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%.]






























