

Impetigo is a confined, infection of the skin caused by S. pyogenes and S. aureus. It begins through colonization of the skin, appearing as red papules, followed by the development of vesicles with clear yellow contents to pustules filled with bacteria and infection at a site where skin integrity is compromised.

How is impetigo diagnosed?

Impetigo is diagnosed clinically, but in order to determine the causative agent, the fluid from the pustules can be cultured.

True or False: Acute rheumatic fever is a nonsuppurative complication of S. pyogenes pharyngitis and skin infections 6-8 weeks post-infection.

False: not skin infections

True or False: S. pneumoniae bacteremia is often a result of sinusitis and/or otitis media.

False: not usually

How is S. pneumoniae treated with penicillin resistance?

If S. pneumoniae is penicillin resistant, then vancomycin + rifampin or vancomycin + ceftriaxone is used.

What is IgA protease and what bacteria express it?

IgA protease, expressed by S. pneumoniae, Neisseria, and Haemophilus, is a protease that destroys IgA, a mucosal Ab.

The greatest risk factor for early-onset GBS disease in an infant is ______.

vaginal-rectal colonization of the mother

Early-onset Group B Streptococcal infections are caused by ______ transmission.

vertical

Victims of S. pneumoniae are (3) ____________.

very young, very elderly, or immunocompromised

S. pyogenes pneumonia is usually preceded by _______ and has a ________ mortality rate.

viral infection or chronic pulmonary disease; high (30%)

Five Virulence Factors of Enterococci

1. Adhesins (MSCRAMMs) 2. Pili: leads to biofilm formation and common in UTIs 3. Aggregation Substance: increases adherence to cells, extracellular matrix proteins, and serum 4. Cytolytic Activity 5. Proteolytic Activity

Enterococci are naturally resistant to _____ (4). _________ (2) are also common.

1. Aminoglycosides 2. Clindamycin 3. Cephalosporins 4. Bactrim 1. Fluoroquinolone 2. Ampicillin

S. pyogenes Virulence Factors

1. Antiphagocytic Capsule 2. M Protein 3. DNAse Sdal (Extracellular DNAse) 4. Streptolysin S and O 5. C5a Peptidase 6. Protein F 7. Superantigens (SPEs) 8. Streptokinase

Major Virulence Factors of S. pneumoniae (6)

1. Antiphagocytic Capsule 2. Pneumolysin 3. Peptidoglycan 4. Teichoic Acid 5. IgA1 6. Host Inflammatory Mechanisms

Late-onset Group B Streptococcal infections include ____.

1. Bacteremia/Sepsis 2. Meningitis 3. Cellulitis: rare 4. Bone/Joint Infections: rare

Diseases Caused by Enterococci (4)

1. Bacteremia: The Enterococcus enters through the urinary tract, pelvic sepsis, or wounds. The mortality is high and is seen commonly in patients with underlying conditions. 2. Endocarditis: About 5-15% of endocarditis cases are Enterococci. However, underlying heart conditions are common in these infections although has been diagnosed in healthy valves. 3. UTI: UTI from enterococci are often associated with catheters, but newborn UTIs are also seen. 4. Wound/Pelvic/Intrabdominal Infections: These infections occur in combination with other bacteria, such as a G- bacteria like Bacteroides.

Three Patient Populations with Cellulitis

1. Burns 2. Surgical Wounds 3. IV Drug Users

Major Virulence Factors of S. agalactiae (3)

1. Capsule: information on another card 2. Hemolysin: S. agalactiae is β hemolytic and contains hemolysins that are toxic for many cell types and confers pigment. 3. C5a Peptidase: destroys complement component C5a, which attracts neutrophils.

Two Risk Factors for Bacteremia by Group C, F, or G Streptococci

1. Cardiovascular Disease 2. Immunocompromised

S. agalactiae Infections in Pregnant Women (2)

1. Cesarean-Related Wound Infection 2. Chorioamnionitis

Four Symptoms/Signs of S. pyogenes Pneumonia

1. Chills 2. Fever 3. Cough with Blood-Tinged Sputum 4. Bacteremia (10-15% of cases)

Three Symptoms of S. pyogenes Bacteremia

1. Chills 2. Fever 3. Exhaustion

What are three ways in which S. pyogenes is diagnosed?

1. Clinical Picture: bacterial culture where a Gram stain will give a preliminary ID. 2. Rapid Strep Test: form a throat swab. Within minutes, it detects bacterial antigens and determines if the patient is colonized with group A Strep. However, a false negative does not rule out Group A Strep. If negative and Group A Strep is high on the differential, a throat culture is performed to determine the presence of GAS. 3. ASO Titer: An antistreptolysin O titer can be taken from the serum of patients with invasive infections to monitor antibiotic increases during infection.

How is S. agalactiae diagnosed (3)?

1. Culture: The organism is cultured from the site of infection. Along with the clinical picture and a positive CAMP test, S. agalactiae can assume to be positive. 2. PCR is performed on pregnant women at 35 to 37 weeks gestation. 3. Neonatal CSF can be Gram stained.

Underlying Medical Conditions for S. agalactiae Infections in Non-Pregnant Adults (6)

1. Diabetes 2. Liver Disease 3. Neurological Impairment 4. Malignancy 5. Cardiovascular Disease 6. Pulmonary Disease

Two Enterococci

1. E. faecium 2. E. faecalis

Symptoms of S. pneumoniae Meningitis (6)

1. Fever 2. Irritability 3. Drowsiness: early 4. Neck Stiffness 5. Seizures 6. Coma: late

Symptoms of Pneumococcal Pneumonia (5)

1. Fever 2. Shaking Chills 3. Productive Cough 4. Blood in Sputum 5. Chest Pain However, not all patients exhibit the classic symptoms.

S. pneumoniae meningitis can result in _____ (5).

1. Hearing Loss 2. Blindness 3. Learning Disabilities 4. Paralysis 5. Death

Four Serotypes of S. agalactiae (Group B Strep) Causing Invasive Disease

1. Ia 2. Ib 3. III 4. V

S. agalactiae Infections in Non-Pregnant Adults Demographics (3)

1. Immunocompromised 2. Underlying Medical Conditions 3. Elderly

Symptoms/Signs of Acute Rheumatic Fever

1. Inflammatory Changes of the Heart, Joints (Arthritis), Blood Vessels, and Subcutaneous Tissues 2. Carditis 3. Chorea

Four Symptoms of Necrotizing Fasciitis

1. Initial Flu-Like Symptoms 2. Diarrhea 3. Vomiting 4. Localized Pain Out of Proportion to Trauma: This usually brings the patient in to seek treatment.

Five Suppurative Complications of S. pyogenes Pharyngitis

1. Otitis Media 2. Peritonsillar Cellulitis 3. Mastoiditis 4. Peritonsillar or Retropharyngeal Abscesses 5. Scarlet Fever

What are five guidelines to follow to prevent the spread of VRE?

1. Patients with VRE should be isolate patient and perhaps visited patient last on rounds to avoid hospital spread. 2. All persons entering the room should wear gloves and a gown. 3. Noncritical items, such as a thermometer, should remain in room. This should prevent spread. 4. Wash hands with antibacterial agent after finished with patient contact. 5. Eliminate the organism. Elimination of organism is very difficult, as it survives on fomites.

What are seven diseases caused by Group C, F, and G Streptococci?

1. Pharyngitis: common 2, Skin and Soft Tissue Infections: rare 3. Bacteremia: rare 4. Endocarditis: rare 5. TSS: rare 6. Septic Arthritis: rare 7. Osteomyelitis: rare

Causative Agents of Meningitis at 6 to 12 months (3)

1. Pneumococcus 2. Meningococcus 3. Hib

Diseases Caused by S. pneumoniae (5)

1. Pneumonia 2. Sinusitis 3. Otitis Media 4. Bacteremia 5. Meningitis

Risk Factors for Enterococci Infection (3)

1. Prolonged Hospitalization 2. Catheters 3. Periods of Treatment with Broad-Spectrum Antibiotics

Four Symptoms/Signs of Scarlet Fever

1. Rash 2. High Fever 3. Strawberry Tongue: a tongue initially covered with a yellow-white coating that is shed revealing a red, raw surface below 4. Skin Desquamation: rash eventually disappears and the skin desquamates

Two Nonsuppurative Complications of S. pyogenes Pharyngitis

1. Rheumatic Fever 2. Glomerulonephritis

How is S. pneumoniae diagnosed? (2)

1. S. pneumoniae is diagnosed by a culture partnered with the clinical picture. S. pneumoniae is optochin susceptible. 2. Gram stain of the CSF is also diagnostic.

S. agalactiae Infections in Non-Pregnant Adults (7)

1. Skin and Soft-Tissue Infections: cellulitis and abscesses are number one 2. Septic Arthritis 3. Osteomyelitis 4. Meningitis 5. Endocarditis 6. Pneumonia 7. Bacteremia/Sepsis

Six Symptoms of Strep Throat (Pharyngitis)

1. Sore Throat 2. Fever 3. Malaise 4. Headache 5. Erythematous Posterior Pharynx 6. Exudative Tonsils

Five Groups of Streptococci (Plus Lancefield Grouping if Applicable) Causing Human Disease

1. Streptococcus pyogenes: Lancefield Group A streptococci 2. Streptococcus agalactiae: Lancefield Group B streptococci 3. Streptococcus pneumoniae: no group 4. Enterococcus faecalis and E. faecium: Lancefield Group D 5. viridans Streptococci: most have no group except S. gallolyticus/bovis, which are Group D

Five Similarities between Group C, F, and G Streptococci and Group A Streptococci

1. Streptolysins S and O 2. Streptokinase 3. M Proteins 4. Pyrogenic Exotoxins 5. β-Hemolytic

What are two types of complications that may. occur when S. pyogenes pharyngitis is not treated?

1. Suppurative 2. Non-Suppurative

What are the three major functions of the M protein?

1. The M protein is an antiphagocytic defense from neutrophils. 2. The M protein binds to fibrinogen, collagen, and/or fibronectin depending on M serotype. Different M proteins bind to different host receptors. 3. The M protein decreases C3b deposition by binding H factor.

Victims of Enterococci Infections (3)

1. Wounded 2. Chronically Ill 3. Immunocompromised It is an opportunist and generally does not cause disease is healthy humans.

S. pyogenes bacteremia is a consequence of these four prodromes:

1. wound infections 2. pneumonia 3. necrotizing fasciitis 4. TSS

Three Types of Hemolysis with Example Species

1. α hemolysis: cause greening of blood agar due to the effect of H2O2 or pneumolysin and lead to incomplete lysis; i.e. S. pneumoniae and most viridans 2. β hemolysis: complete red blood cell lysis due to exotoxins; i.e. GAS and GBS 3. γ hemolysis: no hemolysis; i.e. most Enterococci

Late-onset Group B Streptococcal infections occur within ______.

7 to 89 days after birth (mean is 36 days)

What is acute glomerulonephritis?

Acute glomerulonephritis is a nonsuppurative complication following some strains S. pyogenes pharyngitis or pyoderma characterized by acute inflammation of the renal glomeruli with edema, hypertension, hematuria, and proteinuria. It is thought to be an autoimmune reaction through molecular mimicry. Young patients typically have an uneventful recovery; however, adult patients have progressive, irreversible loss of renal function.

Epidemiology of Scarlet Fever Age: Prevalence:

Age: ages of 3 to 7 Prevalence: rare today in contrast to latter half of 19th century, when mortality was 25-35%

Epidemiology of Impetigo Age: Associations:

Age: young children Associations: poor hygiene and moist climates

What is C5a peptidase? What species of Streptococcus produces this peptidase?

C5a peptidase is a peptidase produced by S. pyogenes and Group B Strep that degrades the complement component C5a, impairing neutrophil chemotaxis.

CSF Comparisons Cause: Bacterial Appearance: Opening Pressure: PMN: Lymphocytes: Protein: Glucose:

CSF Comparisons Cause: Bacterial Appearance: yellow and turbid Opening Pressure: increased PMN: markedly increased Lymphocytes: slightly increased or normal Protein: markedly increased Glucose: decreased

CSF Comparisons Cause: Fungal Appearance: Opening Pressure: PMN: Lymphocytes: Protein: Glucose:

CSF Comparisons Cause: Fungal Appearance: yellow and viscous Opening Pressure: increased PMN: slightly increased or normal Lymphocytes: markedly increased Protein: slightly increased or normal Glucose: normal or decreased

CSF Comparisons Cause: TB Appearance: Opening Pressure: PMN: Lymphocytes: Protein: Glucose:

CSF Comparisons Cause: TB Appearance: yellow and viscous Opening Pressure: increased PMN: slightly increased or normal Lymphocytes: markedly increased Protein: increased Glucose: decreased

CSF Comparisons Cause: Viral Appearance: Opening Pressure: PMN: Lymphocytes: Protein: Glucose:

CSF Comparisons Cause: Viral Appearance: clear Opening Pressure: normal to increased PMN: slightly increased or normal Lymphocytes: markedly increased Protein: slightly increased or normal Glucose: normal

What is cellulitis? What causes it?

Cellulitis is a skin infection by S. pyogenes or S. aureus that involves the superficial and deep subcutaneous tissues. Cellulitis must be treated expediently, as it can lead to bacteremia. Bacteremia particularly by Group A Strep has a high mortality.

What is the number one underlying medical condition for S. agalactiae infections in non-pregnant adults?

DM

What is DNAse Sda1? What species produces this virulence factor? How does it work?

DNAse Sda1 is an extracellular DNAse produced by S. pyogenes that degrades neutrophil extracellular traps ("NETs"), allowing GAS to evade NET-mediated killing by these structures. Sometimes, neutrophils lyse and release their DNA attached to granules with antimicrobial properties. So, even dead neutrophils have the capability of killing pathogens by ensnaring bacteria into this web-like structure of DNA called NETs. GAS utilizes DNAse Sda1 to cleave the DNA of the neutrophil, so the bacteria is able to escape from the extracellular trap.

Why is early GBS disease becoming "past tense?"

Early GBS disease is become "past tense" because expecting mothers are screened for GBS. If the organism is present, then the mother is given antibiotics to prevent early onset GBS disease.

What causes early onset GBS disease?

Early onset GBS disease is transmitted through vertical transmission. About a quarter of women are naturally and asymptomatically colonized by Group B strep in the vaginal wall. In about 50% of infants, the bacteria migrates into the amniotic fluid and aspirates into the fetus, and the fetus' lungs become infected. So, the fetus is already infected before they are born. So, when they are born, the infant will present with neonatal pneumonia and sepsis usually, but rarely neonatal meningitis. Early-onset GBS can lead to stillbirth. However, this only occurs in 2% of colonized infants while the other 98% will be asymptomatic.

How is early-onset S. agalactiae infection prevented?

Early-onset S. agalactiae infection is prevented through vaginal-rectal screening on pregnant women from 35-37 weeks pregnant. About 25% of women test positive. These women who test positive or have other risk factors are administered penicillin IV at least four hours prior to delivery. The administration of penicillin prevents early-onset disease, but does not affect late-onset disease.

How are Enterococci diagnosed?

Enterococci are diagnosed via culture partnered with the clinical picture.

Where is Enterococcus found?

Enterococci are hardy, so they are able to survive on dry surfaces, hands, and other fomites. However, it is a normal resident of the human colon.

What is erysipelas? What causes it?

Erysipelas is a skin infection caused by S. pyogenes or S. aureus defined by local pain, inflammation, lymph node enlargement, chills, and fever. Erysipelas particularly caused by S. pyogenes have clear lines of demarcation that can be marked and no muscle involvement.

What is the progression of necrotizing fasciitis?

First, S. pyogenes gains entry through a trivial wound or blunt trauma. Then, initially, the skin has a cellulitis-like appearance. However, the pain is out of proportion to how it presents. The toxins elaborated by the organism destroy the tissue rapidly (3 cm/h), leading to bacteremia. After, patients experience shock, multiple organ failure, and death if not treated expediently.

Streptococci are Gram-_________, catalase __________ shape. .

G+, catalase negative cocci

The number one cause for neonatal meningitis is ______.

GBS

What prevents the spread of Enterococci?

Handwashing is key in preventing the spread of Enterococci.

Late-onset Group B Streptococcal infections are caused by serotypes (2) _____.

Ia (20%) and III (60%)

Early-onset Group B Streptococcal infections are caused by serotypes (3) _____.

Ia, III, and V

How does viridans Streptococci cause endocarditis? How is it prevented?

In patients with heart valve pre-conditions, endocarditis can be caused by a simple teeth cleaning. So, prior to going to the dentist, these patients undergo antibiotic prophylaxis, as oral bacteria can colonize the heart from oral bleeding.

Lancefield Group: Group A Gram Stain: Shape: Hemolysis: Bacitracin:

Lancefield Group: Group A Gram Stain: G+ Shape: cocci in chains Hemolysis: β Bacitracin: susceptible

Lancefield Group: Group B Gram Stain: Shape: Hemolysis: Bacitracin:

Lancefield Group: Group B Gram Stain: G+ Shape: cocci in chains Hemolysis: β Bacitracin: resistant

What is the M protein? In what species of Streptococci is this protein found?

M protein is a linear microfibrillar protein appearing similar to a pilus found in Group A Strep that is only observable only an electron microscope. They are highly variable antigenically with over 200 serotypes based on M protein sequence. This sequence, particularly the portion of the M protein susceptible to the environment, is highly variable. However, the C-terminus, which attaches to the cell wall, is highly conserved. Particular M serotypes are predominate in certain diseases.

What is the drug of choice in major S. agalactiae infection?

Major S. agalactiae infection can be treated with ampicillin + gentamicin.

Epidemiology of S. pyogenes Pharyngitis Age:

Most patients with S. pyogenes pharyngitis are from the pediatric population, so most cases of pharyngitis are actually viral. If a patient younger than 5 has a sore throat, it is probably viral. The key population of S. pyogenes pharyngitis is around 5 to 15 years of age.

How is necrotizing fasciitis treated?

Necrotizing fasciitis is treated with intensive antibiotic therapy (penicillin derivative with clindamycin to penetrate deep tissues) and surgical debridement of the affected tissue.

How are VRE treated?

New antibiotics such as linezolid, daptomycin, or quinupristin/dalfopristin (streptogramins) have been used successfully against vancomycin-resistant enterococci (VRE).

Why are patients with splenectomy more prone to pneumococcal infection?

Patients with splenectomy are more prone to pneumococcal infection because B cell response against the polysaccharide capsule is involved in clearing the pathogen, and the spleen produces B-cells.

Organism: S. pneumoniae Lancefield Group: Gram Stain: Shape: Hemolysis: Encapsulated: Oxygen Tolerance: Optochin:

Organism: S. pneumoniae Lancefield Group: none Gram Stain: G+ Shape: lancet-shaped diplococci Hemolysis: α Encapsulated: yes (>90+) Oxygen Tolerance: aerotolerant anaerobe Optochin: susceptible

Organism: Viridans Streptococci Lancefield Group: Hemolysis: Optochin: Gas Requirement:

Organism: Viridans Streptococci Lancefield Group: N/A (except for bovis, which is non-Enterococcus Group D) Hemolysis: α-hemolytic Optochin: resistant Gas Requirement: requires 5-10% CO2

Otitis Media Epidemiology Age:

Otitis Media Epidemiology Age: young children

Symptoms of Otitis Media (2)

Otitis media is indicated by inflammation and redness of the TM.

Why are penicillin allergies a problem in the treatment of S. agalactiae infection?

Penicillin allergies are a problem in the treatment of S. agalactiae infection because GBS are resistant to many other antibiotics. Third generation cephalosporins are generally well-tolerated; however, broad penicillin allergies are problematic.

Drug of Choice for Group C, F, or G Streptococci

Penicillin or Cephalosporins

What is the mortality rate of pneumococcal pneumonia?

Pneumococcal pneumonia has a 5% mortality rate although some serotypes have a higher mortality rate than others. Patients usually recover rapidly with appropriate antimicrobial therapy.

What is pneumolysin? In what species is it found?

Pneumolysin, found in S. pneumoniae, is a toxin for many cell types as well as an α hemolysin. It functions to activate complement and suppress phagocytic oxidative burst.

Prior to the pneumococcal vaccine, infants from six to 12 months of age were at risk of pneumococcal meningitis. Why?

Prior to the pneumococcal vaccine, infants from six to 12 months of age were at risk. Newborns are protected from pneumococcal meningitis because IgG crosses the placenta and immunizes the newborn, so the newborn is protected from pneumococcal meningitis. However, once the antibody begins to drop, the population becomes susceptible.

What is Protein F? What species of Streptococcus produces this protein?

Protein F is an adherence factor produced by S. pyogenes that binds fibronectin and fibrinogen.

_____ is the number one cause of neonatal sepsis and meningitis.

S. agalactiae (Group B Strep)

_________ is a major pathogen of neonates.

S. agalactiae (Group B Strep)

What is the drug of choice in minor S. agalactiae infection?

S. agalactiae infections can be treated with penicillin/ampicillin or a third generation cephalosporin.

Why are S. agalactiae infections in non-pregnant adults problematic?

S. agalactiae infections in non-pregnant adults have a mortality rate of 25%.

Where is S. agalactiae found?

S. agalactiae is a normal membrane of the GI flora, vaginal flora, and sometimes the oropharynx via the fecal-oral route (about 20% of older adults). Partners are often colonized with the same strain, so there is some person-to-person transmission.

What is unique about the hemolysins produced by S. agalactiae?

S. agalactiae produces an organic compound, not a protein, hemolysin.

____________ is linked to bacteremia in patients with colorectal cancer.

S. bovis/gallolyticus (Group D non-enterococci)

What is the only G+ diplococcus (in this course, at least)?

S. pneumoniae

________ is a leading bacterial pathogen in terms of death.

S. pneumoniae

_________ is the cause of 50% of bacterial meningitis in adults.

S. pneumoniae

How does S. pneumoniae bacteremia occur? What can it lead to?

S. pneumoniae bacteremia can occur in patients (about 25-30%) with pneumococcal pneumonia. S. pneumoniae bacteremia can lead to meningitis or endocarditis. The bacteria crosses the blood brain barrier, leading to meningitis.

How is S. pneumoniae treated without any resistance?

S. pneumoniae has obtained penicillin susceptibility in recent years due to the vaccine killing antibiotic resistant strains of the bacteria. So, S. pneumoniae can be treated with amoxicillin with or without clavulanate or a third generation cephalosporin. A third generation cephalosporin like cefotaxime is preferred in cases of meningitis due to its ability to penetrate the meninges.

How is S. pneumoniae infection prevented in children?

S. pneumoniae infection can be prevented through a pneumococcal conjugate vaccine called PCV-13 (Prevnar 13 with diphtheria toxoid) for children under 5. The pneumococcal polysaccharide vaccine stimulates both T-cell and B-cell response. It has decreased the incidence in kids (90%) and elderly indirectly by eliminating transmission from kids.

How is S. pneumoniae infection prevented in adults?

S. pneumoniae infection can be prevented through a pneumococcal conjugate vaccine called PPSV23 for elderly over 65 or patients with underlying risk factors, such as smokers, asthma, and HIV+. The pneumococcal polysaccharide vaccine stimulates both T-cell and B-cell response.

Where is S. pneumoniae found?

S. pneumoniae is found asymptomatically colonizing the upper respiratory tract of about a third humans. Colonization is seasonal and contributes to spread and infection in susceptible populations.

S. pneumoniae is naturally transformable. What does this mean?

S. pneumoniae is naturally transformable. This means that they are able to take up DNA from the environment. They can use this DNA to gain antibiotic resistance as well as gain and lose capsular genes.

How does S. pneumoniae cause pneumonia?

S. pneumoniae is often seen in 30-40% of adult pneumonia cases, particularly in smokers. Cilia are utilized to cough out bacteria that are breathed in every day. Smokers have compromised cilia, so this population is prone to pneumococcal pneumonia. The bacteria enter the lung, resisting phagocytosis due to its capsule. The organism, since it is G+, contains peptidoglycan and teichoic acid, sheds its cell wall and elicits and inflammatory response to recruit phagocytic cells. Most of the damage in the URT is due to host response, as frustrated phagocytosis damages the lung tissue. The patient then becomes cyanotic due to the lack of oxygen.

How is S. pneumoniae presumptively identified?

S. pneumoniae is presumptively identified via optochin.

How is S. pneumoniae spread?

S. pneumoniae is spread by close contact, such as daycares, military camps, prisons, homeless shelters, and nursing homes.

How does S. pneumoniae cause sinusitis and otitis media?

S. pneumoniae sinusitis and otitis media is often preceded by viral infection of the upper respiratory tract and are often associated with underlying health conditions. PMN infiltrate obstructs the sinuses and ear canal, and this accumulated fluid provides growth medium for bacteria.

S. pyogenes are the champions of avoiding phagocytosis. How?

S. pyogenes are the champions of avoiding phagocytosis through their capsule and the M protein. Particularly the M protein, the presence of this protein increases the likelihood of this organism's escape from phagocytosis.

How is S. pyogenes introduced to cause Streptococcal toxic shock syndrome?

S. pyogenes can be introduced to a skin lesion or during surgery in about 50% of cases. However, some cases have no obvious portal of entry.

How is major S. pyogenes infection treated?

S. pyogenes can be treated by clindamycin, which inhibits protein synthesis, to impede toxin synthesis. This is partnered with penicillin to treat TSS and necrotizing fasciitis. If the patient has necrotizing fasciitis, then surgical debridement and possibly hyperbaric O2 are used.

How is S. pyogenes introduced to cause necrotizing fasciitis (Streptococcal gangrene)?

S. pyogenes gains entry through a trivial wound or blunt trauma.

Where is S. pyogenes found?

S. pyogenes is an asymptomatic colonizer of the upper respiratory tract and skin and is especially prevalent in children ages 5 to 15, in residential schools, and detention centers. The carriage rate of S. pyogenes in these areas can approach 50%. Colonization is also high for individuals who have wound and skin disease as well as areas where streptococcal pyoderma is common.

How is minor S. pyogenes infection treated?

S. pyogenes is treated with ten days of penicillin. A cephalosporin or a macrolide can be used for penicillin allergies.

Why does S. pyogenes spread better during cold months?

S. pyogenes spreads better in cold months due to individuals being indoors.

How does S. pyogenes spread?

S. pyogenes spreads through respiratory secretions, food, water, and fomites since it can survive on dry surfaces for long periods of time. It can also be spread through breaks in skin after direct contact with infected/colonized person or an arthropod vector.

What causes scarlet fever?

Scarlet fever is caused by a strain of S. pyogenes infected by bacteriophage, which stimulate elaboration of pyrogenic exotoxins.

Since both Group A and Group B Strep are β hemolytic, how can you differentiate between the two species?

Since both Group A and Group B Strep are β hemolytic, bacitracin can be applied as a disk onto a plate. Group A are bacitracin susceptible while Group B are bacitracin resistant.

Sinusitis Epidemiology Age:

Sinusitis Epidemiology Age: any age

Species: Enterococci Gram Stain: Shape: Catalase: Hemolysis:

Species: Enterococci Gram Stain: G+ Shape: cocci in pairs or short chains Catalase: negative Hemolysis: usually non-hemolytic

What are streptococcal pyrogenic exotoxins (SPEs)? What do they do? What organism produces these toxins?

Streptococcal pyrogenic exotoxins (SPEs) are superantigens produced by S. pyogenes that are involved in several of the diseases caused by GAS, including scarlet fever, TSS, and necrotizing fasciitis. These superantigens, particularly SpeA, lead to the excessive release of cytokines followed by shock.

What causes Streptococcal toxic shock syndrome? What symptoms are associated with this disease?

Streptococcal toxic shock syndrome is caused by S. pyogenes introduction to a skin lesion or during surgery, although 50% of cases have no obvious portal of entry. S. pyogenes can multiply at the site of infection, producing toxins. The patient becomes bacteremic with symptoms including fever, chills, malaise, nausea, vomiting, and diarrhea along with necrotizing fasciitis, hypotension, renal impairment, liver abnormalities, and coagulopathy.

Why are Streptococci known as pyogenic cocci?

Streptococci, along with Staphylococci and Neisseria, are known as pyogenic cocci because they produce pus full of bacteria and neutrophils.

What is the causative agent of Strep throat?

Streptococcus pyogenes

What is a positive use of streptokinase?

Streptokinase can be used to dissolve clots in some cases of heart attack, pulmonary embolism, or thrombosis. However, streptokinase is typically used only for first heart attacks.

What is streptokinase? What species produces this virulence factor?

Streptokinase is a virulence factor produced by S. pyogenes that promotes the dissemination of GAS by dissolving fibrin used by the host to contain bacterium. This activates plasminogen to plasmin, allowing spread.

What are streptolysins (S and O)? What species produces this protein?

Streptolysins, particularly S and O subtypes, are β hemolysins produced by S. pyogenes that lyses leukocytes, platelets, and erythrocytes.

Group A Strep, similar to S. aureus, produce superantigens. What is the significance of this?

Superantigens are antigens that bind outside of the peptide-binding groove of MHC Class II. Instead of stimulating a single T-cell receptor, superantigens stimulate a large repertoire of T-cell receptors, triggering a cytokine storm with massive inflammation.

What is the CAMP test? What is it used for?

The CAMP test is used to identify Group B Strep. A plate is streaked in one direction with S. aureus, which is β-hemolytic. In perpendicular, the unknown isolate is streaked. Group B Strep will produce an arrowhead-like appearance due to the synergy between the two β hemolysins, the one from S. aureus and the one from S. agalactiae. This is a CAMP positive test.

Enterococci are considered "wimpy" pathogens due to very few virulence factors. Why are they still considered so virulent?

The Enterococci ability to cause disease is substantially related to ability to survive in the presence of antibiotics and other antimicrobials, not their virulence factors. Essentially, they are good at surviving and resisting antibiotics.

What is the major virulence factor of S. pneumoniae?

The antiphagocytic polysaccharide capsule is the major virulence factor of S. pneumoniae.

Why is the capsule for S. agalactiae (Group B Strep) difficult to vaccinate against?

The capsule for S. agalactiae (Group B Strep) is difficult to vaccinate against because sialic acid is present on our host cell surface.

What is the major concern with VRE?

The major concern with VRE is the transfer of vancomycin resistance genes to other bacteria, including S. aureus. However, whenever this transfer does occur, there seems to be a fitness cost associated in S. aureus. Thank God.

What is the major feature of Enterococci?

The major feature of Enterococci is their resistance to antibiotics. E. faecium more inherently resistant to antibiotics than E. faecalis, but E. faecalis encountered much more frequently in specimens E. faecium is a major problem, as it is resistant to penicillin and ampicillin in about 80% of isolates. About 80% of isolates are vancomycin resistant.

Why is there no vaccine against S. pyogenes?

There is no vaccine against S. pyogenes because it has a capsule composed of hyaluronic acid, the same substance that composes our ECM. It is difficult to produce a vaccine with a capsule that is the same composition as our ECM.

Meningitis caused by S. pneumoniae can be preceded by ______ (3).

bacteremia, otitis media, or sinusitis

Early-onset Group B Streptococcal infections include ____.

bacteremia/sepsis, pneumonia, and meningitis (>10%)

CSF glucose is decreased in _____.

bacterial meningitis

True or False: Acute glomerulonephritis is a nonsuppurative complication of S. pyogenes pharyngitis and skin infections (pyoderma).

True

True or False: Enterococci are able to grow in high salt and bile.

True

What is the most common infection caused by Enterococci?

UTI

Adult-onset Group B Streptococcal infections are caused by serotype _____.

V

Where are viridans Streptococci found?

Viridans Streptococci are found in the normal flora of the oral cavity, GI and genitourinary tract.

What is a common cause of dental caries?

Viridans Streptococci, including S. mutans, are a common cause of dental caries. Glucose that is consumed is taken by S. mutans and deposited as a biofilm, producing plaque.

Does S. agalactiae (Group B Strep) have a capsule?

Yes, S. agalactiae (Group B Strep) has a capsule composed of polysialic acid. This enhances the ability of this bacterium to evade the host's defenses. There are ten serotypes of S. agalactiae based on capsule.

Does S. pyogenes have a capsule?

Yes, S. pyogenes has a capsule. It is composed of hyaluronic acid. Since hyaluronic acid is a part of the ECM, then the bacterium mimics our own cell molecules. This is known as molecular mimicry and will result in disease in otherwise healthy individuals.

E. faecalis are/are not usually vancomycin susceptible.

are not

Early-onset Group B Streptococcal infections occur within ______.

first six days of life (mean age is 12 hours)

The mortality rate of S. pyogenes bacteremia is ______ in patients with necrotizing fasciitis or TSS.

high (40%)

Late-onset Group B Streptococcal infections are caused by ______ transmission through ______.

horizontal; nosocomial or community exposure

A 3 week old male who was born at term by C-section had a left diaphragmatic hernia at birth requiring intubation and continued respiratory support. Over a 24 hour period, the infant developed bulging anterior fontanelles (margins of cranial bones), increased respiratory and heart rates, wide fluctuations in blood pressure, difficulties maintaining adequate tissue perfusion and his peripheral WBC count increased from 6300 to 13,700/ml. The child began to have focal seizures as well. A cerebrospinal fluid (CSF) exam showed 3900 WBC/ml with 92% neutrophils, glucose of 2 mg/dL (normal = 50-80 mg/dL) and protein of 350 mg/dL (normal =20-45 mg/dL). Gram stain and culture of CSF revealed catalase-negative Gram-positive cocci in chains that were beta-hemolytic. What is the organism and diagnosis at hand?

late-onset neonatal meningitis by Group B Strep

Viridans Streptococci are _____-grade pathogens.

low

The case fatality rate of early GBS disease is _________ than late onset GBS disease.

lower (about 5% compared to )

Enterococci is one of the top causes of ____________ infections.

nosocomial

S. anginosus can cause _____.

periodontal disease and abscesses with pyrogenic toxins

Scarlet fever is a complication of S. pyogenes _______ and _______.

pharyngitis and skin infections

A 70-year-old female who smoked for 45 years was previously diagnosed 1 year ago with multiple myeloma and had been recently treated with 5 cycles of immunosuppressive drugs, including prednisone, presents with a 2-day history of dyspnea and a productive cough with phlegm. She denied hemoptysis, night sweats, abdominal pain, vomiting or chest pain. On physical exam, she had a fever of 38.8C, pulse of 120/min and respiratory rate of 20/min. Chest exam was significant for bilateral crackles and expiratory wheezes. Chest X-ray showed bilateral, diffuse pulmonary infiltrates with effusion. WBC count was 1700/ml. Two sets of blood cultures and sputum were obtained and a Gram positive diplococci was observed. The organism was susceptible to optochin, was alpha hemolytic and the colonies were mucoid. Antimicrobial susceptibility testing revealed the organism was resistant to erythromycin, penicillin, and trimethoprim/sulfamethoxazole, but susceptible to clindamycin and cefotaxime. The latter two antibiotics were given IV. What is the organism and diagnosis at hand?

pneumococcal pneumonia

Enterococci are ________ to 3% hydrogen peroxide.

resistant This is interesting because it is catalase negative.

Streptococcal toxic shock syndrome is associated with strains of S. pyogenes that cause ________, not ________.

skin disease; pharyngitis

S. pneumoniae is soluble/insoluble in bile, making it susceptible to optochin.

soluble