Infectious Disease Flashcards

1
Q

Necrotizing fasciitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute infectious arthritis

A
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Osteomyelitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Myositis

A

infection of the muscle that leads to muscle inflammation. Can be caused by many different microorganisms including viruses, bacteria, and helmniths.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bacteremia

A

the presence of bacteria in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Viremia

A

the presence of virus in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Septicemia

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Streptococcus pyogenes

A

gram +, cocci, catalase -, beta-hemolytic, bacitracin sensitive.
Causes necrotizing fasciitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

White Blood Cell Count

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

C-Reactive Protein

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

synovial fluid

A

foul smell means obligate anaerobe infection

the more cloudy, the more infected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acute Infectious Arthritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Staphylococcus aureus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Neisseria gonorrhoeae

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Osteomyelitis

A

Staphylococcus aureus

Salmonella typhi

Pasteurella multocida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Salmonella typhi

A

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).

17
Q

Pasteurella multocida

A

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.

18
Q

Salmonella, sickle cell, osteomyelitis

A

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.

19
Q

Myositis

A

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.

20
Q

Clostridium perfringens

A

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).

21
Q

Coxsackievirus A & B

A

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.

22
Q

Acute infectious arthritis in Adolescents and adults

A

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

23
Q

Acute infectious arthritis in Neonates

A

organism: Group B streptococci, Escherichia coli, Staphylococcus aureus
source: Maternal-fetal transmission; IV punctures or catheters with bacteremic dissemination

24
Q

Acute infectious arthritis in Children 3-years-old or younger

A

organism: Streptococcus pyogenes, Streptococcus pneumoniae, Staphylococcus aureus
source: Bacteremia (otitis media, URIs, skin infections, meningitis, etc)

25
Q

Acute infectious arthritis in Age 3 years to adolescence

A

organism: Staphylococcus aureus, streptococci, Neisseria gonorrhoeae, Pseudomonas aeruginosa, Kingella kingae
source: Bacteremia or contiguous spread

26
Q

Acute infectious arthritis in All ages

A

organism: Viruses (parvovirus B19, HBV, HCV, rubella virus, VZV, mumps virus, adenoviruses, coxsackieviruses A and B, HIV, EBV)
source: Viremia or immune complex deposition

27
Q

Acute infectious arthritis in Patients with possible tick exposure

A

organism: Borrelia burgdorferi (Lyme disease)
source: Bacteremia

28
Q

Acute infectious arthritis in Patients with bite wounds (human, dog, cat, rat)

A

organism: Often polymicrobial. Human bites – Eikenella corrodens, group B streptococci, Staphylococcus aureus, oral anaerobic bacteria. Dog and cat bites – Staphylococcus aureus, Pasteurella multocida, Pseudomonas species, Moraxella species, Haemophilus species. Rat bites – Staphylococcus aureus, Streptobacillus moniliformis, Spirillum minus
source: Direct joint penetration, usually of the small joints of the hands

29
Q

Acute infectious arthritis in The elderly, patients with severe joint trauma or serious disease (immunosuppression, hemodialysis, SLE, RA, diabetes, cancer)

A

organism: Staphylococci (particularly in RA), gram-negative bacteria, Salmonella species (particularly in SLE)
source: Urinary tract, skin

30
Q

Dengue Fever Virus:

A

this virus is found in the tropics worldwide. Dengue hemorrhagic fever is most common in southern Asia.

Clinical presentation: Dengue fever – “breakbone fever” (flu-like with severe joint and muscle pain). Dengue hemorrhagic fever – (dengue fever with hemorrhage and shock).

Pathology: humans, monkeys, and birds are all normal reservoirs for this virus. It is transmitted through a mosquito bite and enters the bloodstream to cause transient viremia. From here the virus infects macrophages causing acute inflammation release of pyrogens and pain mediators to create “breakbone fever”. If this initial infection is followed by a second infection of a different serotype, then antibodies from the first serotype infection increase and cross-react to form immune complexes and a type III hypersensitivity reaction which can lead to hemorrhage and shock (Dengue Hemorrhagic Fever).

Diagnosis: Serology, clinical presentation, patient history

Treatment: Prevention against mosquito bites. Supportive.

31
Q

Trichinella spiralis

A

In the United States, trichinosis infections have decreased following legislation that prohibits feeding pigs uncooked garbage.

Clinical presentation: gastroenteritis, myalgia.

Pathology: Reservoir is in pigs. Encysted larvae ingested from uncooked meat. Larvae mature into adults in the small intestine. Adult worms mate and eggs mature to larvae. The larvae can then penetrate the intestinal wall and gain access to the bloodstream. The main cause diarrhea and pain.

The larvae can be carried by the blood to the skeletal muscle (often to the extraoculars, masseters, tongue, and diaphragm) where localized inflammation ensues which leads to myalgia. Here the larvae can form a fibrous cyst that can last for years and may calcify.

If many encysted larvae are ingested this can lead to a severe infection where the larvae can migrate to the heart and brain causing myocarditis and encephalitis.

Diagnosis: eosinophilia. Striated muscle biopsy contain cysts with larvae. Serology for chronic infection.

Treatment: Mebendazole/thiabendazole (against adult worms in the small intestine). No treatment to remove cysts from muscle. Steroids for severe myositis and myocarditis.

32
Q

Taenia solium

A

In cysticercosis the larvae sometimes can be detected swimming in the vitreous humor of the eyes.

Clinical presentation: intestinal infection – asymptomatic, malnutrition, abdominal discomfort. Tissue infection – cysticerosis (neurological defects, blindness).

Pathology: intestinal infection: larvae found as cystercerci in pig muscle which get ingested in poorly cooked pork. In the small intestine the larvae mature and grow to generate adult worms consisting of a scolex (head) and numerous proglotids (autonomous segments). The scolex attaches to the intestinal wall, proglotids containing eggs passed in feces. The worm consumes the food that is ingested by the host leading to malnutrition.

Tissue infection: humans ingest eggs from infected feces and the eggs hatch into oncospheres in the small intestine. Oncosheres penetrate the intestinal wall and travel to other tissues (brain, skeletal muscle, and eye) to form cysticerci containing larvae. The cysts grow slowly eventually leading to neurological defects (seizures, focal symptoms) or blindness. When cysts die (several years later) this caused increased inflammation and aggravated symptoms.

Diagnosis: intestinal infection: proglottids, eggs in stool. Tissue infection: calcified cysticerci in muscle, brain on X-ray or CT scan. Eosinophilia in muscle, brain also seen in X-ray or CT scan.

Treatment: intestinal infection: niclosamide + cathartic; praziquantel. Tissue infection: praziquantel or albendazole + steroids (reduce inflammation from the dying cysts).