5: Infection Flashcards
What is the most common organism overall in surgical wound infections?
Staphylococcus aureus
[Coagulase positive]
[UpToDate: The predominant organisms causing surgical site infections (SSIs) after clean procedures are skin flora, including streptococcal species, Staphylococcus aureus, and coagulase-negative staphylococci. In clean-contaminated procedures, the predominant organisms include gram-negative rods and enterococci in addition to skin flora. When the surgical procedure involves a viscus, the pathogens reflect the endogenous flora of the viscus or nearby mucosal surface; such infections are typically polymicrobial.]
What is the most common source of fever 48 hours - 5 days after surgery?
Urinary tract infection
[UpToDate: There are many causes of fever in the first week after surgery. Nosocomial infections are common during this period. Occasionally, fever or other symptoms predate surgery and are manifestations of community-acquired infection, such as a viral upper respiratory tract infection.
While SSI and intravascular catheter infections can cause acute postoperative fever, other infections are more frequently identified, including pneumonia and urinary tract infection (UTI).
Patients receiving mechanical ventilation during surgery are at risk for ventilator-associated pneumonia (VAP). The risk of VAP increases with the duration of mechanical ventilation. The risk of pneumonia tapers to a stable, lower rate over the first postoperative week and with the discontinuation of mechanical ventilation.
Patients with depressed mental status or gag reflex due to anesthesia and analgesia are more susceptible to aspiration if they vomit after surgery. A nasogastric tube also increases gastroesophageal reflux and the risk for aspiration.
UTI is a frequent cause of postoperative fever in patients with indwelling urethral catheters. The risk of UTI increases with the duration of catheterization. UTI is more common in patients who have undergone a genitourinary procedure and in those who have chronic, indwelling catheters prior to surgery.
SSI most often presents in the subacute period, one week or more after surgery. However, two organisms, group A streptococcus (GAS) and Clostridium perfringens, can cause fulminant SSI within a few hours after surgery.
Catheter exit site infections and bacteremia associated with intravascular catheters also tend to occur subacutely but should be considered as sources of fever in any patient with a catheter in place, especially if insertion was performed under emergent or nonsterile conditions.
Acute fever can also be caused by noninfectious conditions. Pancreatitis, myocardial infarction, pulmonary embolism, thrombophlebitis, alcohol withdrawal, and acute gout can complicate the acute postoperative period.]
Which bacteria usually cause a furuncle (boil)?
Staph epidermidis or staph aureus
[Treat with drainage +/- antibiotics]
What is the risk of someone contracting HIV from mucous membrane exposure to an HIV positive individual?
0.1%
[UpToDate: The risk of transmission of HIV infection following inadvertent exposure varies widely depending upon the type of exposure. The risk is increased when the source has a high viral load, the volume is large, and the exposure is deep. The healthcare personnel (HCP) at highest risk are those who have percutaneously been inoculated with blood from an HIV-infected source. All known seroconversions have occurred with exposure to blood, bloody fluids, or viral cultures.
The risk of becoming infected with HIV after exposure to body fluids from an HIV-infected patient is low. In the United States, there were 58 confirmed and 150 possible cases of occupationally-acquired HIV reported to the Centers for Disease Control from 1985 to 2013; there was only 1 confirmed case from 2000 to 2012.
A review of prospective studies of seroconversion following occupational exposure to an HIV-infected source in the era before the introduction of potent antiretroviral therapy (ART) found the following:
HIV transmission occurred in 20 of 6135 cases (0.33%) following percutaneous exposure
One case of HIV was transmitted out of 1143 exposures (0.09%) on the mucosa of HCP
There were no cases after 2712 intact skin exposures
A similar frequency of HIV seroconversion after needlestick injury (0.36%) was found in a later report from the Centers for Disease Control and Prevention (CDC) Cooperative Needlestick Surveillance Group and in another meta-analysis (0.23%). The risk of HIV infection following an occupational mucosal exposure was subsequently estimated to be 0.03%]
What is the most common gram negative rod in surgical wound infections?
E. coli
What is the treatment for lymphoma in HIV patients?
Usually chemotherapy
[May need surgery with significant bleeding or perforation]
[UpToDate: The optimal initial therapy for lymphomas in the setting of HIV has yet to be defined. Antiretroviral therapy (ART) is started or modified (if already begun) to control the HIV infection and allow for the administration of chemotherapy and/or radiation therapy. As in the HIV-seronegative population, the choice of therapy is principally determined by the subtype of NHL and the stage of disease. Modifications are made based upon the degree of immunosuppression from HIV as measured by the CD4 count.
The following represents our approach for patients with diffuse large B cell lymphoma (DLBCL). A similar approach may be taken for other types of clinically aggressive NHL, although rituximab is not used for NHL that lacks expression of CD20.
For most patients with DLBCL who have a CD4 count >50 cells/microL, we suggest the combination of CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus rituximab (R-CHOP) rather than CHOP alone (Grade 2B).
The decision to use rituximab in the setting of a CD4 count <50 cells/microL must be individualized. For most patients with DLBCL who have a CD4 count <50 cells/microL, we suggest CHOP chemotherapy without rituximab rather than the combination (Grade 2B). Caution is advised if rituximab is incorporated into CHOP chemotherapy in the setting of CD4 count <50/microL.
For DLBCL patients with >80% growth fraction, or plasmablastic histology in the setting of CD4 count >50/microL, we suggest the standard dose-adjusted EPOCH (etoposide, vincristine, and doxorubicin plus oral prednisone and IV bolus cyclophosphamide) regimen plus rituximab rather than R-CHOP (Grade 2C). In such cases, we suggest concurrent rather than sequential rituximab (Grade 2B).
If treatment with R-EPOCH is chosen, supportive care should include prophylaxis for Pneumocystis jiroveci pneumonia (PCP, previously Pneumocystis carinii pneumonia), and antibiotic prophylaxis for enteric organisms. Given the high incidence of recurrent Herpes simplex, Herpes zoster, and Candida infections in this population, many clinicians also advise instituting antiviral and antifungal prophylaxis.
Lumbar puncture should be performed at diagnosis in the setting of >2 extranodal sites of disease accompanied by elevated LDH, or specific high-risk sites such as paranasal sinuses, testes, epidural space, and bone marrow. CNS prophylaxis is not routinely administered.]
Should clippers or razors be used preoperatively to shave an area?
Clippers to decrease chance of wound infections
[UpToDate: Shaving hair with razors at the planned operative site should be avoided; if hair removal is absolutely necessary, it may be performed with clippers or depilatory agents.
Preoperative hair removal has been associated with an increased risk for SSI. One meta-analysis including 19 trials concluded no hair removal was associated with a significantly lower risk of SSI compared with hair removal via shaving (relative risk [RR] 0.56; 95% CI, 0.34 to 0.96). Of hair removal methods, shaving was associated with the highest risk of SSI, followed by clipping and depilatory creams. In one study, rates of SSI associated with shaving, clipping, or depilatory creams were 5.6%, 1.7%, and 0.6%, respectively.
Scanning electron micrographs have demonstrated that razors cause gross skin cuts and clippers cause less injury than razors; depilatory agents cause no injury to the skin surface. The timing of hair removal is also important; the lowest rates of SSI have been observed when hair was removed just prior to the surgical incision.]
Cirrhotic patients with ascitic protein concentrations below 1 g/dL are at what risk of developing primary spontaneous bacterial peritonitis (SBP) compared to individuals with higher concentrations?
10 times more likely to develop SBP when ascitic protein concentration is below 1 g/dL
[UpToDate: The vast majority of patients with SBP have advanced cirrhosis. Other risk factors (most of which are associated with cirrhosis) include:
- Ascitic fluid total protein concentration less than 1 g/dL (<10 g/L)
- Prior episode of SBP
- Serum total bilirubin concentration above 2.5 mg/dL
- Variceal hemorrhage
- Possibly malnutrition
- Use of proton pump inhibitors
The combination of certain clinical and laboratory features is also associated with an increased risk of SBP:
- An ascitic fluid total protein <1.5 g/dL (<15 g/L) with
- Child-Pugh score ≥9 points with serum bilirubin ≥3 mg/dL or with
- Plasma creatinine ≥1.2 mg/dL, blood urea nitrogen ≥25 mg/dL or plasma sodium ≤130 mEq/L
Patients who meet the above combination criteria should be considered candidates for antibiotic prophylaxis.]
The microflora of which part of the gastrointestinal tract contains 10^5 bacteria (mostly gram positive cocci)?
Proximal small bowel
What is the risk of Hepatitis C infection with blood transfusion today?
0.0001% per unit of blood
[UpToDate: Blood transfusion was a major risk factor for acute infection in the past, with more than 10% of transfusion recipients acquiring infection in some studies. The screening of blood donors for historical risk factors, serologic evidence of hepatitis B infection (HBsAg and anti-HBc), and elevated serum ALT caused a striking reduction in the rates of non-A, non-B post-transfusion hepatitis, even before HCV was identified. The subsequent initiation of donor screening for anti-HCV antibodies in 1990 has nearly eliminated the risk of posttransfusion acute HCV infection. The estimated risk is now less than one in a million per unit transfused.]
Fungal infection with which organism is most commonly associated with CNS symptoms in AIDS patients?
Cryptococcus
[UpToDate: Disseminated Cryptococcus neoformans infection is a serious opportunistic infection that occurs in patients with untreated AIDS. Although cryptococcal infection begins in the lungs, meningitis is the most frequently encountered manifestation of cryptococcosis among those with advanced immunosuppression. However, the infection is more properly characterized as “meningoencephalitis” rather than meningitis since the brain parenchyma is almost always involved on histologic examination.
Symptoms of cryptococcal meningoencephalitis typically begin indolently over a period of one to two weeks. The most common symptoms are fever, malaise, and headache. Stiff neck, photophobia, and vomiting are seen in one-fourth to one-third of patients. Patients rarely present with coma and fulminant death in days.
Other symptoms suggesting disseminated disease include cough, dyspnea, and skin rash. Visual and hearing loss has also been reported.
The initial physical examination may be notable for lethargy or confusion in association with fever. In one report, 24% of patients had altered mentation on presentation, and 6% presented with focal neurologic deficits. Other manifestations of disseminated disease may be evident, including tachypnea and skin lesions resembling molluscum contagiosum. Increased diastolic hypertension may be reflective of increased intracranial pressure.
General laboratory studies are nonspecific. Patients with advanced immunosuppression may have leukopenia, anemia, hypoalbuminemia, and an increased gamma globulin antibody fraction.
We have a high index of suspicion for cryptococcal meningitis in patients with advanced HIV infection (CD4 cell count <100 cells/microL) who have isolated fever and headache. Initial evaluation includes a careful history, neurologic exam, and serum cryptococcal antigen. Evaluation should also include a lumbar puncture to assess for increased intracranial pressure and culture of cerebrospinal fluid (CSF) to confirm the diagnosis in those with symptoms and/or a positive serum cryptococcal antigen (CrAg).]
What is the most common anaerobe in the colon?
Bacteroides fragilis
[UpToDate: The largest concentrations of anaerobic bacteria are found in the relatively stagnant terminal ileum and colon, where concentrations reach 1011 per gram, and anaerobic bacteria account for approximately 99.9% of the cultivable flora. The most important and frequent anaerobic bacteria are Bacteroides spp (principally members of the B. fragilis group), Prevotella spp, Clostridium spp, and Peptostreptococcus spp.]
The exoslime released by staph species is composed of what?
Exopolysaccharide matrix
What is the treatment for acute septic arthritis?
Drainage, 3rd generation cephalosporin and vancomycin until cultures show which organism is responsible
[Commonly gonococcus, staph, H. influenzae, strep]
[UpToDate: Treatment of acute bacterial arthritis consists of antibiotic therapy and joint drainage. The initial choice of antibiotics for treatment of septic arthritis is based on the Gram stain. The initial regimen should be tailored to culture and susceptibility results when available. The typical duration of therapy is three to four weeks.
If the initial Gram stain of the synovial fluid shows gram-positive cocci, we suggest treatment with vancomycin (Grade 2B). If the initial Gram stain of the synovial fluid shows gram-negative bacilli, we suggest treatment with a third-generation cephalosporin (Grade 2B).
If the initial Gram stain is negative and the patient is immunocompetent, we suggest treatment with vancomycin (Grade 2C). If the initial Gram stain is negative and the patient is immunocompromised, we suggest treatment with vancomycin plus a third-generation cephalosporin (Grade 2C).
In general, we recommend joint drainage in the setting of septic arthritis (Grade 1B), as this condition represents a closed abscess collection. Options for drainage include needle aspiration (single or multiple), arthroscopic drainage, or arthrotomy (open surgical drainage).]
What is the treatment for Nocardia infection?
Drainage and sulfonamides (Bactrim)
[UpToDate: Nocardiosis is an uncommon gram-positive bacterial infection that usually causes infection in immunocompromised hosts. Two characteristics that distinguish nocardiosis are the ability to disseminate to virtually any organ, particularly the central nervous system, and the tendency to relapse or progress despite appropriate therapy.
Patients with systemic disease require antibiotic therapy. We also recommend antibiotic therapy even in patients with limited cutaneous disease (Grade 1C).
Antibiotics that are typically effective against Nocardia spp include trimethoprim-sulfamethoxazole (TMP-SMX), amikacin, imipenem, and third-generation cephalosporins (ceftriaxone and cefotaxime). However, antibiotic susceptibilities vary among isolates. The suggested regimens discussed below are empiric and should be tailored once information on susceptibilities is available. Dosing is presented in the table.
Patients with isolated cutaneous infection can usually be managed with oral monotherapy. We suggest initial therapy with oral TMP-SMX (Grade 2C). Patients who do not respond require intravenous therapy as discussed below for severe disease.
For patients with nonsevere mycetomas, we suggest initial therapy with oral TMP-SMX with or without dapsone (Grade 2C). For patients with severe mycetomas, we suggest initial therapy with imipenem with or without amikacin (Grade 2C).
For patients with mild to moderate pulmonary nocardiosis without involvement of other organs, we suggest monotherapy with oral TMP-SMX (Grade 2C).
Most experts would treat severe infection with two or three intravenous agents while awaiting results of susceptibility testing. In patients without central nervous system (CNS) disease, we suggest treating with TMP-SMX plus amikacin (Grade 2C). In patients with CNS disease, we suggest TMP-SMX plus imipenem (Grade 2C). In patients with CNS disease who have multiorgan involvement, we also add amikacin.
In selected patients with severe disease who have improved after receiving three to six weeks of intravenous therapy and do not have CNS disease, treatment can be switched to an oral regimen. In these patients, we suggest a monotherapy oral regimen to complete the treatment course (Grade 2C). The oral agent is selected based on susceptibility testing; we use TMP-SMX if the isolate is susceptible.
The optimal duration of antimicrobial treatment for severe disease has not been determined, but most recommend a prolonged course because of the relapsing nature of Nocardia infection. We usually treat for a duration of 3 to 6 months for isolated cutaneous infection in immunocompetent patients but for 6 to 12 months in immunocompromised patients with isolated cutaneous infection. For patients with serious pulmonary infection, we treat for 6 to 12 months or longer. All immunocompromised patients (except those with isolated cutaneous infection) as well as patients with CNS involvement should be treated for at least one year. Within these ranges, the duration of therapy is based upon the severity and extent of disease and the clinical and radiographic response to treatment.]
What is/are the oral treatment option(s) for Clostridium Difficile Colitis?
Oral Vancomycin or Flagyl
[Lactobacillus can help]
[UpToDate: For initial treatment of nonsevere CDI, we suggest oral metronidazole (Grade 2B).
For treatment of severe CDI, we recommend vancomycin 125 mg four times daily for 10 to 14 days (Grade 1B). For patients with severe disease who do not demonstrate clinical improvement, we suggest treatment with oral vancomycin 500 mg four times daily (Grade 2C); fidaxomicin may be considered in patients who cannot tolerate vancomycin, although more data are needed. In critically ill patients with fulminant or refractory disease, we suggest oral vancomycin 500 mg four times daily and intravenous metronidazole 500 mg every eight hours (Grade 2C); fidaxomicin may be considered in patients who cannot tolerate vancomycin, although more data are needed.
For treatment of severe disease in patients with profound ileus, we suggest addition of intracolonic vancomycin (Grade 2C), but there is risk of colonic perforation. Therefore, use of intracolonic vancomycin should be restricted to patients who are not responsive to oral therapy, and the procedure should be performed by personnel with expertise in administering enemas.
For treatment of a nonsevere initial recurrence of CDI, we suggest oral metronidazole (Grade 2A). Alternatives include oral vancomycin or fidaxomicin.
For treatment of a second recurrence of CDI, we suggest intermittent and tapering vancomycin therapy or fidaxomicin. For treatment of subsequent recurrences of CDI, we suggest administering either fidaxomicin or vancomycin followed by rifaximin (Grade 2C).
We recommend urgent surgical evaluation for patients with a white blood cell count ≥20,000 cells/microL and/or a plasma lactate between 2.2 and 4.9 mEq/L (Grade 1B). In addition, surgical intervention should be strongly considered in the setting of peritoneal signs, severe ileus, or toxic megacolon.]
What is the treatment for diabetic foot infections?
Broad-spectrum antibiotics such as Unasyn (Ampicillin/Sulbactam)
[Commonly mixed staph, strep, gram negative rods, and anaerobes]
[UpToDate: Management of diabetic foot infections requires attentive wound management, good nutrition, antimicrobial therapy, glycemic control, and fluid and electrolyte balance. Wound management includes attentive local wound care including debridement of callus and necrotic tissue, wound cleansing, and relief of pressure on the ulcer. Consultation with a surgeon with experience in diabetic foot infection is important for cases of severe infections and most cases of moderate infections. Prompt surgical debridement is critical for cure of infections complicated by abscess, extensive bone or joint involvement, crepitus, necrosis, gangrene or necrotizing fasciitis and is important for source control in patients with severe sepsis.
The microbiology of diabetic foot wounds varies with the severity and extent of involvement. Superficial infections are likely due to aerobic gram-positive cocci whereas deep, chronically infected, and/or previously treated ulcers are more likely to be polymicrobial. Anaerobic organisms may also be involved in wounds with extensive local inflammation, necrosis, or gangrene. When there is concern for multidrug-resistant organisms or in cases of moderate or severe infection (including deep infections and osteomyelitis), aerobic and anaerobic cultures of deep tissue or bone biopsies should be obtained at the time of debridement. Organisms cultured from superficial swabs are not reliable for predicting the pathogens responsible for deeper infection.
Empiric antibiotic therapy should be selected based upon the severity of infection and the likelihood of involvement of resistant organisms:
- For patients with mild infections, we suggest an empiric antimicrobial regimen with activity against skin flora including streptococci and Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA] if risk factors are present) (Grade 2C).
- For patients with deep ulcers, we suggest an empiric antimicrobial regimen with activity against streptococci, S. aureus (and MRSA if risk factors are present), aerobic gram-negative bacilli and anaerobes (Grade 2C). Oral antibiotics may be appropriate for ulcers that extend to the fascia, whereas parenteral regimens should be used for deeper infections.
- For patients with limb-threatening diabetic foot infections or evidence of systemic toxicity, we suggest treatment with a broad-spectrum parenteral antibiotic regimen with activity against streptococci, MRSA, aerobic gram-negative bacilli, and anaerobes (Grade 2C).
Antimicrobial therapy should be tailored to culture and susceptibility results when available, and a switch to an oral from parenteral regimen is reasonable following clinical improvement. Antibiotics need not be administered for the entire duration that the wound remains open. Close follow-up is important to ensure continued improvement and to evaluate the need for modification of antimicrobial therapy, further imaging, or additional surgical intervention.
Many patients with osteomyelitis of the foot benefit from surgical resection. However, in certain cases, limited surgical debridement combined with prolonged antibiotic therapy may be appropriate. The duration of antibiotic therapy of osteomyelitis depends on the extent of residual affected tissue.]
What are 2 risk factors for Fournier’s gangrene (a severe infection in the perineal and scrotal region)?
- Diabetes mellitus
- Immunocompromised state
[UpToDate: Necrotizing infection of the male perineum, known as Fournier’s gangrene, can result from a breach in the integrity of the gastrointestinal or urethral mucosa. Infection can occur in all age groups but is most common in older men. Necrotizing infection involving the labia and perineum can also occur in females, particularly in the setting of diabetes. Fournier’s gangrene begins abruptly with severe pain and may spread rapidly to the anterior abdominal wall, the gluteal muscles, and, in males, onto the scrotum and penis. In the setting of Fournier’s gangrene, early aggressive drainage or debridement is essential. Affected patients may require cystostomy, colostomy, or orchiectomy.]
What are 2 causes of surgical infection within 48 hours of a procedure?
- Injury to bowel with a leak
- Invasive soft tissue infection (clostridium perfringens and beta-hemolytic strep can present within hours postoperatively)
[UpToDate: SSI most often presents in the subacute period, one week or more after surgery. However, two organisms, group A streptococcus (GAS) and Clostridium perfringens, can cause fulminant SSI within a few hours after surgery.]
How soon after surgical procedures can necrotizing soft tissue infections occur?
Within hours
What is the line salvage rate with antibiotics?
50%
[Much less likely with yeast line infections]
[UpToDate: Following diagnosis of catheter-related infection, catheter salvage may be attempted in the setting of uncomplicated CRBSI involving long-term catheters due to pathogens other than S. aureus, P. aeruginosa, fungi, or mycobacteria. Salvage is also difficult in the setting of CRBSI due to organisms of relatively low virulence that are difficult to eradicate (eg, Bacillus spp, Micrococcus spp, or Propionibacteria). Catheter salvage in the setting of coagulase-negative staphylococcal infection does not influence resolution of bacteremia but may be a risk factor for recurrence (relative risk 6.6 in a retrospective series of 175 cases).
If salvage is attempted, both systemic and antimicrobial lock therapy may be administered through the colonized catheter for the duration of therapy, depending upon the microorganism. The efficacy of antibiotic lock therapy remains uncertain and concerns have been raised about the emergence of antimicrobial resistance and fungal superinfection. The optimal antimicrobial dosing for lock therapy is also uncertain. Antibiotic lock therapy is not warranted for management of catheter infection for devices in place for <2 weeks; these are usually extraluminal infections.
Two sets of blood cultures should be obtained after 72 hours of appropriate antimicrobial therapy (for neonates, one set is acceptable); positive cultures should prompt catheter removal.
Catheter removal is not necessary for hemodynamically stable patients with unexplained fever in the absence of documented bloodstream infection and without endovascular prosthetic material (such as a prosthetic valve, pacemaker, or vascular graft).]
The microflora of which part of the gastrointestinal tract contains 10^11 bacteria consisting almost entirely of anaerobes, some gram negative rods, and some gram positive cocci?
Colon
Which endotoxin gets released in gram-negative sepsis?
Lipopolysaccharide lipid A
[UpToDate: Anaerobic gram-negative bacteria, like all gram-negative bacteria, contain lipopolysaccharide (LPS) that can be extracted from the envelope, but the biologic activity of this endotoxin (mouse lethality assays, the chick embryo death test, and the Shwartzman reaction) is 100 to 1000 times less than that of LPS from Enterobacteriaceae. The LPS of B. fragilis contains a lipid A moiety (the endotoxin portion of LPS), but there are structural and chemical composition differences that render this LPS less potent than the LPS of Escherichia coli. The inability of B. fragilis LPS to activate TLR 2 may be responsible for this difference.
Lipid A is the biologically active component of lipopolysaccharide (LPS) found in the cell wall of Salmonella and other gram-negative bacteria. Lipid A is toxic to mammalian cells and is a potent immunomodulator. Certain features of the lipid A in Salmonella may correlate with virulence or with activation of host inflammation. Lipid A induces toll-like receptor 4 (TLR4)-mediated responses, which are important for host defense against Salmonella infection, and modifications in lipid A as part of Salmonella’s adaptation to host environments reduce this signaling. Death in mice from Salmonella may be related to the toxic effect of lipid A, which triggers further production of TNF-alpha and IL-1 beta. S. typhimurium mutants with a defective lipid A molecule have greatly attenuated virulence in mice. Structural modifications of lipid A are influenced by the Salmonella virulence regulatory locus (phoP/phoQ) which responds to a variety of host intracellular environmental signals. For example, antimicrobial peptides have been shown to be part of the first step in signal transduction across the bacterial membrane, resulting in activation of phoQ and promotion of bacterial virulence. PhoP has also been found to bind a promoter region of a drug efflux system, thus connecting virulence with possible drug resistance.]
Which 2 locations in the body are the most common sites of lymphoma in HIV patients?
- Stomach
- Rectum
[UpToDate: The GI tract is a frequent presenting site in patients with HIV-associated lymphoma, though the prevalence of GI involvement may have declined in the post-antiretroviral therapy (ART) era. Virtually any area of the GI tract may be involved, but the most common sites are the stomach, duodenum, perianal/anal area, and the oropharynx. The major presenting features are abdominal or perianal pain, fever, diarrhea, and/or weight loss; life-threatening complications such as bleeding, perforation and obstruction are not uncommon. When GI involvement is suspected, the evaluation includes imaging studies, upper and lower endoscopy with evaluation of the small bowel, and biopsy.
Most information regarding gastrointestinal (GI) lymphoma in the HIV-positive population comes from the era before the routine implementation of ART, since this condition is most commonly associated with advanced HIV and low CD4 counts. Based on older series, the gastrointestinal tract is the presenting site of AIDS-related systemic lymphoma in 30% to 50% of patients, and is the most frequent site of extranodal disease. A more recent series indicates the rate of GI involvement to be 14% of AIDS-related lymphoma. The area of gastrointestinal tract involvement is different from that in the non-HIV setting. Virtually any area of the gastrointestinal tract may be involved, including the oral cavity, esophagus, bile duct, pancreas, mesentery, small bowel, perianal area, and anal canal.
In one series of 48 patients with HIV-associated gastrointestinal lymphoma, involvement was multifocal in 23%. Areas of involvement included:
- Stomach – 50%
- Duodenum – 25%
- Perianal/anal – 15%
- Oropharynx – 10%
- Small bowel – 8%
- Esophagus – 6%
- Liver, cecum, and rectum – Each <5%
The major presenting features of these tumors are abdominal or perianal pain, fever, diarrhea, and/or weight loss; life-threatening complications such as bleeding, perforation, and obstruction have been reported in 16% to 55%.]
What percent of abdominal abscesses have anaerobes?
90%
What is the most common source of fever within 48 hours of surgery?
Atelectasis
[UpToDate: The potential causes of fever in the immediate operative and postoperative period are mainly limited to: medications or blood products to which the patient was exposed during preoperative care either in the operating room or in the recovery area; trauma suffered prior to surgery or as part of surgery; infections that were present prior to surgery; and rarely malignant hyperthermia.
Adverse medication reactions that produce immediate fever include immune-mediated reactions, such as reactions to antimicrobials and to transfused blood products. The vasodilation that often accompanies these reactions makes hypotension a common presenting sign; rash may accompany fever in some patients with medication reactions.
The initial clinical signs (ie, hypercarbia) of malignant hyperthermia typically present within 30 minutes following the administration of a triggering agent (eg, inhaled anesthetics, succinylcholine), but have been reported later in the operative course and also following cessation of anesthesia. If the malignant hyperthermia response is not recognized and aborted with dantrolene, high fever may develop as result of hypermetabolism.
Fever due to the trauma of surgery usually resolves within 2 to 3 days. The severity and duration of these self-limited postoperative fevers depends on the type of surgery, but tends to be greater in patients with longer and more extensive surgical procedures. Fever caused by severe head trauma can be persistent and may resolve gradually over days or even weeks.
Atelectasis is often used as an explanation for otherwise unexplained postoperative fever. Both atelectasis and fever occur frequently after surgery, but their concurrence is probably coincidental rather than causal.
- In one study of 270 consecutive patients after abdominal surgery, the sensitivity and negative predictive value of fever as a predictor of atelectasis were both less than 50%, and the specificity and positive predictive value were 68% and 66% respectively.
- In another study, there was also no association between fever and the presence of, or the degree of, atelectasis. Therefore, ascribing a postoperative fever to atelectasis is probably false reassurance and may mislead the clinician from pursuing the true cause of the fever.]
What is the optimal glucose level in a septic patient?
100-120 mg/dL
[UpToDate: For hyperglycemic critically ill adult patients:
- We recommend a blood glucose target of 140 to 180 mg/dL (7.7 to 10 mmol/L), rather than a more stringent target (eg, 80 to 110 mg/dL [4.4 to 6.1 mmol/L]) (Grade 1A).
- We also suggest a blood glucose target of 140 to 180 mg/dL (7.7 to 10 mmol/L), rather than a more liberal target (eg, 180 to 200 mg/dL [10 to 11.1 mmol/L]) (Grade 2C).
The Volume Substitution and Insulin Therapy in Severe Sepsis (VISEP) trial was a multicenter two-by-two factorial trial conducted in medical and surgical ICU patients with severe sepsis. It compared IIT (target blood glucose level of 80 to 110 mg/dL [4.4 to 6.1 mmol/L]) to conventional glucose control (target blood glucose level of 180 to 200 mg/dL [10 to 11.1 mmol/L]), as well as comparing two methods of volume resuscitation. The IIT arm of the trial was stopped after 488 patients were enrolled because IIT significantly increased the rate of hypoglycemia (12.1% vs 2.1%) and serious adverse events (10.9% vs 5.2%). The trial then continued with only patients in the conventional therapy group until 537 patients were enrolled. The following outcomes were detected when IIT was compared to conventional glucose control:
- Mean morning blood glucose was significantly lower in the IIT group (112 vs 151 mg/dL [6.2 vs 8.4 mmol/L])
- Hypoglycemia (blood glucose ≤40 mg/dL [2.2 mmol/L]) was significantly more common in the IIT group (17% vs 4.1%)
- There was no significant difference in 28 day mortality (24.7% vs 26% in the conventional glucose control group), morbidity, or organ failures
- There was a nonstatistically significant increase in 90 day mortality in the IIT group (39.7% vs 35.4%)
The Glucontrol trial was a multicenter trial that randomly assigned 1101 critically ill medical and surgical patients to IIT (target blood glucose of 80 to 110 mg/dL [4.4 to 6.1 mmol/L]) or conventional glucose control (target blood glucose of 140 to 180 mg/dL [7.8 to 10 mmol/L]). The trial was terminated early because of a high rate of unintended protocol violations. IIT significantly increased the rate of hypoglycemia (8.7% vs 2.7%). There was no difference in ICU mortality, although the IIT group had a nonsignificant trend toward increased 28 day mortality and hospital mortality.
Meta-analysis — Meta-analyses have been performed in an effort to consolidate the data from numerous randomized trials. One such meta-analysis of 15 randomized trials (10,140 patients) compared IIT (defined as a target blood glucose level ≤150 mg/dL [8.3 mmol/L]) to less stringent glycemic control in mixed medical and surgical ICU patients. Patients who received IIT had a similar mortality to those who received less stringent glycemic control (26.7% vs 25.6%, relative risk 0.99, 95% CI 0.87-1.12).
Summary - In mixed adult populations of critically ill medical and surgical patients, IIT (target blood glucose of 80 to 110 mg/dL [4.4 to 6.1 mmol/L]) increased the incidence of severe hypoglycemia and either increased mortality or had no effect on mortality, when compared to the more permissive blood glucose ranges of 140 to 180 mg/dL (7.8 to 10 mmol/L) and 180 to 200 mg/dL (10 to 11.1 mmol/L). Similar trends have been noted in children.]
Which are most common in the GI tract: Aerobes or anaerobes?
Anaerobes
What must be ruled out if primary spontaneous bacterial peritonitis is not responding to antibiotics or if cultures are polymicrobial?
Intra-abdominal source (IE bowel perforation)
[UpToDate: Patients with suspected secondary bacterial peritonitis should receive broader coverage with cefotaxime and metronidazole. A similar regimen should be used with polymicrobial bacterascites.]
What is the risk of someone contracting HIV from a needle stick from an HIV positive patient?
0.3%
[UpToDate: The risk of transmission of HIV infection following inadvertent exposure varies widely depending upon the type of exposure. The risk is increased when the source has a high viral load, the volume is large, and the exposure is deep. The healthcare personnel (HCP) at highest risk are those who have percutaneously been inoculated with blood from an HIV-infected source. All known seroconversions have occurred with exposure to blood, bloody fluids, or viral cultures.
The risk of becoming infected with HIV after exposure to body fluids from an HIV-infected patient is low. In the United States, there were 58 confirmed and 150 possible cases of occupationally-acquired HIV reported to the Centers for Disease Control from 1985 to 2013; there was only 1 confirmed case from 2000 to 2012.
A review of prospective studies of seroconversion following occupational exposure to an HIV-infected source in the era before the introduction of potent antiretroviral therapy (ART) found the following:
- HIV transmission occurred in 20 of 6135 cases (0.33%) following percutaneous exposure
- One case of HIV was transmitted out of 1143 exposures (0.09%) on the mucosa of HCP
- There were no cases after 2712 intact skin exposures
A similar frequency of HIV seroconversion after needlestick injury (0.36%) was found in a later report from the Centers for Disease Control and Prevention (CDC) Cooperative Needlestick Surveillance Group and in another meta-analysis (0.23%). The risk of HIV infection following an occupational mucosal exposure was subsequently estimated to be 0.03%]
Which bacteria has alpha toxin that is a membrane-disrupting toxin with phospholipase C activity, directly responsible for gas gangrene and myonecrosis?
Clostridium perfringens
[UpToDate: Many extracellular toxins are produced by C. perfringens; of these, alpha and theta toxins have been implicated in pathogenesis:
Alpha toxin is a hemolytic toxin with both phospholipase C (PLC) and sphingomyelinase activities. Two independent studies have identified alpha toxin as an essential toxin in disease. First, genetic interruption of the alpha toxin gene in C. perfringens rendered the organism avirulent in a mouse myonecrosis model. Complementation of the chromosomal mutation with a recombinant plasmid carrying a wild-type gene fully restored ability to cause disease. Second, vaccination with the C-terminal domain of alpha toxin (amino acids 247 to 370) protected mice from experimental C. perfringens infection in part by improving tissue perfusion and restoring the tissue inflammatory response.
Theta toxin (also known as perfringolysin O) is a member of the cholesterol-dependent cytolysin family that includes streptolysin O, pneumolysin, listeriolysin, septicolysin, and others. These pore-forming toxins contain a conserved amino acid motif. Theta toxin appears to contribute to pathogenesis by its effects on cells of the vascular and immune systems. However, theta toxin is not essential in causing mortality since isogenic mutant strains lacking an intact theta toxin structural gene (pfoA) remained lethal in the mouse myonecrosis model.
Molecular and animal studies have shown that alpha toxin is largely responsible for both the widespread tissue necrosis and the characteristic absence of tissue inflammatory response. Alpha toxin potently stimulates platelet aggregation and upregulates adherence molecules on PMN and endothelial cells. Experimental intramuscular alpha toxin injection causes a rapid, irreversible decline in muscle blood flow and concomitant ischemic necrosis of tissue due to the formation of occlusive intravascular aggregates composed of activated platelets, leukocytes, and fibrin. The perfusion deficits expand the anaerobic environment and contribute to the rapidly advancing margins of tissue destruction characteristic of clostridial gas gangrene.
Shock associated with gas gangrene may be attributable to both direct and indirect effects of alpha and theta toxins. Alpha toxin directly suppresses myocardial contractility and may contribute to profound hypotension via a sudden reduction in cardiac output. In experimental models, theta toxin causes markedly reduced systemic vascular resistance combined with a markedly increased cardiac output (ie, “warm shock”). This likely occurs via induction of endogenous mediators such as prostacyclin, platelet activating factor, and other lipid autocoids that cause vasodilation.]
What is the risk of surgical site infection in a clean contaminated procedure (IE. elective colon resection with prepped bowel)?
3-5%
[UpToDate: A widely accepted wound classification system has been developed by the National Academy of Sciences and the National Research Council based upon the degree of expected microbial contamination during surgery. It stratifies wounds as clean, clean-contaminated, contaminated, or dirty using the following definitions:
Clean wounds are uninfected operative wounds in which no inflammation is encountered and the wound is closed primarily. By definition, a viscus (respiratory, alimentary, genital, or urinary tract) is not entered during a clean procedure.
Clean-contaminated wounds are operative wounds in which a viscus is entered under controlled conditions and without unusual contamination.
Contaminated wounds are open, fresh accidental wounds, operations with major breaks in sterile technique, or gross spillage from a viscus. Wounds in which acute, nonpurulent inflammation was encountered also were included in this category.
Dirty wounds are old traumatic wounds with retained devitalized tissue, foreign bodies, or fecal contamination or wounds that involve existing clinical infection or perforated viscus.
Several studies have found a moderate correlation between the wound classification and the SSI rate. SSI rates according to wound class were:
Clean – 1.3% to 2.9%
Clean-contaminated – 2.4% to 7.7%
Contaminated – 6.4% to 15.2%
Dirty – 7.1% to 40.0%
While widely used, this classification scheme may be a poor predictor of overall risk of SSI. Other factors, such as the operative technique, length of surgery, and health of the surgical patient, may be as important as wound classification in predicting infectious risks for SSI.
Available data suggest that the relative risk reduction of SSI from the use of antimicrobial prophylaxis is the same in clean and in higher-risk procedures. Antimicrobial prophylaxis is justified for most clean-contaminated procedures. The use of antimicrobial agents for dirty procedures or established infection is classified as treatment of presumed infection, not prophylaxis.]
What are the bacterial causes of necrotizing soft tissue infections?
- Beta-hemolytic strep (Group A)
- C. perfringens
- Mixed organisms
[UpToDate: Necrotizing soft tissue infections are comprised of two distinct bacteriologic entities: type I (polymicrobial infection) and type II (group A streptococcal [GAS] infection). There are also case reports of monomicrobial necrotizing soft tissue infections due to other organisms, including Haemophilus influenzae.
In type I infection, at least one anaerobic species (most commonly Bacteroides, Clostridium, or Peptostreptococcus) is isolated in combination with one or more facultative anaerobic streptococci (other than group A) and members of the Enterobacteriaceae (eg, Escherichia coli, Enterobacter, Klebsiella, Proteus). An obligate aerobe, such as P. aeruginosa, is only rarely a component of such a mixed infection. Necrotizing fasciitis of the head and neck is usually caused by mouth anaerobes, such as Fusobacteria, anaerobic streptococci, Bacteroides, and spirochetes. Fournier’s gangrene is caused by facultative organisms (E. coli, Klebsiella, enterococci) along with anaerobes (Bacteroides, Fusobacterium, Clostridium, anaerobic or microaerophilic streptococci).
In type II, necrotizing fasciitis is generally mono-microbic, most commonly caused by group A Streptococcus (also known as hemolytic streptococcal gangrene). Aeromonas hydrophila has been associated with traumatic lesions in fresh water, and Vibrio vulnificus can cause necrotizing fasciitis in association with seawater injuries (Gulf coast and South Atlantic seaboard) or among patients with cirrhosis who ingest raw oysters. Group A streptococci or other beta-hemolytic streptococci are isolated alone or in combination with other species, most commonly Staphylococcus aureus. In communities with relatively high prevalence of community-acquired methicillin-resistant S. aureus (CA-MRSA) infection, this organism is also a potential cause of monomicrobial necrotizing infection.
An important virulence determinant of GAS, M protein, is a filamentous protein anchored to the cell membrane. M protein has antiphagocytic properties. Many M types of GAS have been associated with necrotizing fasciitis; types 1 and 3 are most common. These strains can produce one or more of the pyrogenic exotoxins A, B, or C. Necrotizing fasciitis caused by these strains is associated with streptococcal toxic shock syndrome in about 50% of cases.
Group A streptococci may localize to the exact site of muscle injury due to increased surface expression of vimentin, which specifically binds the microbe. In an in vitro model, investigators demonstrated that injured skeletal muscle cells in tissue culture increased adherence of GAS twofold due to specific binding of GAS by vimentin on the surface of these cells.
Pyrogenic exotoxins lead to cytokine production, which may explain some of the clinical findings of necrotizing fasciitis. The exotoxins bind to the MHC class II portion of antigen presenting cells, such as macrophages. This complex can then bind to a specific V beta segment of the T cell receptor in the absence of classical antigen processing by the macrophage. Thus, pyrogenic exotoxins are superantigens and cause rapid proliferation of T cells bearing specific V beta repertoires. Such stimulation of the host’s immune cells is associated with production of both monokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1, and IL-6) and lymphokines (IL-2 and TNF-beta). Expression of these cytokines in vivo probably contributes to shock, tissue destruction, and organ failure.]
When should an infected peritoneal dialysis catheter be removed?
For peritonitis that lasts for 4-5 days (First treat with intraperitoneal Vancomycin and gentamicin)
[Some say need removal of peritoneal dialysis catheter for all fungal, tuberculous, and pseudomonas infections]
[UpToDate: If the exit site remains infected after two weeks of antibiotics, compliance should be ensured and a thorough repeat examination performed. One should also examine the exit site to see if the external cuff is exposed since an exposed cuff may cause infection. Ultrasonography, computed tomography (CT) scanning, or less often gallium scanning may be performed to exclude an abscess. If the cuff is not exposed and there is no evidence of abscess or tunnel infection, additional antibiotic therapy may be attempted or salvage techniques may be employed to rescue the infected catheters.
Catheter removal is required for some exit-site and tunnel infections such as those complicated by a tunnel abscess or peritonitis, or if the infection does not respond or progresses after several weeks of antibiotic therapy. In all cases, perioperative antibiotics should be given and then continued for one to two weeks after catheter removal.
If there is no peritonitis associated with the exit-site infection, the infected catheter can be removed and a new catheter placed simultaneously in the opposite lower quadrant. A new catheter should not be placed at the time the infected catheter is removed if active peritonitis is present.]
What is the most common type of lymphoma in HIV patients?
Non-Hodgkin’s B-cell lymphoma
[UpToDate: AIDS-related non-Hodgkin lymphoma (NHL) can be divided into three general categories based on location:
- Systemic NHL
- Primary central nervous system (CNS) lymphoma
- Primary effusion (or body cavity) lymphoma
Systemic NHL accounts for the great majority of AIDS-related lymphomas, while primary CNS lymphoma accounts for approximately 15%, and primary effusion lymphoma for less than 1%. Systemic NHL can be further divided into common subtypes described in the World Health Organization (WHO) classification system. The most common systemic NHL subtypes seen in HIV-positive persons are:
●Burkitt lymphoma (approximately 25%)
●Diffuse large B cell lymphoma (DLBCL, approximately 75%)
●Plasmablastic lymphoma (less than 5%)
●T cell lymphoma (1% to 3%)
●Indolent B cell lymphoma (less than 10%)
The WHO classification does not order lymphoid neoplasm according to their aggressiveness, in part due to recognition that the natural history of these tumors shows significant patient-to-patient variability. However, some studies have separated histologic subtypes into three general categories (highly aggressive, aggressive, and indolent) according to the usual clinical behavior of each of the lymphoid neoplasms.]
What is the most common anaerobe in surgical wound infections?
Bacteroides fragilis
What is the treatment for Histoplasma infection (Histoplasmosis)?
Liposomal amphotericin for severe infections
[UpToDate: Histoplasmosis is a common endemic mycosis that is usually asymptomatic but occasionally results in severe illness. Histoplasmosis and its causative agent, Histoplasma capsulatum, are found worldwide but particularly in North and Central America. Pulmonary histoplasmosis should be considered in patients with the following clinical presentations, particularly in the appropriate epidemiologic setting:
- Pneumonia with mediastinal or hilar lymphadenopathy
- Mediastinal or hilar masses
- Pulmonary nodule
- Cavitary lung disease
- Pericarditis with mediastinal lymphadenopathy
- Pulmonary manifestations with arthritis or arthralgia plus erythema nodosum
- Dysphagia caused by esophageal narrowing
- Superior vena cava syndrome or obstruction of other mediastinal structures. These manifestations place pulmonary histoplasmosis in the differential diagnosis of sarcoidosis, tuberculosis, and malignancy.
Histopathology using stains for fungi, cultures, antigen detection, and serologic tests for Histoplasma-specific antibodies can all help make a diagnosis of pulmonary histoplasmosis.
The clinical and radiographic findings in pulmonary histoplasmosis and sarcoidosis may be similar. A mistake in diagnosis can be disastrous if the patient is treated with corticosteroids or other immunosuppressive medications. As a result, histoplasmosis must be excluded before treating patients with presumed sarcoidosis with immunosuppressive medications.
The yield of the diagnostic modalities differs depending upon the extent of the infection and timing following exposure. A battery of tests is required to achieve the highest sensitivity for diagnosis. Antigen tests and serology may be negative when first performed but become positive later as the illness progresses.
The optimal treatment for histoplasmosis varies according to the patient’s clinical syndrome. Most infections caused by H. capsulatum are self-limited and require no therapy. However, patients who are exposed to a large inoculum of Histoplasma and those who are immunocompromised usually require antifungal therapy.
Itraconazole is generally preferred for mild to moderate histoplasmosis, and amphotericin B for the treatment of moderately severe to severe infections.
Therapy should be considered in patients with more than four weeks of symptoms but may not be indicated in those with mild symptoms who are already improving. Therapy is indicated without delay in patients with moderately severe or severe disease.
Treatment is indicated in all patients with chronic pulmonary histoplasmosis because the infection results in progressive loss of pulmonary function in most patients and death in as many as 30% of cases.]
What percent of the population is infected with Hepatitis C?
1%-2%
[UpToDate: The prevalence of antibodies to hepatitis C virus (anti-HCV) in the United States is approximately 1.6% (equating to about 4.1 million anti-HCV positive persons), while the prevalence of positive HCV RNA is approximately 1.3% (or about 3.2 million persons who are HCV RNA-positive). The peak prevalence is observed among persons born between 1945 and 1964.
Most patients infected with HCV in the United States and Europe acquired the disease through intravenous drug use or blood transfusion, the latter of which has become rare since routine testing of the blood supply for HCV began in 1990.]
What is the treatment for Coccidiodomycosis infection?
Liposomal amphotericin for severe infections
[UpToDate: Otherwise healthy patients without evidence of extensive coccidioidal infection or risk factors for more serious infection usually do not need antifungal therapy. However, for patients with severe illness, and for those at increased risk of dissemination or complications (eg, immunocompromised hosts or pregnant women), we suggest antifungal therapy (Grade 2C).
When treatment is indicated, we recommend fluconazole or itraconazole for most nonpregnant patients (Grade 1C). Amphotericin B should be used as initial therapy only in the most severe cases due to its toxicity; it is also used for treatment of pregnant women during the first trimester.
We generally treat immunocompetent patients, and those without severe underlying immunocompromise, for three to six months. The duration of treatment for patients with other immunocompromising conditions (eg, malignancy, AIDS, transplant recipients, patients receiving immunosuppressive therapy for autoimmune diseases) and pregnant women is discussed separately.
It is important that patients with coccidioidal infection (regardless of treatment) be followed for a year or longer to monitor for the development of complications (eg, chronic cavitary pneumonia, extrapulmonary disease).
Some patients may develop fatigue and lethargy associated with coccidioidal pneumonia without evidence of complications, and this may persist for many weeks or months. For such patients, developing a structured physical rehabilitation program and referral to a physical therapist for reconditioning training is often very helpful.]
How does a necrotizing C. perfringens infection present on physical exam?
- Pain out of proportion to exam
- Skin signs may not be evident with a deep infection
[UpToDate: Traumatic gas gangrene usually presents with sudden onset of severe pain at the site of surgery or trauma. The mean incubation period is less than 24 hours (range 6 hours to several days), depending on the size of the bacterial inoculum and the extent of vascular compromise. Pain is likely related to toxin-mediated ischemia.
The skin over the infected area initially may appear pale then rapidly develops a bronze appearance, followed by purple or red discoloration. The skin becomes tense and exquisitely tender. Overlying bullae may be clear, red, blue, or purple.
Signs of systemic toxicity develop rapidly including tachycardia and fever, followed by shock and multiorgan failure. In one series, shock was present in 50% of patients at the time of presentation to the hospital.
Bacteremia occurs in about 15% of cases and may be associated with brisk intravascular hemolysis. One case report described a patient whose hematocrit dropped from 37% to 0% over a 24-hour period; despite transfusion with 10 units of packed red blood cells over 4 hours, the hematocrit never exceeded 7%. Both alpha and theta toxins appear to contribute to the marked intravascular hemolysis based upon studies performed with recombinant toxins in the laboratory.
Bacteremia with C. perfringens can occur transiently in patients without gas gangrene, although the majority of C. perfringens and C. septicum blood isolates are associated with clinically significant infection.
Additional complications of clostridial myonecrosis include jaundice, renal failure, hypotension, and liver necrosis. Renal failure is largely due to the combined effects of hypotension, hemoglobinuria, and myoglobinuria. Bacterial toxins may also exert a direct effect on renal tubular cells.]
Which bacteria has alpha toxin that is a membrane-disrupting toxin that creates pores causing hemolysis and tissue damage?
Staphylococcus aureus
[Wikipedia: Alpha-toxin, also known as alpha-hemolysin (Hla), is the major cytotoxic agent released by bacterium Staphylococcus aureus and the first identified member of the pore forming beta-barrel toxin family. This toxin consists mostly of beta-sheets (68%) with only about 10% alpha-helices. The hla gene on the S. aureus chromosome encodes the 293 residue protein monomer, which forms heptameric units on the cellular membrane to form a complete beta-barrel pore. This structure allows the toxin to perform its major function, development of pores in the cellular membrane, eventually causing cell death.]
[UpToDate: Alpha-hemolysin is a well-characterized toxin capable of forming pores in selected host cells, including erythrocytes, macrophages, and lymphocytes; it appears to play a critical role in the pathogenesis of infection in a mouse model. In mice infected with isogenic strains of USA300, alpha-hemolysin was essential for development of pneumonia, but PVL was not. Subsequent studies demonstrated vaccination with the toxin protected mice from infection.]
Fungal infection with which organism is most commonly associated with pulmonary symptoms and can cause tortuous abscesses in cervical, thoracic, and abdominal areas?
Actinomyces
[Not a true fungus]
[UpToDate: Actinomycetes are commensal inhabitants of the oral cavity and intestinal tract but acquire pathogenicity through invasion of breached or necrotic tissue. As the infection progresses, granulomatous tissue, extensive reactive fibrosis and necrosis, abscesses, draining sinuses, and fistulas are formed.
Infection involving the cervicofacial area is most common (50%), followed by abdominal involvement (20%) and thoracic involvement (15% to 20%). In abdominal actinomycosis, the appendix and ileocecal region are usually involved. The disease tends to remain localized as the infection spreads contiguously, disregarding tissue planes. Lymphadenopathy is not a clinical feature. Hematogenous dissemination is also rare.
Actinomycotic abscesses can also present in the abdomen following cholecystectomy complicated by spilled gallstones during gallbladder removal. Because of the slow growth characteristics of the pathogen, such patients may present months to years after cholecystectomy.
Factors that predispose to abdominal actinomycosis include recent abdominal surgery, trauma, neoplasia, or a perforated viscus. In addition, there have been multiple reports of abdominopelvic actinomycosis associated with the use of intrauterine contraceptive devices.
Actinomycosis is a difficult disease to diagnose preoperatively by virtue of its rarity, nonspecific symptoms, and imitation of more common conditions such as malignancy, Crohn’s disease, and tuberculosis. It has been estimated that fewer than 10% of cases are diagnosed preoperatively. As a result, a high index of suspicion is required in patients presenting with constitutional or nonspecific abdominal symptoms and an abdominal mass. The disease is characterized by a chronic, indolent course with symptoms such as fatigue, fever, weight loss, and abdominal pain. Physical findings may include a palpable mass, visible sinus tracts, or fistulas. Laboratory abnormalities may show anemia and leukocytosis.]
What are the 2 most common organisms in ICU pneumonia?
- Staph aureus
- Pseudomonas
[UpToDate: Hospital-acquired (or nosocomial) pneumonia (HAP) and ventilator-associated pneumonia (VAP) may be caused by a wide variety of pathogens and can be polymicrobial. Common pathogens include aerobic gram-negative bacilli (eg, Escherichia coli, Klebsiella pneumoniae, Enterobacter spp, Pseudomonas aeruginosa, Acinetobacter spp) and gram-positive cocci (eg, Staphylococcus aureus, including methicillin-resistant S. aureus [MRSA], Streptococcus spp). Nosocomial pneumonia due to viruses or fungi is significantly less common, except in the immunocompromised patient.
There is a paucity of data regarding whether the pathogens that cause VAP differ from those that cause HAP in patients who are not mechanically ventilated. One prospective observational study evaluated 158,519 patients admitted to a single center over a four-year period. A total of 327 episodes of VAP and 261 episodes of HAP in nonventilated patients were identified:
The infecting flora in patients with VAP included methicillin-susceptible S. aureus (MSSA; 9%), MRSA (18 percent), P. aeruginosa (18%), Stenotrophomonas maltophilia (7%), Acinetobacter spp (8%), and other spp (9%).
The infecting flora in nonventilated patients with HAP was similar, except non-Enterobacteriaceae gram-negative bacilli (P. aeruginosa, Acinetobacter, and S. maltophilia) were less likely. Specifically, it included MSSA (13%), MRSA (20%), P. aeruginosa (9%), S. maltophilia (1%), Acinetobacter spp (3%), and other spp (18%).
These findings are supported by a prospective, multicenter, observational study of 398 intensive care unit (ICU) patients with suspected VAP. In this study, there was a similar distribution of pathogens: MRSA (14.8%), P. aeruginosa (14.3%), and other Staphylococcus species (8.8%).
Of 8474 cases of VAP reported to the United States Centers for Disease Control and Prevention from 2009 to 2010, the distribution of pathogens associated was S. aureus (24.1%), P. aeruginosa (16.6%), Klebsiella species (10.1%), Enterobacter species (8.6%), Acinetobacter baumannii (6.6%), and E. coli (5.9%). Similar findings were observed in another surveillance study.
A frequent criticism of such studies is that they may underestimate the prevalence of certain pathogens (eg, anaerobes) because special culturing techniques are required to identify them. However, a study performed anaerobic cultures using protective brush specimens and bronchoalveolar lavage fluid from 185 patients with possible VAP identified only one anaerobic organism, nonpathogenic Veillonella spp. This suggests that the practice of including anaerobic coverage in the treatment of VAP is unnecessary.]
PMNs greater than what amount in the peritoneal fluid is diagnostic of spontaneous bacterial peritonitis?
PMNs greater than 500 cells/cc fluid
[UpToDate: Spontaneous bacterial peritonitis (SBP) is typically diagnosed if there is an elevated ascitic fluid absolute polymorphonuclear cell (PMN, also referred to as neutrophils) count (≥250 cells/mm3), a positive ascitic fluid bacterial culture, and absence of secondary causes of peritonitis, such as bowel perforation. However, in some cases, additional tests may be needed to support the diagnosis or to differentiate SBP from secondary bacterial peritonitis.
What is the treatment for Actinomyces infection?
Drainage and Penicillin G
[UpToDate: We recommend high-dose penicillin as the treatment of choice for actinomycosis. Initial intravenous therapy is required for larger lesions with abdominal abscesses or draining sinus tracts. The recommended dose is penicillin G (10 to 20 million units per day divided every four to six hours) for 4 to 6 weeks, followed by oral penicillin (2 to 4 g/day) or amoxicillin for 6 to 12 months. For penicillin-allergic patients, tetracycline, erythromycin, or clindamycin are acceptable alternatives.
Surgery is usually reserved for patients with extensive lesions with severe necrosis and large abscess formation and for removal of persistent fistulas, recurrent disease, or inability to rule out neoplasm. Patients who undergo resection should also be treated with high-dose antibiotic therapy.
With combined medical and surgical treatment, the outcome is favorable in more than 90% of cases. Mortality is rare.]
What is the ratio of anaerobic bacteria to aerobic bacteria in the colon?
1,000 to 1
What is the risk of surgical site infection in a clean procedure (IE. hernia repair)?
2%
[UpToDate: A widely accepted wound classification system has been developed by the National Academy of Sciences and the National Research Council based upon the degree of expected microbial contamination during surgery. It stratifies wounds as clean, clean-contaminated, contaminated, or dirty using the following definitions:
Clean wounds are uninfected operative wounds in which no inflammation is encountered and the wound is closed primarily. By definition, a viscus (respiratory, alimentary, genital, or urinary tract) is not entered during a clean procedure.
Clean-contaminated wounds are operative wounds in which a viscus is entered under controlled conditions and without unusual contamination.
Contaminated wounds are open, fresh accidental wounds, operations with major breaks in sterile technique, or gross spillage from a viscus. Wounds in which acute, nonpurulent inflammation was encountered also were included in this category.
Dirty wounds are old traumatic wounds with retained devitalized tissue, foreign bodies, or fecal contamination or wounds that involve existing clinical infection or perforated viscus.
Several studies have found a moderate correlation between the wound classification and the SSI rate. SSI rates according to wound class were:
Clean – 1.3% to 2.9%
Clean-contaminated – 2.4% to 7.7%
Contaminated – 6.4% to 15.2%
Dirty – 7.1% to 40.0%
While widely used, this classification scheme may be a poor predictor of overall risk of SSI. Other factors, such as the operative technique, length of surgery, and health of the surgical patient, may be as important as wound classification in predicting infectious risks for SSI.
Available data suggest that the relative risk reduction of SSI from the use of antimicrobial prophylaxis is the same in clean and in higher-risk procedures. Antimicrobial prophylaxis is justified for most clean-contaminated procedures. The use of antimicrobial agents for dirty procedures or established infection is classified as treatment of presumed infection, not prophylaxis.]
Which bacteria is found in dog and cat bites?
Pasteurella multocida
[UpToDate: The predominant pathogens in animal bite wounds are the oral flora of the biting animal and human skin flora. About 85% of bites harbor potential pathogens, and the average wound yields five types of bacterial isolates; 60% have mixed aerobic and anaerobic bacteria. Skin flora such as staphylococci and streptococci are isolated in about 40% of bites.
Pasteurella species are isolated from 50% of dog bite wounds and 75% of cat bite wounds. Capnocytophaga canimorsus, a fastidious gram-negative rod, can cause bacteremia and fatal sepsis after animal bites, especially in asplenic patients or those with underlying hepatic disease. Anaerobes isolated from dog and cat bite wounds include Bacteroides, fusobacteria, Porphyromonas, Prevotella, propionibacteria, and peptostreptococci.]
What are the percentages of patients infected with Hepatitis C that develop each of the following?
- Chronic infection
- Cirrhosis
- Hepatocellular carcinoma
- Chronic infection: 60%
- Cirrhosis: 15%
- Hepatocellular carcinoma: 1%-5%
[UpToDate: Following infection with the hepatitis C virus (HCV), chronic infection typically occurs, with approximately 50% to 85% of cases developing chronic hepatitis. However, chronic HCV infection is usually slowly progressive and may not result in clinically apparent liver disease in many patients. Approximately 5% to 30% of chronically infected individuals develop cirrhosis over a 20- to 30-year period of time.
HCV-associated mortality is more likely to be due to end stage liver disease rather than hepatocellular carcinoma. Nevertheless, in the United States, HCV accounts for approximately one-third of hepatocellular carcinoma cases. Estimates of the risk of developing hepatocellular carcinoma once cirrhosis has developed have varied from 0% to 3% per year in various reports.
In contrast to hepatitis B virus infection, hepatocellular carcinoma in patients with HCV occurs almost exclusively in those with cirrhosis, suggesting that cirrhosis is the major risk factor. One study found that obesity may also be an independent risk factor. There is also suggestive experimental evidence that HCV infection itself can promote the development of hepatocellular carcinoma. Mice that were made transgenic for the HCV core gene developed adenomas and subsequent carcinoma within the adenomas.]
The microflora of which part of the gastrointestinal tract is virtually sterile, with some gram positive cocci and some yeast?
Stomach
What will a CT head show in a patient with sinusitis?
Air-fluid levels in the sinus
[UpToDate: Normal imaging can rule out sinusitis; however, abnormal imaging is not useful in the diagnosis of acute rhinosinusitis, as healthy adults often have abnormal sinuses on imaging. Imaging also does not distinguish between viral and bacterial etiology.
Common findings of sinusitis on CT scan include air-fluid levels, mucosal edema, and air bubbles within the sinuses. CT findings are not specific for sinusitis. Mucosal abnormality on CT scan may be observed in as many as 42% of asymptomatic healthy individuals. Abnormalities in the sinuses are also often seen in patients with the common cold.
CT scan without contrast may be used to evaluate for findings of sinusitis and can be used to rule out sinusitis. When concerned about complications of sinusitis, CT scan with contrast or magnetic resonance imaging (MRI) should be used.]
What is a carbuncle?
A multiloculated furuncle (boil)
[UpToDate: A carbuncle is a coalescence of several inflamed follicles into a single inflammatory mass with purulent drainage from multiple follicles.]
What is the treatment for peritoneal dialysis catheter infections?
Intraperitoneal vancomycin and gentamicin
[Increased dwell time and intraperitoneal heparin may help]
[UpToDate: As noted in the 2010 International Society for Peritoneal Dialysis (ISPD) guidelines, oral antibiotic therapy is as effective as intraperitoneal antibiotic therapy, with the exception of the treatment of methicillin-resistant S. aureus.
If the patient has a history of methicillin-resistant S. aureus (MRSA) and there is drainage from the exit site, most centers would obtain a culture and treat with an appropriate antibiotic to cover MRSA. At our center, in these cases, we use oral cephalexin or ciprofloxacin for broad-spectrum coverage and also give intraperitoneal vancomycin to cover possible MRSA.
Mild infection can be treated with topical antimicrobial agents, such as chlorhexidine and dilute hydrogen peroxide. Moderate infection with drainage requires culture of drainage and an oral antibiotic. Gram stain of the drainage or the microbiologic history of a preceding exit-site infection can help to direct therapy. If a gram-negative infection is suspected, the patient should be treated with an antipseudomonal antibiotic such as ciprofloxacin. Empiric therapy may need to be based on local patterns of infection and resistance and also based on the type of exit-site antimicrobial prophylaxis being used.
If the exit site remains infected after two weeks of antibiotics, compliance should be ensured and a thorough repeat examination performed. One should also examine the exit site to see if the external cuff is exposed since an exposed cuff may cause infection. Ultrasonography, computed tomography (CT) scanning, or less often gallium scanning may be performed to exclude an abscess. If the cuff is not exposed and there is no evidence of abscess or tunnel infection, additional antibiotic therapy may be attempted or salvage techniques may be employed to rescue the infected catheters.
Catheter removal is required for some exit-site and tunnel infections such as those complicated by a tunnel abscess or peritonitis, or if the infection does not respond or progresses after several weeks of antibiotic therapy. In all cases, perioperative antibiotics should be given and then continued for one to two weeks after catheter removal.
If there is no peritonitis associated with the exit-site infection, the infected catheter can be removed and a new catheter placed simultaneously in the opposite lower quadrant. A new catheter should not be placed at the time the infected catheter is removed if active peritonitis is present.
The first step in the evaluation of recurrent exit-site infection is to determine if the patient received a complete course of therapy for the first infection and if the organism responsible was sensitive to the antibiotic prescribed. Breaks in the proper maintenance and hygiene of the exit site should be identified and the patient retrained as necessary. Tunnel infection should be excluded by ultrasonography or CT scanning. Mupirocin or gentamicin should be considered.]
What is the risk of surgical site infection in a contaminated procedure (IE. gunshot wound to colon with repair)?
5-10%
[UpToDate: A widely accepted wound classification system has been developed by the National Academy of Sciences and the National Research Council based upon the degree of expected microbial contamination during surgery. It stratifies wounds as clean, clean-contaminated, contaminated, or dirty using the following definitions:
- Clean wounds are uninfected operative wounds in which no inflammation is encountered and the wound is closed primarily. By definition, a viscus (respiratory, alimentary, genital, or urinary tract) is not entered during a clean procedure.
- Clean-contaminated wounds are operative wounds in which a viscus is entered under controlled conditions and without unusual contamination.
- Contaminated wounds are open, fresh accidental wounds, operations with major breaks in sterile technique, or gross spillage from a viscus. Wounds in which acute, nonpurulent inflammation was encountered also were included in this category.
- Dirty wounds are old traumatic wounds with retained devitalized tissue, foreign bodies, or fecal contamination or wounds that involve existing clinical infection or perforated viscus.
Several studies have found a moderate correlation between the wound classification and the SSI rate. SSI rates according to wound class were:
- Clean – 1.3% to 2.9%
- Clean-contaminated – 2.4% to 7.7%
- Contaminated – 6.4% to 15.2%
- Dirty – 7.1% to 40.0%
While widely used, this classification scheme may be a poor predictor of overall risk of SSI. Other factors, such as the operative technique, length of surgery, and health of the surgical patient, may be as important as wound classification in predicting infectious risks for SSI.
Available data suggest that the relative risk reduction of SSI from the use of antimicrobial prophylaxis is the same in clean and in higher-risk procedures. Antimicrobial prophylaxis is justified for most clean-contaminated procedures. The use of antimicrobial agents for dirty procedures or established infection is classified as treatment of presumed infection, not prophylaxis.]
What is the risk of surgical site infection in a gross contaminated procedure (IE. abscess)?
30%
[UpToDate: A widely accepted wound classification system has been developed by the National Academy of Sciences and the National Research Council based upon the degree of expected microbial contamination during surgery. It stratifies wounds as clean, clean-contaminated, contaminated, or dirty using the following definitions:
Clean wounds are uninfected operative wounds in which no inflammation is encountered and the wound is closed primarily. By definition, a viscus (respiratory, alimentary, genital, or urinary tract) is not entered during a clean procedure.
Clean-contaminated wounds are operative wounds in which a viscus is entered under controlled conditions and without unusual contamination.
Contaminated wounds are open, fresh accidental wounds, operations with major breaks in sterile technique, or gross spillage from a viscus. Wounds in which acute, nonpurulent inflammation was encountered also were included in this category.
Dirty wounds are old traumatic wounds with retained devitalized tissue, foreign bodies, or fecal contamination or wounds that involve existing clinical infection or perforated viscus.
Several studies have found a moderate correlation between the wound classification and the SSI rate. SSI rates according to wound class were:
Clean – 1.3% to 2.9%
Clean-contaminated – 2.4% to 7.7%
Contaminated – 6.4% to 15.2%
Dirty – 7.1% to 40.0%
While widely used, this classification scheme may be a poor predictor of overall risk of SSI. Other factors, such as the operative technique, length of surgery, and health of the surgical patient, may be as important as wound classification in predicting infectious risks for SSI.
Available data suggest that the relative risk reduction of SSI from the use of antimicrobial prophylaxis is the same in clean and in higher-risk procedures. Antimicrobial prophylaxis is justified for most clean-contaminated procedures. The use of antimicrobial agents for dirty procedures or established infection is classified as treatment of presumed infection, not prophylaxis.]
What percent of abdominal abscesses have both anaerobic and aerobic bacteria?
80%
What is the most common neoplasm in AIDS patients?
Kaposi sarcoma
[Surgery is rarely needed]
[UpToDate: AIDS-related or epidemic KS is the most common tumor arising in HIV-infected persons. KS is considered an AIDS-defining illness in the Centers for Disease Control and Prevention (CDC) guidelines. In the United States, KS was over 20,000 times more common in persons with AIDS than in the general population prior to the widespread use of potent antiretroviral therapy (ART), although its incidence has declined substantially since that time.
Although KS has been reported among all risk groups for HIV infection, it is most common in homosexual or bisexual men. AIDS-related KS is much less common in heterosexual injection drug users, transfusion recipients, women or children, and hemophiliacs.
In patients with AIDS-related KS, the CD4 count appears to be an important factor associated with the development of KS. In a series of 70 patients who presented with a new diagnosis of KS while on treatment with combined antiretroviral therapy (ART), the rate ratios for developing KS for patients with CD4 counts <200, 200-349, and 350-499 cells/mm3 were 18.9, 3.6, and 4.1, compared to those with ≥500 cells/mm3.
However, trends in earlier initiation of antiretroviral therapy (ART) and improved health care continuity have altered the epidemiology of AIDS-related malignancies. In a study including 466 patients with AIDS-related KS, less than half of KS cases diagnosed between 2007 and 2011 were in patients with CD4 counts <200, with 29% having a viral load <500 copies/mL. This reflects the growing proportion of the HIV population that, due to ART, has higher CD4 counts and suppressed viral loads, rather than an increased risk of cancer among such patients. In resource-rich areas, AIDS-related KS is predominantly a disease of men. In contrast, in resource poor areas such as sub-Saharan Africa, AIDS-related KS is also more frequent in males, although the difference is less pronounced.]
What is the treatment for Brown recluse spider bites?
Dapsone initially
[May need resection of area and skin graft for large ulcers later]
[UpToDate: For patients with ulceration or systemic complaints, the evidence supporting the use of Loxoscelism specific treatments (eg, dapsone, antivenom) is lacking. Care providers should weigh the relative risks versus potential benefits with the understanding of the controversies surrounding effectiveness.
The treatment of acute local findings following a recluse spider bite involves local wound care, pain management, and, if indicated, tetanus prophylaxis. Initial treatment measures following any spider bite include:
- Clean the bite with mild soap and water.
- Apply cold packs, taking care not to freeze the tissue.
- Maintain the affected body part in an elevated or neutral position (if possible).
- Administer pain medication as needed. Some patients will respond to nonsteroidal antiinflammatory medications, while others may require opioids.
- Administer tetanus prophylaxis if indicated.
Most bites can be managed with minimal intervention and heal without scarring. Resolving bites should be monitored for the development of secondary bacterial infection.
Antibiotics are prescribed only if there are signs of infection such as increased erythema, fluctuation, and suppuration. If infection is suspected, it should be treated with antibiotics for cellulitis.]
What is characterized by a severe infection in the perineal and scrotal region caused by mixed organisms including gram positive cocci, gram negative rods, and anaerobes?
Fournier’s gangrene
[UpToDate: Necrotizing infection of the male perineum, known as Fournier’s gangrene, can result from a breach in the integrity of the gastrointestinal or urethral mucosa. Infection can occur in all age groups but is most common in older men. Necrotizing infection involving the labia and perineum can also occur in females, particularly in the setting of diabetes. Fournier’s gangrene begins abruptly with severe pain and may spread rapidly to the anterior abdominal wall, the gluteal muscles, and, in males, onto the scrotum and penis. In the setting of Fournier’s gangrene, early aggressive drainage or debridement is essential. Affected patients may require cystostomy, colostomy, or orchiectomy.]
Fungal infection with which organism is most commonly associated with pulmonary symptoms and is common in the Southwest United States?
Coccidiodes
[UpToDate: Coccidioidomycosis is the infection caused by the dimorphic fungi of the genus Coccidioides (Coccidioides immitis and Coccidioides posadasii). Most infections are caused by inhalation of spores. The clinical expression of disease ranges from self-limited acute pneumonia (Valley Fever) to disseminated disease, especially in immunosuppressed patients.
For those who develop symptoms, a wide spectrum of manifestations are possible. Primary infection due to Coccidioides species most frequently manifests as a community-acquired pneumonia (CAP) approximately 7 to 21 days after exposure. The most common presenting symptoms are chest pain, cough, and fever. In a study from Pima County, Arizona, 29% of patients diagnosed with CAP were serologically positive for coccidioidal infection. If hemoptysis occurs, it suggests the development of a pulmonary cavity.
Some patients also develop systemic complaints, often lasting for weeks to months. Patients can experience constitutional symptoms, such as fever, drenching night sweats, and weight loss. Patients can also develop extreme fatigue that can interfere with activities of daily living, and may last for many months.
Patients with early coccidioidal infection can also present with dermatologic or rheumatologic complaints. The frequent complaint of arthralgias has contributed to the alternate name of “desert rheumatism” for this illness. Cutaneous manifestations of primary coccidioidal infection include erythema nodosum and erythema multiforme. Erythema nodosum is much more common in women than in men, and often is the symptom prompting evaluation for Valley Fever.
Cases of coccidioidomycosis in the United States are concentrated in the southwestern part of the country. Coccidioides spp are endemic to certain lower deserts of the western hemisphere, including southern Arizona, the southern and central valleys of California, southwestern New Mexico, and west Texas in the United States. They are also found in parts of Mexico and Central and South America.]
What is the treatment for sinusitis?
Broad-spectrum antibiotics
[Rare to have to tap sinus percutaneously for systemic illness]
[UpToDate: Acute viral rhinosinusitis (AVRS) is expected to improve or resolve within 10 days. Patients with AVRS should be managed with supportive care. Patients who fail to improve after ≥10 days of symptomatic management are more likely to have acute bacterial rhinosinusitis (ABRS) and should be managed as ABRS.
Symptomatic management of acute rhinosinusitis (ARS) aims to relieve symptoms of nasal obstruction and rhinorrhea. We suggest over-the-counter (OTC) analgesics and saline nasal irrigation (Grade 2C). We suggest treatment with intranasal glucocorticoids (Grade 2B). Decongestants may be useful when eustachian tube dysfunction is a factor for patients with AVRS but are not likely to be helpful for patients with ABRS and have adverse side effects.
ABRS may also be a self-limited disease. Systematic reviews and meta-analyses have found that 70% to 80% of immunocompetent patients improve within two weeks without antibiotic therapy. We suggest symptomatic management and observation (watchful waiting) for immunocompetent patients with ABRS who have good follow-up (Grade 2B). We start antibiotic therapy after diagnosis for patients who do not have good follow-up.
Antibiotics should be started in patients who have been managed with observation who have worsening symptoms. Patients with stable symptoms (no worsening or improvement) after 7 days may be managed either with an additional 10 days of observation and symptomatic management or antibiotic therapy depending on patient presentation, comorbidities, and social factors. Patients with worsening symptoms or who fail to improve with an additional 10 days of watchful waiting should be started on antibiotics.
There are also a variety of reasons for patients to have a suppressed immune system, and treatment decisions for immunocompromised patients should be made on a case-by-case basis. They may warrant immediate antibiotic treatment and/or specialist referral. Treatment decisions for patients with other comorbidities that can affect immune function (eg, diabetes) should also be individualized.
In light of increasing microbial resistance to antibiotics, we suggest initial empiric treatment with amoxicillin-clavulanate rather than macrolides (clarithromycin or azithromycin), trimethoprim-sulfamethoxazole, or oral second- or third-generation cephalosporins (Grade 2B).]
Fungal infection with which organism is most commonly associated with pulmonary symptoms and is common along the Mississippi and Ohio river valleys?
Histoplasma
[UpToDate: Histoplasmosis is the most prevalent endemic mycosis in the United States. Histoplasmosis and its causative agent, Histoplasma capsulatum, are found worldwide but particularly in North and Central America. Within the United States, infection is most common in the midwestern states located in the Ohio and Mississippi River valleys.
While most infections are asymptomatic or self-limited, some individuals develop acute pulmonary infections or severe and progressive disseminated infection. Progressive disseminated histoplasmosis occurs in about one in 2000 patients with acute infection. Among the endemic mycoses, it is the most common cause for hospitalization.
Although hematogenous dissemination probably occurs in most patients during the acute infection before cellular immunity develops, progressive illness is unusual except in the host with altered immunity and those at the extremes of age. The diagnosis of disseminated histoplasmosis requires a high index of suspicion, recognition of the common modes of presentation, and familiarity with the appropriate diagnostic tests.
The clinical manifestations of disseminated histoplasmosis as well as the timing of presentation vary based on host immunodeficiency and the degree of exposure to the fungus. Patients may present shortly after the exposure or years later and may experience asymptomatic periods interrupted by symptomatic relapses. Progressive disseminated histoplasmosis occurs in two forms, partly based upon the time course of the illness and partly upon the extent of infection:
- Acute infection, which is mostly seen in infants and heavily immunocompromised hosts
- Chronic infection is noted mostly in older adults and in men more often than women
Patients with chronic infection often present with pancytopenia, hepatosplenomegaly, hepatic enzyme elevation, and oropharyngeal or gastrointestinal lesions. Other sites include the skin, brain, and adrenal glands.
Patients with acute infection present with fever, fatigue, hepatosplenomegaly, and pancytopenia. Diarrhea and dyspnea occur less commonly. Severely immunodeficient patients, such as those with AIDS or those receiving treatment with immunosuppressive medications, can present with overwhelming infection manifested by shock, respiratory distress, hepatic and renal failure, obtundation, and coagulopathy. The mortality in spite of amphotericin B treatment approaches 50% in such cases.
These manifestations were more common early in the course of the AIDS epidemic, prior to the wide recognition of the importance of histoplasmosis as a complication of AIDS and AIDS as a risk factor for histoplasmosis. Since the introduction of potent antiretroviral therapy, unusual manifestations of disseminated disease have been reported in severely immunosuppressed patients within three months of initiating antiretroviral therapy. Atypical signs (eg, splenic infarction, ulcerative skin lesions) were attributed to the immune reconstitution inflammatory syndrome.]
What is the treatment for cat/dog/human bites?
Broad-spectrum antibiotics like amoxicillin/clavulanic acid (Augmentin)
[Alternatives include combinations of an anti pseudomonas antibiotic like Doxycycline or TMP-SMX plus an antianaerobic antibiotic like Metronidazole or Clindamycin. Cephalexin, Dicloxacillin, and Erythromycin have poor activity against Pseudomonas and should be avoided.]
[UpToDate: Prophylactic amoxicillin-clavulanate has been shown to reduce the rate of infection due to animal bite wounds. This was illustrated in a prospective trial of 185 patients with full-thickness animal bite wounds; prophylactic antibiotics significantly reduced the infection rate among patients presenting 9 to 24 hours after injury. No significant benefit was observed in patients presenting less than nine hours following bite injury. These findings suggest that patients with more than just superficial wounds who present greater than eight hours after a bite should receive prophylactic antibiotics. In addition, antibiotic prophylaxis should be administered for animal bites that are less than eight hours old in the following circumstances:
- Deep puncture wounds (especially due to cat bites)
- Moderate to severe wounds with associated crush injury
- Wounds in areas of underlying venous and/or lymphatic compromise
- Wounds on the hand(s) or in close proximity to a bone or joint (particularly the hand, as well as prosthetic joints)
- Wounds on the face or in the genital area
- Wounds requiring surgical repair
- Wounds in immunocompromised hosts
Prophylactic oral antibiotics should be administered for three to five days, with close follow-up. On follow-up evaluation, signs of infection should prompt further evaluation (with radiographic imaging and/or surgical consultation, if needed) and an extension of the antibiotic course.]
Necrotizing fasciitis is usually caused by which bacteria?
Beta-hemolytic group A strep
[UpToDate: There are an estimated 3.5 cases of invasive group A Streptococcus infections per 100,000 persons in the United States; necrotizing infections make up approximately 6% of these cases. Conditions associated with necrotizing soft tissue infection include diabetes, drug use, obesity, immunosuppression, recent surgery, and traumatic wounds. In the United States, there are no convincing data that suggest an increase incidence of necrotizing fasciitis; in New Zealand, the incidence increased from 0.18 to 1.68 per 100,000 per year between 1990 and 2006. In New Zealand, the prevalence was similar among different ethnic groups, but the mortality was greater among older adults and native Pacific Islanders. In addition, in the United States and Scotland, mini-epidemics of necrotizing fasciitis and gas gangrene, caused by Clostridium sordellii and C. novyii, respectively, have been reported among drug abusers injecting black tar heroin subcutaneously.
Diabetes is a particularly important risk factor; several forms of necrotizing infection have been described more frequently among diabetics. These include nonclostridial anaerobic cellulitis, synergistic necrotizing cellulitis, and type I necrotizing fasciitis. These infections occur most frequently in the lower extremities. In addition, diabetic patients are also predisposed to developing necrotizing fasciitis in the head and neck region and the perineum.
There are two bacterial forms of necrotizing fasciitis: type I and type II.
Type I necrotizing fasciitis is a mixed infection caused by aerobic and anaerobic bacteria. Risk factors include diabetes, peripheral vascular disease (PVD), immune compromise, and recent surgery, including minor procedures such as circumcision in newborn infants. Patients with diabetes and/or PVD frequently have lower extremity involvement. Neonates usually have abdominal or perineal involvement.
Type II necrotizing fasciitis due to group A Streptococcus (GAS) or other beta-hemolytic streptococci, either alone or in combination with other species, most commonly S. aureus. It can occur among healthy individuals with no past medical history, in any age group. Predisposing factors include a history of skin injury, such as laceration or burn, blunt trauma, recent surgery, childbirth, injection drug use, and varicella infection (chickenpox). In cases with no clear portal of entry, the pathogenesis of infection likely consists of hematogenous translocation of GAS from the throat (asymptomatic or symptomatic pharyngitis) to a site of blunt trauma or muscle strain. Traumatic injuries in the setting of fresh or seawater can predispose to necrotizing infection due to A. hydrophila or V. vulnificus, respectively; the latter can also cause necrotizing infection in patients with underlying cirrhosis who ingest contaminated oysters.
During the 1990s, there was a dramatic increase in the number of invasive infections caused by GAS. In one Canadian report, the incidence of GAS necrotizing fasciitis increased from 0.085 to 0.4 per 100,000 between 1991 and 1995. Most cases were community acquired; 20% were nosocomial or acquired in a nursing home. Almost one-half of patients had streptococcal toxic shock syndrome; this rate is similarly noted in other studies.
In a retrospective review of 14 adults with necrotizing fasciitis due to community-associated methicillin-resistant S. aureus (MRSA), risk factors for infection included injection drug use (43%), diabetes (21%), hepatitis C infection (21%), malignancy (7%), and HIV infection (7%).]
What is the treatment for secondary spontaneous bacterial peritonitis?
Laparotomy to find source
[UpToDate: Patients with suspected secondary bacterial peritonitis should receive broader coverage with cefotaxime and metronidazole. A similar regimen should be used with polymicrobial bacterascites.
A diagnosis of SBP is made if the polymorphonuclear cell (PMN, also referred to as neutrophils) count in the ascitic fluid is ≥250 cells/mm3, culture results are positive, and secondary causes of peritonitis are excluded. However, in selected cases, fluid chemistries may be needed to support the diagnosis or to differentiate SBP from secondary bacterial peritonitis.
The distinction of secondary bacterial peritonitis from SBP is crucial because the former usually requires antibiotics and surgical treatment, whereas the latter only requires antibiotics.]
The microflora of which part of the gastrointestinal tract contains 10^7 bacteria consisting of gram positive cocci, gram positive rods and gram negative rods?
Distal small bowel
Primary spontaneous bacterial peritonitis is monobacterial and most commonly caused by which 3 bacteria?
- E. Coli (50%)
- Streptococcus (30%)
- Klebsiella (10%)
[Fluid cultures are negative in many cases of SBP]
[UpToDate: Pathogens commonly associated with SBP included Escherichia coli, streptococcal species, and Klebsiella pneumoniae.]
What is the most common source of fever more than 5 days after surgery?
Wound infection
[UpToDate: SSI is a common cause of fever more than one week after surgery; many patients have already been discharged from the hospital by this time.
Central venous catheters, if used, can be a source of infection and fever.
Fever from antibiotic-associated diarrhea, typically attributed to Clostridium difficile, also occurs more commonly during this period.
Febrile drug reactions are a frequent cause of subacute fever. Beta-lactam antibiotics and sulfa-containing products are commonly implicated, but other medications, such as H2-blockers, procainamide, phenytoin, and heparin, should be considered.
Thrombophlebitis should be considered as a cause of subacute fever in a patient with impaired mobility. Deep venous thrombosis and pulmonary embolism can cause fever and are more frequent in patients who are debilitated either by chronic medical problems or by the surgery.
Patients who require critical care after surgery are at higher risk for the development of subacute fever. These patients typically develop a variety of postoperative complications. Nosocomial infections are more common in these patients because of their treatment with invasive medical devices. Device-related infections due to bacteria and fungi include intravascular catheter-related infection with or without bacteremia, VAP, UTI, and sinusitis.]
