Micro 6: Examples of Bacteria Flashcards
1
Q
Case 1: A 24 y/o female has sexual intercourse with her fiancé. She usually urinates right after sex, but is too tired and goes to sleep instead. About 24-36 hours later she experiences dysuria (painful urination), urinary frequency and malodorous urine. She goes to her PCP and gives a urine sample which shows a lot of WBCs and grows Escherichia coli. She is placed on Ciprofloxacin for treatment.
A
Case 1: A 24 y/o female has sexual intercourse with her fiancé. She usually urinates right after sex, but is too tired and goes to sleep instead. About 24-36 hours later she experiences dysuria, urinary frequency and malodorous urine. She goes to her PCP and gives a urine sample which shows a lot of WBCs and grows Escherichia coli. She is placed on Ciprofloxacin for treatment.
2
Q
Where did the E. coli come from?
A
Her GI tract. E. Coli is the second most common normal flora in the GI
3
Q
How did the E. coli reach her urinary tract and
bladder?
A
Translocation to the urinary tract and entered the bladder through the urethra by swimming because uropathogenic E. Coli (UPEC) are motile
4
Q
Would it be unusual to detect some E. coli in her urine?
A
No, the diagnosis of a UTI is based not the simple presence of flora but the elevated NUMBER.
5
Q
Did it make a difference that she did not urinate after sex?
A
Yes, it flushes the area
6
Q
Is there a downside to treating with Cipro?
A
she could get a yeast infection and gram negative rods like E. Coli can develop multi-drug resistance (mechanism: efflux pump)
C
7
Q
What are some possible side-effects of Cipro (and Fluoroquinolones in general)
A
spontaneous tendon rupture (like Achilles tendon) and spontaneous retinal detachment. These drugs should be used sparingly because of these side effects and the potential for multi-drug resistance to develop
8
Q
What is cystitis?
A
Cystitis is the result of the ascension of normal flora bacteria from the urethra to the bladder. Because the urethra is shorter in women and near the vagina and anus, UTIs are more common in women
9
Q
What bacteria are the major causes of UTIs in women?
A
E. coli cause 90% of UTIs in women, but Klebsiella, Proteus, Enterococci, and Staph saprophyticus also cause UTIs.
UTIs keep slutty sorority pledges engaged
10
Q
T or F. In elderly men and women, bacteriuria occurs more equally.
A
T. NOT UTIs, just the presence of bacteria
11
Q
What are some common symptoms of bacteriuria?
A
pain while urinating (dysuria), frequent but low volume urination, suprapubic pain, and blood in the urine (hematuria). Most patients are afebrile
12
Q
What does febrile mean?
A
showing a fever
13
Q
What is pyelonephritis?
A
it basically means that the bacteria have made their way to the kidney
14
Q
What should you suspect is a patient presenting with symptoms of a UTI are febrile?
A
if febrile, an upper UTI (pyelonephritis) should be considered.
15
Q
T or F. The bladder has normal flora.
A
F. The bladder is normally sterile
16
Q
In WOMEN, what density of bacteria per ml is needed to diagnose UTI?
A
greater than 10^5/ml
17
Q
In MEN, what density of bacteria per ml is needed to diagnose UTI?
A
greater than 10^3/ml
18
Q
What are two alternatives for UTI treatment?
A
Cipro is the go-to but resistance is rising. an alternative is Cotrimoxazole (Trimethoprim-Sulfamethoxazole) OR third-generation cephalosporins
19
Q
When you see a UTI what should your first thought be in terms of bacteria?
A
E. Coli BUT Staph saprophyticus (if its gram-positive) is common!!
20
Q
What are some characteristics of uropathogenic E. Coli (UPEC)?
A
- they are facultative gram negative rods
- they grow aerobically and ferment lactose (i.e. positive on an EMP plate)
- found normally in the gut GI
21
Q
What can uropathogenic E. Coli (UPEC) do in relation to nitrate? Why is this important?
A
convert it to nitrite. This is important because urine dipstick can detect the presence/ratio of nitrate to nitrite as a potential diagnosing factor
22
Q
T or F. Only E. Coli that pick up a PAI are going to cause disease
A
T. Symptom presentation depends on what kinds of virulence factors are picked up
23
Q
What kinds of virulence factors do UPEC bugs have?
A
- Flagella that allow for movement
- Type 1 fimbriae mediate attachment in lower UTI-bladder- (regulated by phase variation)
- P fimbriae mediate attachment in upper- kidney and ureter- UTI (receptor is same as P blood group antigen)
24
Q
Case 2
• A 70 y/o female presents to the ED with shortness of breath and wheezing. She has been hospitalized 5 times in the last 2 years with similar presentations. PMH includes COPD. She smokes 2 ppd and has for 50 years. Admission vitals: T 98.6°F, BP 120/76, HR 100, RR 30, O2 saturation 85% on RA. Her labs are unremarkable and chest x ray was clear.
• She is admitted and placed on oxygen by nasal cannula and nebulizer treatments for a COPD exacerbation, however she soon develops worsening respiratory failure and has to be intubated and placed on a ventilator. Her oxygenation initially improves over the next few days.
On day 5 of hospitalization, she develops increased O2 requirements, thick tracheal secretions, and a fever to 102°F. Labs show a WBC count of 15,000. CXR shows infiltrates. She is started on Vancomycin but does not improve.
- A sputum sample is sent to the lab. You are notified that there is growth on the agar plate, so you go down to look at it. You notice that it has a fruity odor. Here is what the plate looks like:
- Sputum culture grows Pseudomonas aeruginosa.
A
Case 2
• A 70 y/o female presents to the ED with shortness of breath and wheezing. She has been hospitalized 5 times in the last 2 years with similar presentations. PMH includes COPD. She smokes 2 ppd and has for 50 years. Admission vitals: T 98.6°F, BP 120/76, HR 100, RR 30, O2 saturation 85% on RA. Her labs are unremarkable and chest x ray was clear.
• She is admitted and placed on oxygen by nasal cannula and nebulizer treatments for a COPD exacerbation, however she soon develops worsening respiratory failure and has to be intubated and placed on a ventilator. Her oxygenation initially improves over the next few days.
On day 5 of hospitalization, she develops increased O2 requirements, thick tracheal secretions, and a fever to 102°F. Labs show a WBC count of 15,000. CXR shows infiltrates. She is started on Vancomycin but does not improve.
- A sputum sample is sent to the lab. You are notified that there is growth on the agar plate, so you go down to look at it. You notice that it has a fruity odor. Here is what the plate looks like:
- Sputum culture grows Pseudomonas aeruginosa.
25
What is the normal WBC count?
~3000-8000
26
What is the normal respiratory rate (RR)?
12-16. RR is the breaths taken in a minute
27
In general terms, what type of infection is this?
| i?
opportunistic, nosocomial
28
How would you know this is a good sputum sample and not just saliva?
FYI: sputum is a mixture of saliva and mucus coughed up from the respiratory tract, typically as a result of infection or other disease and often examined microscopically to aid medical diagnosis.
you want to see few epithelial cells from saliva and more PMNs as a sign of infection
29
Nosocomial pneumonias are most often caused by G- rods or Staph. How might Pseudomonas (a G- rod) be distinguished from E. coli?
lactose fermentation (pseudomonas does not!!), oxidase positive vs negative
30
Why was the patient immediately started on Vancomycin? Why didn’t she improve?
Vancomycin was administered assuming they were treating the Staph (a gram positive strain- and a very common cause of nosocomial infection- so this isn't the worst assumption but wrong here).
So she didn't improve because Vanco doesn't cover gram-neg (which it probably will), or anaerobes
31
T or F. Nosocomial pneumonia (aka HAI pneumonia) is the leading cause of death among hospital- acquired infections.
T. The greatest risk for infection occurs when the patient is placed on a ventilator. Infection occurs through micro-aspiration of oropharyngeal tract or GI tract bacteria, or from the introduction of bacteria from the hospital setting.
32
What are the most common pathogens that cause Nosocomial pneumonia (aka HAI pneumonia)?
The most common pathogens are Gram-negative rods (E. coli, Klebsiella, Enterobacter, Ps. aeruginosa, or Acinetobacter) and Gram-positive cocci (Staph aureus and Streptococci).
Two MOST common are: Staph. aureus and Ps. aeruginosa
Multidrug resistance is common among isolates, which is typical of HAI infections.
33
What are some common symptoms of Nosocomial pneumonia (aka HAI pneumonia)?
May be characterized by a patient that comes in and is placed on a ventilator, gets better, and then gets worse and develops more symptoms such as fever.
Symptoms include fever, purulent sputum, and decline in oxygenation, cough if not on ventilator. Infiltrates will be seen on lung x-ray.
34
What is the appropriate treatment for Nosocomial pneumonia (aka HAI pneumonia)??
Treatment starts with empiric therapy (like Vanco?) to cover most possible organisms but should be narrowed when a definitive diagnosis is made.
However, nosocomial pneumonias can be polymicrobial requiring broad spectrum coverage.
35
What are some characteristics of Psuedomonas aeruginosa?
1. aerobic, gram-negative rod
2. releases a fruity odor
3. Produces pyocyanin (blue) and fluorescin (yellow) to produce blue-green color
4. Some strains produce a slime layer commonly seen in CF patients
36
Is Pe. aeruginosa ever found normally in the body? If so, where?
Yes, in 10% of the population it is found in the GI tract.
Most it is mostly found in the environment- e.g. soil, water, vegetation
37
T or F. Pse. aeruginosa is a frank pathogen
F. it is opportunistic
38
Where do Pse. aeruginosa infections usually occur in the body?
They can infect a wide range of places including pulmonary, urinary, and soft tissue sites
39
The vast majority of Pse. aeruginosa infections impact what types of patients?
burn victims, HAI infections, and CF patients
40
What kinds of antibiotic are currently used in treating Pse. aeruginosa infections?
3rd and 4th generation cephalosporins, carbapenems, some beta- lactams with beta lactamase inhibitors, and newer aminoglycosides are used in treatment
41
What is an antibiogram?
A machine at hospitals that log the effectiveness of certain antibiotics to certain bacteria over a time period (say in the past year)
42
Case 3
• A 49 y/o male presents to the ED with cough and shortness of breath x 1 week’s duration and a one-day history of severe headache and vomiting. His spouse reports that he has been acting funny over the last 24 hours, and what actually brought them in was she witnessed him having what she thinks was a seizure earlier that day. He has been having fevers up to 102°F, rigors, and night sweats for the past 5 days as well.
• PMH: splenectomy after splenic injury from car accident 10 years ago. Has not seen a primary care provider ever.
Has never received any vaccinations.
• Social history: smokes 1 ppd, drinks a 6 pack of beer every 1- 2 days.
Vital signs: T 101.6oF, BP 90/60, HR 125, RR 28, O2 saturation 88% on RA. Patient appears toxic. Eye exam is abnormal.
• Antibiotics (Vancomycin and Ceftriaxone) plus dexamethasone (steroid) are administered for suspected bacterial meningitis.
• Head CT is done immediately. No acute abnormalities are found.
• Lumbar puncture is then done. Sample Gram stains of the CSF and diagnosis is made as Streptococcus pneumoniae meningitis
• The doctor discontinues the Vancomycin but continues the Ceftriaxone and Dexamethasone.
• However, the patient’s condition deteriorates even further over the next 48 hours and he dies.
Case 3
• A 49 y/o male presents to the ED with cough and shortness of breath x 1 week’s duration and a one-day history of severe headache and vomiting. His spouse reports that he has been acting funny over the last 24 hours, and what actually brought them in was she witnessed him having what she thinks was a seizure earlier that day. He has been having fevers up to 102°F, rigors, and night sweats for the past 5 days as well.
• PMH: splenectomy after splenic injury from car accident 10 years ago. Has not seen a primary care provider ever.
Has never received any vaccinations.
• Social history: smokes 1 ppd, drinks a 6 pack of beer every 1- 2 days.
Vital signs: T 101.6oF, BP 90/60, HR 125, RR 28, O2 saturation 88% on RA. Patient appears toxic. Eye exam is abnormal.
• Antibiotics (Vancomycin and Ceftriaxone) plus dexamethasone (steroid) are administered for suspected bacterial meningitis.
• Head CT is done immediately. No acute abnormalities are found.
• Lumbar puncture is then done. Sample Gram stains of the CSF and diagnosis is made as Streptococcus pneumoniae meningitis
* The doctor discontinues the Vancomycin but continues the Ceftriaxone and Dexamethasone.
* However, the patient’s condition deteriorates even further over the next 48 hours and he dies.
43
What feature of the Gram stain distinguishes S. pneumoniae from other streptococci?
diplococci (all other streps are chains) and they have a characteristic 'lancid' shape where their ends are pointed
44
Why was the vancomycin dropped? Did that likely cause the patient’s death?
The doctor assumed that the Strep. peumn was susceptible to ceftriaxone, as to has been for years in practice. ONLY RECENTLY, has resistance been developed
You can no longer assume that Strep. pen meningitis are susceptible to third generation cephalosporins
The recommendation is to continue the Vanco and Ceftrixaone until susceptibility testing returns
45
If not, what is a possible reason the patient died?
the lack of a spleen makes a patient more susceptible to infection from bacteria with CAPSULES such as Strep. pneumo
46
Was there anything significant in his history that could have contributed to this severe infection?
– If so, which virulence factor was responsible?
the lack of a spleen makes a patient more susceptible to infection from bacteria with CAPSULES such as Strep. pneumo
47
Can you think of a way this infection might have been prevented?
Vaccination is needed with a splenectomy
48
How does the presence of a capsule in bacteria such as Strep. peumo. cause increased virulence?
it is antiphagocytic and that property allows it an increased chance to reach the CSF.
49
How does the lack of a spleen cause increased susceptibility to bacteria with capsules?
the spleen is the major site in the body for removal on ENCAPSULATED bacteria from systemic circulation
50
What is Pneumococcal meningitis?
Meningitis is an infection of the meninges, most commonly by hematogenous spead of a nasopharyngeal infection
51
What are the classic symptoms of Pneumoccoal meningitis?
Early symptoms include fever, headache, and stiff neck. This can be followed by irrational behavior and seizures, eventually resulting in coma
52
What is the most common cause of Pneumococcal meningitis?
S. pneumoniae is the most common cause overall, but other bacteria can affect select age groups. Viral (or aseptic) meningitis is also possible, but less severe and generally self-limiting.
53
How can the dissemination of Strep. pneumo be diagnosed?
S. pneumoniae meningitis can be diagnosed by Gram stain (gram-positive) and culture of CSF
54
T or F. S. pneumoniae remains largely sensitive to penicillin
T. however it is gaining resistance and vancomycin should always be continued until susceptibilities are back. Empiric therapy should be initiated as soon as bacterial meningitis is suspected.
Capsular polysaccharide vaccine is available for prevention.
55
What should you do if you suspect meningitis in the ER?
give vancomycin, ceftriaxone, plus dexamethasome (dexamethasone is only shown to improve outcomes in ADULTS with Strep. Pneumo meningitis)
56
What happens if you find out it is not Strep. pneumo causing the meningitis?
you stop the dexamethasome in ADULTS (children are different)
57
What are the most common pathogens that cause meningitis in neonates?
GBS (group B strep), E. Coli, Listeria monocytogenes
58
What are the most common pathogens that cause meningitis in young children?
S. pneumo., N. meningitidis, and Haemophilus infleunzae (significant reduction with vaccine)
59
What are the most common pathogens that cause meningitis in young adults?
S. pneumo., N. meningitidis
60
What are the most common pathogens that cause meningitis in elderly patients?
S. pneumo., N. meningitidis, L. monocytogenes
61
What happens to the treatment regimen if you suspect meningitis in an elderly patient, an immunocompromised person, or neonates?
have to cover for Listeria with ampicillin
So you'll give vancomycin, ceftriaxone, and ampicillin
62
What are some characteristics of Strep. pneumo (aka pneumococcus)?
1. Gram positive lancet-shaped diplococcus
– Alpha-hemolytic
– Optochin (Taxo P) sensitive
• Respiratory route of transmission
63
What kinds of virulence factors does pneumococcus have?
– Capsule
– Secretory IgA protease
– Pneumolysin (helps lyse cells during infection)
64
How can infection via. Strep. pneumo be prevented?
vaccination with Prevnar (marketed to 60+ individuals and babies), a polyvalent capsular vaccine
65
Case 4
• A 33 y/o Hispanic male presents to his primary care provider with a 6-week history of low-grade fevers, night sweats, loss of appetite, unintended weight loss of 15 pounds, and cough productive of blood-streaked sputum. He moved to the U.S. from Mexico 5 years ago. He has no known medical problems.
• Family history: His father died 10 years ago of some type of pneumonia.
• Exam: vital signs normal. Patient appears mildly chronically ill. Lung exam reveals coarse sounds in right upper lobe.
• The patient is admitted to the hospital for further workup.
• Basic labs are unremarkable.
• Chest x ray shows a right upper lobe infiltrate and mediastinal lymphadenopathy.
• The doctor orders sputum Gram stain and culture as well as AFB (acid-fast bacillus) stain on the sputum.
* Gram stain is negative and routine culture is also negative at 48 hours. AFB smear is positive and a presumptive diagnosis of active pulmonary tuberculosis is made.
* The patient is immediately started on treatment consisting of 4 different drugs: Isoniazid, Rifampin, Pyrazinamide, and Ethambutol (PIRE).
* The pulmonologist decides to take the patient for bronchoscopy to get lung samples and also for a lymph node biopsy.
* Here is a picture of the biopsy specimen: This shows a caseating granuloma.
Case 4
• A 33 y/o Hispanic male presents to his primary care provider with a 6-week history of low-grade fevers, night sweats, loss of appetite, unintended weight loss of 15 pounds, and cough productive of blood-streaked sputum. He moved to the U.S. from Mexico 5 years ago. He has no known medical problems.
• Family history: His father died 10 years ago of some type of pneumonia.
• Exam: vital signs normal. Patient appears mildly chronically ill. Lung exam reveals coarse sounds in right upper lobe.
• The patient is admitted to the hospital for further workup.
• Basic labs are unremarkable.
• Chest x ray shows a right upper lobe infiltrate and mediastinal lymphadenopathy.
• The doctor orders sputum Gram stain and culture as well as AFB (acid-fast bacillus) stain on the sputum.
* Gram stain is negative and routine culture is also negative at 48 hours. AFB smear is positive and a presumptive diagnosis of active pulmonary tuberculosis is made.
* The patient is immediately started on treatment consisting of 4 different drugs: Isoniazid, Rifampin, Pyrazinamide, and Ethambutol.
* The pulmonologist decides to take the patient for bronchoscopy to get lung samples and also for a lymph node biopsy.
* Here is a picture of the biopsy specimen: This shows a caseating granuloma.
66
Why were the patient’s Gram stain and culture negative?
high mycolic acid content blocks the stain.
67
What is a granuloma?
macrophages (and other cells) containing the infection
68
Which part of the immune system is responsible for formation of a granuloma?
T-cell mediated
69
Do you think this could be a chronic infection? Latent?
yes it is both, he was probably infected in Mexico. This is an example of secondary TB
70
Antibiotic treatment of tuberculosis lasts for several (6-9) months. Why do you think that is, and why are 4 drugs needed to treat tuberculosis?
this prevents multi-drug resistance from arising and that granuloma is essentially walled-off and hard to get to easily
Also, an acid-fast culture takes up to 6 weeks to come positive for TB so it is a slow grower and there are metabolically-inactiving proteins in the granuloma so treatment takes a while
71
What is TB?
TB is a complex infection where initial infection is only apparent due to our immune response. The disease can progress, or more often, become latent for years before symptoms arise. Reactivation leads to a chronic pneumonia characterized by cough, fever, bloody sputum, night sweats, and weight loss.
A staggering number of TB cases occur each year, but most are confined to developing nations. AIDS patients have accounted for an increase in TB cases in industrialized nations.
* Individuals previously infected with TB (or who have received the BCG vaccine) will test positive in a tuberculin skin test. This is a DTH reaction that does not distinguish active vs latent infection. Newer interferon-based assays can do so.
* Because of the prolonged treatment regimen that is required, compliance is an issue and patients should be directly observed taking their medications ('direct-observed therapy is necessary).
72
What things are key to TB pathogenesis?
Key to TB pathogenesis is the formation of granulomas (tubercles), in which the latent bacteria reside.
73
Upon reactivation, where do sites of infection tend to be?
in well-oxygenated sites, such as the upper lobe of the lung (more oxygenated than the lower lobes)
74
What are some characteristics of Mycobacterium tuberculosis?
```
Acid-fast bacillus (single membrane like G+)
– Mycolic acid in cell wall
– MTB can inhibit phago-lysosome fusion,
survive in unactivated macrophages
• Transmission is respiratory route
– Infectivity is high
```
* AFB on sputum may reveal organism
* The bacillus Calmette-Guerin (BCG, a related mycobacterium) live vaccine is variably effective, but not used in US
* Skin test is based on a purified protein derivative (PPD) of a protein component of the cell wall, tuberculin (a cell wall protein component)
* Combination drug therapy is required because the mycolic acid excludes many conventional antibiotics and resistance is an issue, and it a slow metabolic organism so the drugs are not taken up quickly
– 6-9 months, susceptibility testing required
75
Mycobacterium TB diagnosis requires growth on what kind of agar?
Growth on Lowenstein-Jensen agar can take 3 weeks
76
Is MTB an extracellular or intracellular pathogen?
intracellular
77
Why is Rifampin very commonly given with other antibiotics?
because resistance to it occurs extremely fast in bacteria
78
Case 5
• An 18 y/o male currently in basic training in the army develops sore throat, headache, dry cough, low-grade fevers, and fatigue. He presents to the infirmary after 3-4 days and is prescribed amoxicillin. His symptoms do not improve. He goes back to the infirmary. Gram stain is performed on his sputum and shows white cells but no bacteria.
Case 5
• An 18 y/o male currently in basic training in the army develops sore throat, headache, dry cough, low-grade fevers, and fatigue. He presents to the infirmary after 3-4 days and is prescribed amoxicillin. His symptoms do not improve. He goes back to the infirmary. Gram stain is performed on his sputum and shows white cells but no bacteria.
79
Why was the Gram stain of the sputum negative? Was it a bad sample?
could have been a viral infection or Mycoplasma (no cell wall)
No, because of presence of WBCs
80
Why might the amoxicillin have been ineffective?
No cell wall to act on
81
Could this be a viral infection?
Could be
82
Can you think of a way to detect a bacterial infection rapidly besides Gram stain?
PCR that shit
83
Nasopharyngeal PCR for Mycoplasma pneumoniae is done and is positive. He is started on Azithromycin.
Why might Azithromycin be effective when amoxicillin was not in treating Mycoplasma infection?
Effective against ribosome function
84
What is atypical pneumonia?
Technically, any pneumonia that does not present like pneumococcal pneumonia, ie, abrupt onset of fever, chills
Atypical or “walking” pneumonia is a less severe, chronic form
Most courses of infection are benign but may still be treated
85
What three organisms cause atypical pneumonia?
Mycoplasma pneumoniae (young adults)
Chlamydia (Chlamydophila) pneumoniae (young and older adults)
Legionella pneumophila (Legionnaire’s disease) (elderly)-Legionnaire’s is a much more severe disease
86
What are some of the common symptoms of a mycoplasma induced atypical pneumonia?
Mycoplasma pneumonia usually includes a nonproductive cough, fever, and headache. Sore throat and otitis media are common. Patchy infiltrates on x-ray
87
What are some characteristics of mycoplasma pneumoniae?
• Aerobic, pleomorphic bacterium
– Lacks cell wall (no Gram stain)
– Contains sterol in membrane
– Can grow on synthetic medium
• Smallest free living organism
• Transmission is by respiratory route
– Pharyngitis
– Otitis media
– Atypical pneumonia
* Formation of cold agglutinins () in two- thirds of patients, can be diagnostic
* Treat with
88
What is an important virulence factor of mycoplasma pneumoniae?
P1 adhesion protein binds to ciliary cells, causing cell stasis and death
89
What are cold agglutinins?
IgM antibodies that bind RBCs, characteristic of this a mycoplasma pneumoniae infection
90
What is the preferred treatment of mycoplasma pneumoniae?
erythromycin or axithromycin – beta-lactams have no target
91
Case 6
• A 45 y/o male has a motorcycle accident in which he is ejected from his motorcycle, lands in mud in a ditch on the side of the road, and suffers a severe compound fracture of his right lower extremity.
He is found approximately 18 hours after his accident, and is rushed to Regional One. He is taken to the OR immediately for RLE repair.
Vascular injury and ischemia of his RLE are found in the OR. Vasculature is repaired. There is a dusky appearance to his tissues in the OR.
• His RLE pain worsens and his leg became very discolored, almost black. Exam of the leg reveals crepitus (crackling or popping sound when palpating the soft tissues). He is taken back to the OR urgently where significant necrotic tissue is found. Extensive debridement (cleaning of necrotic tissue) is done.
Case 6
• A 45 y/o male has a motorcycle accident in which he is ejected from his motorcycle, lands in mud in a ditch on the side of the road, and suffers a severe compound fracture of his right lower extremity.
He is found approximately 18 hours after his accident, and is rushed to Regional One. He is taken to the OR immediately for RLE repair.
Vascular injury and ischemia of his RLE are found in the OR. Vasculature is repaired. There is a dusky appearance to his tissues in the OR.
• His RLE pain worsens and his leg became very discolored, almost black. Exam of the leg reveals crepitus (crackling or popping sound when palpating the soft tissues). He is taken back to the OR urgently where significant necrotic tissue is found. Extensive debridement (cleaning of necrotic tissue) is done
92
The lab is asked to perform both aerobic and anaerobic cultures. Why might this be?
crepitus indicates gas in the tissue (assumedly from anaerobic bacteria) and he was found in ditch where anaerobes are found commonly
93
Gram stain of the OR specimens reveals large Gram positive bacilli. Aerobic culture is negative, anaerobic culture grew colonies on BAP that produced clear hemolysis. This was consistent with Clostridium perfringens.
• What are the dual benefits of debridement in anaerobic infections?
you get rid of devitalized tissue and only leave behind good tissue and
you get rid of the toxin produced by the bacteria
94
• Crepitus indicates the presence of gas in tissues and this is a case of “gas gangrene,” which is an invasive infection.
1) How might the gas be produced?
2) What type of virulence factor do you suppose is causing the necrotic infection?
1) fermentation (bad smelling is a characteristics of anaerobic infection)
2) cell-lysing exotoxin
95
1) What feature of some Gram positive organisms would allow it to survive long periods of time in the soil?
2) If infection is initially by spores, what patient factor favored development of this invasive infection?
1) spores
| 2) the time in the soil allow the spores to reactivate
96
What is Gas gangrene?
a dreaded disease that begins as a contaminated wound infection but can quickly lead to shock and death in just a few hours. Traumatic injury allows the introduction of spores from the soil.
If the injury is not attended to in a timely way, the spores can germinate in oxygen-poor tissue and lead to infection.
Hydrogen and carbon dioxide production is the result of fermentation of carbohydrates in the infected tissues.
97
In Gas genrene, bacterial growth is accompanied by what?
Bacterial growth is accompanied by the production of **alpha-toxin**, a phospholipase (lecithinase) that lyses cells. Shock is attributable to the spread of alpha-toxin to the bloodstream
Clostridia are not found at the distal sites, just the toxin.
98
How is gas gangrene treated?
Gas gangrene is a medical emergency and requires surgical debridement, often radical, and high doses of penicillin G. You can give desensitizing doses of penicillin G if they are allergic.
99
What is the causative bacteria of gas gangrene?
Clostridium perfringens
100
What are some characteristics of Clostridium perfringens?
* Anaerobic, spore-forming Gram positive bacilli that are large with square ends – “box cars”
* Produce double zone of hemolysis on BAP
* Present in soil and colon of humans and animals
* Gas gangrene or food poisoning
101
What kinds of important virulence factors do Clostridium perfringens have?
• Virulence factors
– Spore formation
– Alpha toxin (lecithinase) in gas gangrene that lyse cells
Pore-forming enterotoxin in food poisoning (5% of strains)
102
What is the difference between gas gangrene and food poisoning?
Food poisoning: spores survive cooking, germinate during reheating to form toxin. Food poisoning is self-limiting, requiring only fluid replacements.
Not caused by the alpha-toxin that causes gas gangrene
103
Case 7
• A 1-month-old girl presents with a diffuse, “sandpaper-like” rash. Her mother noticed the rash while nursing her daughter. The girl does not appear to be severely ill, but is feverish and dehydrated. The rash soon worsens, with widespread loss of skin, with the epidermis appearing to come off in sheets. Hospitalization is required.
• Blood cultures from the girl were negative, but a sample taken from the oral cavity grew Staphylococcus aureus. No S. aureus was cultured from any of the sites of skin loss. Combined with the clinical presentation, this indicated a case of staphylococcal scalded skin syndrome (SSSS).
Case 7
• A 1-month-old girl presents with a diffuse, “sandpaper-like” rash. Her mother noticed the rash while nursing her daughter. The girl does not appear to be severely ill, but is feverish and dehydrated. The rash soon worsens, with widespread loss of skin, with the epidermis appearing to come off in sheets. Hospitalization is required.
• Blood cultures from the girl were negative, but a sample taken from the oral cavity grew Staphylococcus aureus. No S. aureus was cultured from any of the sites of skin loss. Combined with the clinical presentation, this indicated a case of staphylococcal scalded skin syndrome (SSSS).
104
If the cultured bacteria were Gram stained, what would have been seen?
gram-positive cocci in grape-like clusters
105
What would the catalase and coagulase results been?
catalase- positive
| coagulase- positive
106
How might the girl have been infected with S. aureus (does the site of isolation suggest anything)?
breast feeding
107
How can you explain systemic features if S. aureus was not present in the blood or affected tissues?
toxin dissemination
108
Why didn’t the mother have SSSS?
Antibodies and maybe better renal clearance
109
What is SSSS (staph. aureus skin syndrome)? .
it is only one form of S. aureus (very virulent) infection. It is typically found in children under the age of 5, and is often transmitted in daycare settings.
110
What is the cause of SSSS?
Two exfoliative toxins (ETA and ETB) cleave desmoglein-1, a cell-to-cell attachment protein of the superficial epidermis (no scarring).
These exotoxins are phage-encoded and found in only about 5% of S. aureus isolates.
111
What are the types of presentation of SSSS?
SSSS has two types of presentation: the generalized exfoliation described here and a more localized, blistering form occurring at the site of infection.
112
What is the treatment for SSSS?
SSSS treatment includes rehydration therapy, topical wound care, and nafcillin or oxacillin.
If MRSA is involved, then vancomycin or linezolid should be used.
Clindamycin can be used to inhibit toxin production.
113
What are some of characteristics of Staphylococcus aureus?
• Gram positive coccus in grape-like clusters that form golden colonies
– Catalase positive, coagulase positive
– Often beta-hemolytic; growth on mannitol salts agar
• Normal flora of the nose (10-30%)
114
What are some of the virulence factors of Staph. aureus?
• Virulence factors
– Numerous degradative exoenzymes
– Numerous exotoxins (enterotoxins, cytotoxins, exfoliative toxins, TSST)
– Protein A
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What are some of the things St. aureus cause?
• S. aureus is a prolific pathogen
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– Food poisoning
– Pyogenic skin infections (bullous impetigo, folliculitis, styes, carbuncles)
– Toxic shock syndrome
– Necrotizing pneumonia
– Meningitis
– Acute endocarditis
– Osteomyelitis
– Organ abscesses
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116
What is the treatment for a Staph. aureus infection?
Treatment with methacillin or oxacillin, but MRSA is increasing (vancomycin used)
117
How would you treatment Gonorrhea?
Ceftriaxone
118
How would you treat Clamydia?
Azithromycin
119
Administration of Clindamycin and resulting bloody diahhrea is indicative of?
C. Diff infection
