Infectious Disease Flashcards
Necrotizing fasciitis
This infection is typically caused by a mixture of aerobic and anaerobic organisms leading to the necrosis of subcutaneous tissue. Signs of infection include tissues that become hot, red, and swollen, resembling severe cellulitis. Severe pain is common. Without timely treatment the area of infection becomes gangrenous. Patients present acutely ill. Diagnosis is through history and examination, supported by evidence of overwhelming infection. Treatment includes antibiotics and surgical debridement. Prognosis is poor without early aggressive treatment.
Most necrotizing fasciitis cases result from infection with group A streptococcus (Streptococcus pyogenes) or a mixture of aerobic and anaerobic bacteria (Bacteroides species). Organisms establish infection in subcutaneous tissue from an ulcer, infection elsewhere (Streptococci can arrive from a remote site of infection via the bloodstream), or after trauma. Perineal infections usually result from a complication of a recent surgery and perirectal abscesses. Patients with diabetes are also at risk for developing necrotizing fasciitis.
The primary symptom of infection is intense pain (pain out of proportion of clinical findings). Tissue is hot, red, and swollen and rapidly becomes discolored. Bullae, crepitus (resulting from soft tissue gas), and gangrene may develop. Subcutaneous tissues necrose but muscles are spared initially. Patients present acutely ill with a high fever, high heart rate, altered mental status (confusion), and low blood pressure. Patients may be bacteremic or septic. Streptococcal toxic shock syndrome may develop.
Diagnosis is made by history and examination and is supported by leukocytosis, soft-tissue gas on x-ray, positive blood cultures, and deteriorating metabolic and hemodynamic (blood pressure) status. Mortality rate is about 30%. Old age, underlying medical issues, delayed diagnosis, and insufficient surgical debridement worsen prognosis. Treatment is primarily surgical (immediate) with IV antibiotics and fluids.
Acute infectious arthritis
This is a joint infection that progresses very rapidly (within hours to days). The infection resides in synovial or periarticular tissues and is usually bacterial. In young, sexually active adults infections are usually caused by Neisseria gonorrhoeae. Symptoms include a rapid onset of pain, effusion, and restriction of range of motion, usually within a single joint. Diagnosis requires synovial fluid analysis and culture. Treatment is through IV antibiotics and drainage of the pus from the infected joints. Risk factors for infectious arthritis include: • Advanced age (>60 years) • Alcoholism • Arthrocentesis or joint surgery • Bacteremia • Cancer • Chronic illness (lung or liver disease) • Diabetes • Hemodialysis • Hemophila • History of previous joint infection • Immunodeficiency • Immunosuppressive therapy • Injection drug use • Prosthetic joint implant • RA • Risk factors for sexually transmitted diseases (multiple sexual partners, etc) • Sickle cell disease • Skin infections • SLE
Infectious organisms reach the joints by direct penetration (trauma, bites, surgery, etc), extension from an adjacent infection (osteomyelitis, abscess, infected wound, etc), or hematogenesis spread from a remote site of infection. Common microorganisms that cause these infections are classified either as gonococcal or nongonococcal in adults. Distinction is important because gonococcal infections are far less destructive to the joint. Overall, Staphylococcus aureus is the most frequent cause of infection in adults.
Osteomyelitis
inflammation and destruction of bone caused by bacteria, mycobacteria, or fungi. Causes localized bone pain and tenderness. 80% of infections result from contiguous spread or from open wounds.
Myositis
infection of the muscle that leads to muscle inflammation. Can be caused by many different microorganisms including viruses, bacteria, and helmniths.
Bacteremia
the presence of bacteria in the bloodstream
Viremia
the presence of virus in the bloodstream
Septicemia
bloodborne systemic infection. Can lead to spread of the infectious organism to other tissues, massive inflammation, septic shock, and rapid death. Associated with bacterial infections.
Streptococcus pyogenes
gram +, cocci, catalase -, beta-hemolytic, bacitracin sensitive.
Causes necrotizing fasciitis
White Blood Cell Count
Measures the number of leucocytes per milliliter of blood.
WBC – cells of the immune system defending the body against both infections and foreign materials.
Normal range = 4,500 to 11,000 cells/ml
You get high counts during infections, inflammatory diseases, autoimmune systemic diseases, leukemia, and emotional and physical stress.
High lymphocyte count in virus infections, high neutrophil count in bacterial infections (especially banded immature)
C-Reactive Protein
Produced in the liver and is present in circulation at low levels normally. Involved in the promotion of the immune system through the activation of the complement cascade.
Normal: ≤ 1mg/dL
Elevated in bacterial infections, inflammation conditions, acute rheumatic fever, acute rheumatoid arthritis, inflammatory bowel disease, and others.
synovial fluid
foul smell means obligate anaerobe infection
the more cloudy, the more infected
Acute Infectious Arthritis
Rapid onset
Personal history
Pain
Range of motion restriction (single joint)
Synovial fluid analysis and culture
Positive blood cultures
caused by Staphylococcus aureus or Neisseria gonorrhoeae
Staphylococcus aureus
tricuspid valve endocarditis frequently affects IV drug users. Patients with granulomatous disease are vulnerable. Leading cause of osteomyelitis in children and adults.
Clinical presentation: Local = skin/subcutaneous: impetigo, cellulitis, folliculitis, furuncles, carbuncles. Respiratory: pneumonia with cavitations. Systemic = acute endocarditis, meningitis, osteomyelitis, septic arthritis.
Pathology: Bacteria colonize skin (following breach) or nasopharynx (following intubation or viral infection) → overgrow and evade host defenses using protein A, coagulase, hemolysins, and leukocidins. Neutrophils localize to site of infection → purulent abscesses form → skin/subcutaneous infections or pneumonia results. Deeper invasion into the bloodstream relies on the hyaluronidase, staphylokinase, and lipase virulence factors.
Diagnosis: blood culture for Gram (+) clusters, catalase (+), coagulase (+).
Treatment: antibiotic treatment is with either penicillinase-resistant penicillins or vancomycin
Neisseria gonorrhoeae
Obligate human pathogen. Virulence factors include specialized pili (allows attachment to mucosal surface, provides antigenic variation, prevents phagocytosis; endotoxin; capsule; and IgA protease. Higher incidence of infection with menstruation or IUD. Most common cause of septic arthritis in sexually active people. Antigenic variation prevents immunity allowing recurrent infections.
Clinical presentation: Local infection = (genital tract or anorectal infections) either asymptomatic, urethritis, dysuria (men), cervicitis (women), opthalmia neonatorum. Systemic = septic arthritis. Complications = Pelvic Inflammatory Disease (PID), ectopic pregnancy, sterility, Fitz-Hugh-Curtis Syndrome
Pathology: Colonization begins when bacterial pili attach to mucosal cells of the urethra and vagina. Evades mucosal IgA antibodies via IgA protease. Endocytosed by immune cells and kills ciliated cells. Together this leads to inflammatory response leading to urethritis (men) and cervicitis (women). In women, the infection can progress to the uterus, fallopian tubes, and ovaries (PID) which can lead to an increased risk for ectopic pregnancies. From the fallopian tubes the bacteria can spill into the peritoneal cavity causing peritonitis. This can lead to an infection of the liver capsule (Fitz-Hugh-Curtis Syndrome).
The bacteria can also invade the submucosa and enter into the bloodstream where it can collect in synovial fluid causing septic arthritis.
In neonates, it can inoculate the conjunctiva during passage through the birth canal causing opthalmia neonatorum à risk for blindness.
Diagnosis: Gram (-) diplococci within PMNs, metabolizes glucose but not maltose, selectively grows on Thayer-Martin media.
Treatment: Ceftriaxone (+ doxycycline for probable concurrent Chlamydia infections), prophylactic erythromycin eye drops for neonates. Vaccine development difficult.
Osteomyelitis
Staphylococcus aureus
Salmonella typhi
Pasteurella multocida
Salmonella typhi
Key virulence factors include the H antigen (flagella), endotoxin, Vi capsule. Obligate human pathogen. Sickle-cell patients are functionally asplenic and have trouble clearing Vi-encapsulated Salmonella. Patients with impaired gastric acid secretion are more susceptible. Because S. typhi are stored well in gallstones, carriers may present with S. typhi-induced necrotizing cholecystitis. Treating S. typhi infections may actually increase the risk for reinfection due to interference of the development of a suitable host immune response.
Clinical presentation: asymptomatic carrier state, typhoid fever (enteric fever), osteomyelitis in sickle cell patients.
Pathology: Spread through fecal-to-oral transmission. Large inoculum overcomes the gastric acid defense. Bacteria penetrates the mucosal barrier in the distal ileum or colon which leads to transient asymptomatic bacteremia.
Capsular Vi polysaccharide allows survival in phagocytes of Peyer’s patches. Spread via phagocytes to the gallbladder, liver, and spleen where endotoxin is then released. This creates rose spots on the abdomen, fever, diarrhea, and abdominal pain (typhoid fever). This infection can then progress into the carrier state or it may self-resolve.
Carrier state – the bacteria are stored in the gallbladder, especially in gallstones. The bacteria may reenter the bowel lumen to generate more microorganisms that can spread through contaminated feces.
Diagnosis: Gram (-) rod cultured from the blood. Motile by flagella. Produces hydrogen sulfide. Does not ferment lactose.
Treatment: Ceftriaxone for resistant strains. Ciprofloxacin and ampicillin for carriers. Cholecystectomy may be necessary for carriers. Two oral vaccines are available for travelers (killed or live-attenuated).
Pasteurella multocida
Suturing the wound may worsen the infection by creating a closed anaerobic environment which can favor bacterial growth. A cat’s sharp teeth can directly implant bacteria into the bone and cause osteomyelitis.
Clinical presentation: cellulitis, osteomyelitis following cat and dog bites.
Pathology: This bacteria normally inhabits the oral cavity of animals. It enters the human skin via a bite wound and elicits an inflammatory response at the inoculation site. From here the bacteria can spread locally to soft tissue (cellulitis) and bone (osteomyelitis). The infection has the possibility to progress to septicemia.
Diagnosis: Gram (-) coccobacilli with bipolar staining.
Treatment: Penicillin G. Clean and drain wound.
Salmonella, sickle cell, osteomyelitis
The combination of the expanded marrow in sickle cell patients together with high oxygen demand and sluggish circulation means that bone is vulnerable to infarction.
Infarcted areas act as loci for infection.
Gut devitalization due to intravascular sickling leads to an increased incidence of invasion and bacteremia.
Sickle cell patients have reduced bactericidal and opsonic activity against Salmonella and an abnormality in the alternative pathway of complement activation.
Myositis
Infections of the muscles that lead to muscle inflammation come in many forms including clostridial myositis, viral infections, and helminth infections. Although myalgia can occur in most of these infections, severe muscle pain is the hallmark of pleurodynia (coxsackievirus B), trichinellosis, and bacterial infection.
Streptococcus pyogenes may induce primary myositis (referred to as streptococcal necrotizing myositis) in association with severe systemic toxicity. Myonecrosis occurs concomitantly with necrotizing fasciitis in ~50% of cases. Both are part of the streptococcal toxic shock syndrome. Gas gangrene usually follows severe penetrating injuries that result in interruption of the blood supply and introduction of soil into wounds. Such cases of traumatic gangrene are usually caused by the clostridia species (Clostridium perfringens) of bacteria.
Diagnosis is based on the temporal progression of the lesions as well as the patient’s travel history, animal exposure or bite history, age, underlying disease status, and lifestyle. Soft tissue radiography, computed tomography, and magnetic resonance imaging may be useful in determining the depth of infection and should be performed when the patient has rapidly progressing lesions or evidence of a systemic inflammatory response syndrome. These tests are particularly valuable for defining a localized abscess or detecting gas in tissue. Unfortunately, they may reveal only soft tissue swelling and thus are not specific for fulminant infections such as necrotizing fasciitis or myonecrosis caused by group A Streptococcus where gas is not found in lesions.
Treatment includes antibiotics for bacterial and helminth infections.
Clostridium perfringens
this is the only nonmotile Clostridium member. Enteritis necroticans: necrosis of the small intestine caused by β-toxin release. Common in New Guinea following large ingestion of pork (excess protein overwhelms trypsin digestion of β-toxin) 40% mortality.
Clinical presentation: cellulitis, gas gangrene (myonecrosis with crepitus), food poisoning
Pathology: Cellulitis – bacteria normally found in the soil and GI tract. Bacteria infect anaerobic environment of necrotic skin wound and release digestive enzymes (collagenase and hyaluronidase). This generates a slow painless infection and gas production. The infection eventually forms collections of gas under the skin that crackle when touched (crepitus).
Gas gangrene – The infection is initiated from spores found in the soil. These spores are introduced yet deep muscle wounds (military wounds, automobile accidents, crude abortions). Here the spores can germinate and grow in the anaerobic environment to release alpha toxin (lecithinase) which causes deep muscle cell necrosis; degradative enzymes which produce subcutaneous gas bubbles and crepitus. Gangrenous muscles lead to black fluid exudate leaking from the skin. Shock may follow.
Food poisoning – the infection is initiated from spores found in meat and poultry foods. These spores can survive cooking and germinate to contaminate food that is then ingested. The bacteria release heat-labile enterotoxin in the GI tract. This enterotoxin inhibits glucose transport and damages the epithelium. This causes diarrhea, gastric pain, and nausea. Fever and vomiting are not common.
Diagnosis: Gram (+) rod, strict anaerobe, nonmotile.
Treatment: surgical removal of infected areas. Hyperbaric oxygen to kill anaerobic organisms. Penicillin, clindamycin (only effective in local, weak infections).
Coxsackievirus A & B
Coxsackie B virus accounts for 50% of cases of viral myocarditis.
Clinical presentation: Coxsackie B – pleurodynia, myocarditis, pericarditis. A and B – aseptic meningitis, paralysis, upper respiratory tract infection.
Pathology: infections are typical in summer and fall and the virus is transmitted via aerosols or fecal to oral route. The virus travels in the G.I. tract and infects mucosal epithelial cells. Local replication ensues and virus spreads in the bloodstream. From here the virus infects and can lyse heart and pleural surfaces to cause pleurodynia, myocarditis, and pericarditis.
In Group A and B infections the virus can travel to the meninges and anterior horn motor neurons to cause meningitis and paralysis.
Diagnosis: isolate virus, serology.
Treatment: Symptomatic infections – anti-inflammatory agents. No antivirals or vaccines available.
Acute infectious arthritis in Adolescents and adults
organism: Gonococci (young, sexually active adults), nongonococcal bacteria (Staphylococcus aureus, streptococci)
source: Cervical, urethral, rectal, or pharyngeal infection with bacteremic dissemination – gonococci.
Bacteremia – staphylococci and streptococci
Acute infectious arthritis in Neonates
organism: Group B streptococci, Escherichia coli, Staphylococcus aureus
source: Maternal-fetal transmission; IV punctures or catheters with bacteremic dissemination
Acute infectious arthritis in Children 3-years-old or younger
organism: Streptococcus pyogenes, Streptococcus pneumoniae, Staphylococcus aureus
source: Bacteremia (otitis media, URIs, skin infections, meningitis, etc)
