W3P3 Flashcards
What is Viral Hepatitis
Viruses that cause infection and destruction of hepatocytes
Some can cause chronic hepatitis
- Host immune system unable to clear acute infection
- Continuous hepatocyte injury
- End-point: cirrhosis (inflammation/fibrosis within liver)
What are the types of Hepatitis Viruses
- Nucleic Acid
Hep A: ssRNA Hep B: ds DNA Hep C: ss RNA hep delta: ssRNA Hep E: ss RNA
only Hep B is DNA
Transmission of the 5 Hep viruses
Hep A and Hep E: Fecal oral, [sexual, small]
Hep B, C, Delta: Sexual, Vertical, Parenteral
parenteral: administered or occurring elsewhere in the body than the mouth and alimentary canal.
Relation between the Hepatitis Viruses
Bottom line: none of the hepatitis viruses are related (different genetic material, different structures, different classification…)
Only grouped together because they all affect the liver
Hepatitis A
- transmission route
Fecal-oral transmission
Consumption of contaminated water, shellfish, other food
Not associated with chronic hepatitis and no link to hepatic cancers
Hep A clinical manifestations
- Prevention
Kids: mild disease (jaundice, fatigue)
Adults: jaundice, other symptoms of liver inflammation, in rare cases: fulminant hepatic failure
Prevention:
Vaccination
(alone or in combination with HBV)
Post exposure prophylaxis:
Anti-Hep A immunoglobulin if young age or immunocompromised
Otherwise: HAV vaccine within 14 days of exposure
Which antibodies should you measure for Hep A
IgM: will peak first: good if you’re measuring early after exposure, however they will drop
IgG: will rise as IgM falls and STAY high, so this should be measured 8 weeks after infection
Hepatitis E
- transmission
Similar to Hepatitis A in terms of transmission (fecal-oral) and symptoms
Usually no chronic hepatitis
Infection may lead to fulminant hepatic failure in pregnant women
common in farms/travellers
Hepatitis B
- Modes of Transmission
HBV transmitted via blood (highest levels), semen. Virus also found in saliva, cervical secretions.
Can survive for long periods of time on environmental surfaces: potential for horizontal transmission in daycares, institutions for disabled, etc.
IVDU, sexual occupation; high in americas
Perinatal: Africa
Childhood/horizontal: Asia
Which hep infections lead to chronic hepatitis
Hep B and Hep C
Natural history of Hep B
- Areas with high prevalence of disease
Perinatal infx leads to 90% chance of chronic infection - Areas with low prevalence of disease
Adult infection leads to acute hepatitis and there is less than 5% chance it leads to chronic infection
- immune tolerance [inflammation and fibrosis] can last for decades in perinatal infection vs within months for adult
so congential/vertical transmission is WORSE
Hep B viral structure
Hep B core antigen (HBcAg)
Hep B surface antigen (HBsAg)
Acute vs Chronic Hep B serology
Acute Hep B serology:
HBsAg peaks and falss first, IgM anti-HBc same
anti HBs only rises and falls AFTER anti HBsAg falls
total anti HBc rises and STAYS high
Chronic Hep B serology:
HBsAg rises first and STAYs high along with total Anti-HBc
Since HBsAg never falls, there is no anti-HBs
IgM anti HBc rises and falls similar to acute
SO your anti CORE bodies are useless to distinguish because they are the same for chronic vs acute
your HBsAg levels after 24 weeks can determine if the infection is chronic
if there is presence of anti-HBs = this is an ACUTE infection
IMPORTANT:
What Hep B serology test would you order if
a. Is my patient currently infected with hepatitis B?
b. Has my patient ever been infected with hepatitis B?
c. Is my patient immune to hepatitis B?
d. Does my patient have acute hepatitis B infection?
Is my patient currently infected with hepatitis B?
HepBsAg (surface antigen)
Has my patient ever been infected with hepatitis B?
HepBcIgG (core IgG)
Is my patient immune to hepatitis B?
HepBsAb (surface antibody)
Does my patient have acute hepatitis B infection?
HepBcIgM (core IgM)
Interpreting Hep B serology, what values for HBsAg, HBsAb, HBcAb would you expect in the following cases:
No prior exposure
Vaccination
Resolved Acute infection
No prior exposure: all three negative
Vaccination: only HBsAb is positive
Resolved Acute infection: only HBsAb and HBcAb are positive
Interpreting Hep B serology, what values for HBsAg, HBsAb, HBcAb would you expect in the following cases:
Acute or chronic infection *
Chronic infection
Acute or chronic infection: HBsAg, positive. HBsAb NEGATIVE. HBcAB positive
- unable to develop surface antibodies during an active infection. we do develop core antibodies^
Chronic infection, late: HBsAg positive. HBsAb negative. HBcAb positive
yes they are the SAME, you can’t tell the difference with these two measures you need to look at HBeAg which is negative for chronic infection
Prevention of Hepatitis B
Vaccinate, vaccinate, vaccinate
Safer sex practices
Screen pregnant women and protect babies of HBV positive women (give babies hepatitis B Ig and vaccine immediately after birth)
Prevention of Hepatitis B
Vaccinate, vaccinate, vaccinate
Safer sex practices
Screen pregnant women and protect babies of HBV positive women (give babies hepatitis B Ig and vaccine immediately after birth)
Prevention of Hepatitis B
Vaccinate, vaccinate, vaccinate
Safer sex practices
Screen pregnant women and protect babies of HBV positive women (give babies hepatitis B Ig and vaccine immediately after birth)
Treatment of Hep B Goals
Goals
suppress HBV replication (treat patients with high HBV DNA)
Prevent liver-related complications
cirrhosis, hepatocellular carcinoma (20-40% lifetime risk in chronic infection!)
Recall HBV is a DNA virus, so it’ll be there for life* can’t get rid of it only manage it.
Treatment for Hep B
Tenofovir
Entecavir
Laminvudine
HDV
Dependent on HBV for production of envelope proteins; ie. You can only get HDV infection in the presence of HBV
HBV/HDV coinfection occurs commonly in Mediterranean area and parts of South America
Get more severe hepatitis when both viruses are present, and increased risk of complications
Hep C epidemiology in Canada
- greatest route of transmission
Risk factors (Canada):
60%: IDU * [ greatest route of transmission]
20%: immigrants
10% contaminated blood products
Steps for HCV diagnosis
Initial test: test for HCV Ab
If positive: test for HCV RNA
much simpler than HBV diagnosis!!
- much simpler than HBV diagnosis (recall we had to check for core vs surface antibodies/antigens)
Hepatitis C disease
- progression
- Symptoms
Progresses to chronic disease in approx. 80% of people infected
Symptoms:
Most are asymptomatic
If symptoms: anorexia, vague abdominal discomfort, nausea, fatigue, and fever
Long-term: cirrhosis, liver failure (#1 indication for liver transplantation in most centres)
Hep C prevention vs treatment
OPPOSITE compared to HBV
Prevention:
No vaccine!
Blood bank screening, precautions to avoid exposure to blood, safer sex practices (MSM), needle-exchange programs
Treatment:
goal is to CURE, this is RNA virus so we can get rid of it
Direct-acting anti-viral Rx (DAAs)
- shorter treatment - less side effects - much more effective (especially for genotype 1)
Hepatitis and Needlestick injuries
- most to least infectious
Concern re. transmission of HBV, HCV and HIV
HBV most infectious > HCV > HIV
approx 30%/ 3% / 0.3%
What to do if non-immune to HBV:
ASAP: HBV vaccine and ‘HBIg’ (anti- HepBsAg)
Define
Diarrhea
Acute vs Chronic
Diarrhea: ≥ 3 loose or watery stools per day
Acute: ≤ 14 days duration
Chronic: > 30 days duration
Major cause of infant mortality** (malnutrition)
How do people die from Diarrhea
Dehydration (water loss)
Salt imbalances (especially sodium and/or potassium)
Acidosis (bicarbonate losses)
Hemorrhage (if dysentery)
Chronic anemia (hematochezia)
Malnutrition
Sepsis (due to bowel perforation or bacterial translocation into the blood)
Causes of Bacterial Infectious Diarrhea in the Developed World
Escherichia coli* Enterohemorrhagic (EHEC) -> HAMBURGERS DIARRHEA O157:H7 Enterotoxigenic* (ETEC) -> HEMORRAGIC DIARRHEA Salmonella spp* - Non-typhi and typhi Shigella spp* Yersinia enterocolitica Campylobacter jejuni Clostridium difficile Listeria Monocytogenes
- those shared in developing countries, INCLUDING:
Vibrio
Causes of Viral Infectious Diarrhea in the Developed world
Calicivirus/Norovirus
- Norwalk-like
Rotavirus
in developing countries
* HIV, influenze, SARS
Causes of Protozoal Infectious Diarrhea in the Developed World
Giardia lamblia Cyclospora cayetansis Cryptosporidium spp Microsporidium spp Isospora belli Entamoeba histolytica
Purely Toxin-mediated = BACTERIAL
Causes of Infectious Diarrhea : Developed World
Enterotoxigenic E. coli
Traveller’s diarrhea
In North America, which pathogen is most likely to cause diarrhea
VIRAL
Most infectious diarrhea is viral in origin
Over 90% of stool samples have no bacterial pathogen
Visibly bloody stool is a good predictor of isolation of a bacterial pathogen
Especially for EHEC
Blood Diarrhea
- Whare the common pathogens
sign hat is is most likely BACTERIAL Known as dysentery if GROSSLY visible blood Bacterial: SSCYE Shigella spp Salmonella spp Campylobacter jejuni Yersinia enterocolitica Escherichia coli O157
Viral:
None really
Parasitic:
Entamoeba histolytica
Which is the only parasite that causes bloody diarrhea
Entamoeba Histolytics
A closer look at bloody diarrhea
Escherichia coli O157 H7 (EHEC)
Gram negative enteric rods
- Contain a toxin created by a viral plasmid inside the cell
Reservoirs are mammalian GI tracts
A common cause of enteritis due to food poisoning
Most common cause of acute kidney failure in children
DISEASE = enteritis, starts about 1-2 days after infection and lasts for about 5-10 days
Severe cramps, diarrhea is usually very bloody, usually NO fever
Usually self limiting
2-7% develop Hemolytic Uremic Syndrome (HUS)
- Shigatoxin (also known as verotoxin)
- Renal failure
- Consumptive thrombocytopenia
- Vascular hemolysis (shearing of red blood cells called schistocytes or schizocytes)
- Stupor, confusion, and seizures
- Worsens with antibiotic therapy (release of the toxin)
DON’T TREAT WITH ANTIBIOTIC^
A closer look at bloody diarrhea
Salmonella spp
Gram negative enteric rods (only 2 types but many serogroups)
Reservoirs include poultry and reptile GI tracts
Need about 105 bacteria to cause disease
- Disease = diarrhea (usually bloody), abdominal cramps, and fever 2 days after infection
- Lasts about a week
Typhoid fever is the most serious form
Salmonella enterica serogroup typhi
Usually disseminates to various organs (blood, liver etc)
High fever, stupor, cramps, bloody diarrhea, blood sepsis
Fleeting rose spots on skin, leukopenia with left shift
Interestingly: bradycardia
RECURRENCE IS LINKED TO PRESENCE OF BILIARY STONES
Thyphoid we need to treat but the rest of the salmonellas that are non-thyphoid we don’t need to treat cause theyre self limiting
A closer look at bloody diarrhea
Shigella spp
Gram negative enteric rods
Reservoirs are only primates
Need ONNLYYY about 10 (yes..10!) bacteria to cause disease
Disease = DYSENTERY, abdominal cramps, and fever 1-2 days after infection
Lasts about a week
HIGHLY contagious:
High fever, stupor, cramps, bloody diarrhea
BLACK CURRANT JELLY-like stools
Seizures due to shigatoxin; SOMETIMES HUS
NEED TO TREAT, highly contagious
A closer look at bloody diarrhea
Campylobacter jejuni
Curved Gram negative enteric rods
Reservoirs are bird GI tract
Most common cause of bloody diarrhea in daycare settings
One of the most common causes of enteritis due to food poisoning
DISEASE = enteritis, starts about 2 days after infection and lasts for about a week
- Cramps, diarrhea may be bloody, SOMETIMES HUS
- Usually self limiting
- Guillain-Barré syndrome after about 2-3 weeks [*** this can cause peripheral nerve disease]
HIGHLY contagious
A closer look at bloody diarrhea
Yersinia enterocolitica
Gram negative enteric rod
Loves iron (uses it as a growth factor)
- High iron states are a risk factor
Various mammals are the reservoir
- Zoonosis
- Consumption of undercooked meat, or unpasteurized milk, or fecal oral contact
DISEASE = enteritis, starts within a week after infection and lasts 1-3 weeks, sepsis and bacteremia in immune suppressed people
In young children:
- Bloody diarrhea and terminal ileitis
- Mesenteric adenitis
In older children and adults:
- Severe abdominal cramps that may mimic appendicitis (pseudoappendicitis)
Post infectious arthritis
A closer look at bloody diarrhea
Entamoeba histolytica
NOT a bacteria…it’s a protozoan/parasite
Causes amoebic dysentery
DISEASE: DYSENTERY
- Bloody diarrhea, cramps, fever
Dissemination to liver, lungs, brain where it may cause abscesses
- Often happens to immune suppressed people (e.g. HIV infection)
Amoeboma: large mass in intestine can be mistaken for a tumour but it really is a granuloma.
A closer look at WATERY diarrhea
- List the different pathogens
Bacterial
Traveller’s diarrhea (aka “Montezuma’s Revenge”, “Delhi Belly”, etc)
- E. coli (ETEC)
- Major cause of diarrhea in returning travellers
- Self limited disease
- No fever, no systemic illness
Vibrio spp infections
Cholera caused by Vibrio cholerae
- SEVERE EXPLOSIVE watery diarrhea (liters and liters lost!!!!!!!!!!!!!!!!!)
> Developing world
- HIGHLY CONTAGIOUS
Fish-associated disease caused by Vibrio vulnificus
- After eating shellfish or stepping on a stingray
- Diarrhea, vomiting, skin blisters, sepsis, shock
Listeria monocytogenes
Watery diarrhea can progress to disseminated disease in immune suppressed people and pregnant women (CNS disease, bacteremia, still births) after consumption of unpasteurized milk products, cold cuts etc.
Cholera
Rice water stool
it is explosive diarrhea and you die from dehydration
you don’t give anitbiotics, it makes it worse
A closer look at watery diarrhea
- C.difficile
Clostridium difficile
Gram-positive anaerobic rod that forms resistant spores
- that need to be WASHED off hands (alcohol gels NOT ENOUGH)
- Can be found naturally in up to 15% of adult GI tracts
> Up to 75% in infants less than 1 years old
> Means nothing if the patient is asymptomatic
DISEASE= C. difficile-associated colitis (CDAD)
Watery diarrhea, colitis, pseudomembranous colitis
- Toxin mediated (toxins A and B)
Colitis may progress to toxic megacolon
- Septic ileus of the colon
- Perforation…and then septic shock and death
Babies < 6 months DO NOT have receptors for C. difficile toxins…so do not get CDAD!
- Receptors develop between 6 months and 1 year
- Diarrhea in hospitalized children (esp. < 6 months) IS NOT C. difficile
CDAD
C. difficile-associated colitis
Associated with health care contact
- Rare instances of community acquired CDAD
Associated with antibiotic use in the previous 3 months
Classically associated with the use of clindamycin, and broad spectrum antibiotics like the fluoroquinolones
Risk factors: Health care Antibiotic use Debilitated conditions (old age comorbidities) Proton-pump inhibitors?
Serious nosocomial issue in Quebec since the early 2000’s. This has spread to other places in the world.
A closer look at watery diarrhea
Viral
Many causes
Usually acute self limited disease with vomiting and/or diarrhea
2 important ones I want you to remember:
1. Rotavirus
Huge problem with infants
Not too much vomiting
Major cause of morbidity and mortality in infants
- Dehydration
- Norovirus
Most common cause of self limited gastroenteritis (24 hour “stomach flu”; “winter gastro”) – GOOD LORD explosive vomiting and diarrhea!
Highly contagious- Cruise ship and hospital/nursing home outbreaks
Very resistant to alcohol etc. Need to physically wash off hands or use quaternary ammonium compounds (you know…those “wipes” you see at hospitals) to kill the virus
- Cruise ship and hospital/nursing home outbreaks
A closer look at watery diarrhea
Parasitic
- risk factors
- The spora
Many causes
Usually protracted and chronic watery diarrhea
Risk factors
Travel…travel…travel
Fecal oral contact (e.g. contaminated food)
Immune suppression (e.g. HIV infection)
I want you to remember the “spora” - Microsporidium spp - Cryptosporidium spp - Cyclospora cayetanensis - Isospora belli Why? Because you need to ask for special staining (or PCR) to detect them
And remember Giardia lamblia
Why? Because it is common even in developed countries
Usually causes abdominal cramps and bloating but may cause protracted
Algorithmic approach to the management of diarrhea, what should you think of if it is
- Bloody
- Non bloody
Is it bloody?
Think bacterial
- E.coli O157:H7, Salmonella, Shigella, Campylobacter, Yersinia spp
If travel history or risk factors
- Bacterial as above or Entamoeba histolytica
NEVER FORGET INFLAMMATORY BOWEL DISEASE COLITIS!
Is it non-bloody?
Think viral
- With vomiting: Norovirus (esp. if 24-48 hrs duration), Adenovirus, Astrovirus
- Without too much vomiting: Rotavirus
Think bacterial
- If travel or risk factors: ETEC, Vibrio spp (esp. if severe),
Think parasitic
- If travel or risk factors
- If persisting past a few days
Algorithm Based on stool duration
- Acute
- Persistant
Is it acute (less than 2 weeks)? Think infectious - esp. bacterial if bloody - esp. viral if non-bloody - Vibrio spp esp. if severe non-bloody, and/or dietary risk factors - Clostridium difficile if risk factors
Does diarrhea persist past 2 weeks? Think infectious - Parasitic (esp. Giardia lamblia) Think post-infectious - Temporary lactose intolerance following an acute gastroenteritis - Irritable bowel syndrome
NEVER FORGET INFLAMMATORY BOWEL DISEASE COLITIS ( can be due to simple change in diet that has nothing to do with an infection)
Diagnostic Testing for Diarrhea
Things to remember:
Stool cultures are rarely positive
Most infectious causes/symptoms of acute diarrhea are self-limited
- Is it really necessary to document a pathogen?
- In some cases, yes
»_space;(Public Health purposes, highly infectious organisms [Shigella spp, Salmonella typhi])
- In most cases, no.
In which organism infections do stool cultures NOT help
ETEC (self-limited traveler's diarrhea) Self-limited Yersinia enterocolitica infections Self-limited non-typhoid Salmonellosis Diarrhea after 3 days in hospital - Think C. difficile
In which organism infections DO stool cultures help
Yes
EHEC (development of HUS)
- Use of antibiotics may worsen the renal failure
Public Health purposes
- Shigella spp, Salmonella typhi, Vibrio cholerae, outbreak situation (Campylobacter spp infections in daycares)
- When treatment will help
- Help in the diagnosis of Guillain-Barré syndrome
Diagnostic testing When to send for a stool culture?
Severe diarrhea
- Bloody diarrhea, extremely large quantity
Immunocompromised individuals
- HIV, age < 3 months, age > 65 years
Patients with comorbid conditions
- Renal failure
Patients with IBD
Food handlers and health care workers
- Public Health purposes
Patients with Guillain-Barré syndrome
Diagnostic testing When to ask for C.difficile testing?
Symptomatic diarrhea (usually more than 3 watery stools/day) - With or without fever
Suspected nosocomial outbreaks
Risk factors
- Hospitalization
- History of antibiotic use currently or in the preceding 3 months
Diagnostic technique to detect toxins A and/or B
- Enzyme immunoassay
- PCR
Diagnostic testing When to do viral studies?
Only rotavirus testing is currently widely available and used
Diarrhea in hospitalized patients (especially pediatric hospitals)
Other gastroenteritis viruses Disease is self-limited Not cost effective to test No commercially available test Electron microscopy is available \$\$$ expensive! Done by Public Health usually Outbreak investigation eg. Cruise ships and norovirus
Diagnostic testing When to send stool parasitology PCR or stoolfor ova and parasites (microscopy)?
Watery diarrhea especially
Persistent for more than 2 weeks
Travel history
Risk factors
Travel
Dietary risk factors (freshwater consumption)
MSM
Forthe stool PCR (it looks for genetic material only forparasites causing diarrhea(“spora” [if they have HIV/immunesuppressant], Giardia lamblia,andamoebas).
Parasites and their eggs are shed intermittently, so formicroscopy:
- At least 2-3 stools are required (different bowel movements)
- Usually iodine-based staining techniques
- Lab diagnosis is based in morphology
- Results depend on how fast the lab technician can get to the specimens (a few days)
This test:usually reserved for immunocompromisedpeople with diarrhea or new immigrant screens.
Overall Approach to Treatment of Diarrhea
Ensure adequate hydration
- Treat signs and symptoms of dehydration
Diet alteration
- Electrolyte replenishing drinks, avoidance of lactose-containing products
Probiotics?
- Not adequately studied to recommend after acute and non-specific diarrhea
Which diarrhea causing organisms must be treated becuase they are INFECTIOUS
Traveler’s diarrhea
Shigellosis
Cempylobacter infection
Role of Antibiotics in Diarrhea
Typhoid Salmonella typhi Shigella Campylobacter bacteremia
YES for suspected or confirmed typhoid fever
- They are systemically ill
- Ciprofloxacin po/IV or Ceftriaxone IV
YES for confirmed Salmonella typhi in stool specimen
- To prevent typhoid fever
- Ciprofloxacin po/IV or Ceftriaxone IV
YES for Shigella spp
Only 10 organisms are needed to cause infection
public health concern
Ciprofloxacin po/IV or Ceftriaxone IV
YES for Campylobacter spp infection
Azithromycin po
YES for bacteremia with any of the bacterial pathogens
Role of Antibiotics for Diarrhea caused by: traveller's diarrhea C. difficile colitis Parasite Related Diarrhea Spora
YES for traveler’s diarrhea
Empiric or Specific (proven) treatment
Ciprofloxacin po, or Azithromycin po
Can reduce symptoms from 3-5 days to <1-2 days
YES for symptomatic C.difficile colitis
Metronidazole (Flagyl) po/IV, Vancomycin po, Enema with “healthy” stool
YES for parasitic-related diarrhea
E. histolytica, and Giardia lamblia
Metronidazole (Flagyl) po/IV
Spora
Available treatments are not very good
Treat immune suppression
Role of Antibiotic treatment for diarrhea caused by:
EHEC
nonbacteremic, non typhi salmonella spp
NO for suspected or proven EHEC infections
May worsen renal failure and HUS
NO for well-looking and non-bacteremic non-typhi Salmonella spp
Risk for prolonged shedding of organisms
What about anti-motility agents for treating Diarrhea
NO for bloody diarrhea and systemically ill patients
You want to get rid of it…not keep it festering in your intestines so it can invade!
Better to “flush things out”…so to say
Prevention for Diarrhea
Hand and utensil hygiene
Dietary care Especially when traveling - Bottled or boiled water - Peeling fruits and vegetables Avoid undercooked or raw food DON’T EAT SH*T!
Travel vaccines (especially typhoid)!
Acronyms for causes of bloody diarrhea
SSCYE
Viral diarrhea is most often
watery and acute
Think of _____ type of infection with persistent Diarrhea
Parasitic infection
Think of C. difficile caused Diarrhea when:
Post antibiotics
Hospitalized patients
What are some complications of Diarrhea
Complications:
HUS [hemolytic uremic syndrome] with EHEC
Typhoid fever
Guillain-Barré
Treatment is available for Diarrhea caused by….
Traveler’s diarrhea empiric Shigella spp Campylobacter spp Typhoid Systemically ill Symptomatic C.difficile Parasitic in origin
Reserve C. Difficile testing for…
Age > 6 months
Symptomatic patients
NO antibiotics for…
and NO antimotility agents in….
NO antibiotics for EHEC
NO antimotility agents in bloody diarrhea
for Diarrhea DON’T FORGET ABOUT….
IBD
Examples of UNCOMPLICATED soft tissue infections
Cellulitis
Erysipelas
Folliculitis, Furunculosis
Impetigo, Ecthyma
Abcesses are uncomplicated but can’t be treated with ABX
Examples of complicated soft tissue infections
Traumatic wound infection
Bite-related wound infection
Diabetic foot infection
Necrotizing infection
Cellulitis
- which skin layers
- which organisms
- symptoms
- treatment
Constellation of skin manifestations
- Involves the epidermis and dermis
- Organisms: Streptococcus (pyogenes), S. aureus, H. influenza
- Pain, erythema, swelling
- Treatment: antibiotics, incision and drainage (I+D)
Erysipelas
- which part of the skin
- which organism
- nature of infection
- symptoms
- parts of the body it predominantly affects
- treatment
Superficial infection of skin caused by group A Streptococcus
- looks like a red rash
- Spreads rapidly and involves dermal lymphatics
- Fever, pain, “aches”, adenitis
- Legs>face
- Treatment – penicillin G
Skin Abscess
Can result from a number of infections, including cellulitis
- Involve epidermis and dermis and occasionally deeper structures
- Occur anywhere on the body (perianal, sebaceous cyst)
- Usually caused by S. aureus
- Treatment involves I+D, with antibiotics reserved for those with an associated cellulitis
ABX: Cephalexin [covers staph and strep]
Septra: for MRSA
MSSA : Dicloxacilin: oral agent of choice for methicillin-susceptible
Hand Infection: Felon
Distal pulp space of finger is compartmentalized by fibrous septa
Infection arises from direct innoculation with bacteria (puncture wound)
abscess restricted to finger pulp
Less commonly hematogenous spread
Intensely painful, throbbing pulp space
Pressure can lead to necrosis with spread to tendons, ligaments and bone
Treatment is I+D and antibiotics against common Strept and Staph species
Hand Infection: Paronychia
Infection of the skin over the mantle of the nail or of the lateral nail fold
Swollen, tender with progression to felon if untreated
Treatment is I+D with +/- removal of the nail
Purulence about nail fold
Hand Infection: Tenosynovitis
Penetrating injury to volar surface involving tendon sheath
Kanavel’s signs
- Finger held in mild flexion
- Fusiform swelling
- Tender along tendon sheath
- Pain with passive extension
Antibiotics and surgical debridement
- Tendon necrosis, tendon sheath disruption, contracture, proximal extension
EMERG: Won’t be able to move hand/fingers
Management of Tenosynovitis
Usually due to Staphylococcus
treatment recommendation based on stages include minimal invasive drainage and irrigation
severe stages: open depridement, possible amputation
Human Bites
Subtle injury, usually a puncture
Can lead to severe infection
Aerobic and anaerobic
Treatment includes antibiotics and possibly debridement
Should not close puncture site due to high risk of infection
ABX guideline after dog, cat or human bites when
infection not established
Infection established
pts with penicillin hypersensitivity
infection not established: Amoxicillin
Infection established: metronidazole, cefotaxime
pts with penicillin hypersensitivity: Metronidazole, socycycline
Diabetic Foot
Glove and stocking neuropathy, compromised vascular supply +/- microvascular disease
- Cellulitis to chronic osteomyelitis
- Difficult to treat due to poor microcirculation
- Abx, debridement +/- amputation
- revascularization
-STI/Osteomyelitis – GAS, S. aureus, Pseudomonas (deep)
Diabetic Foot Therapy
ABX: amoxicilin for gram positive and gram negative coverage
piptazo: for gram +, gram- AND anaerobic coverage
Necrotizing Infections (NI)
Include Clostridial infections, necrotizing fasciitis, bacterial syngergistic gangrene and Streptococcal gangrene
Early diagnosis is vitally important for early treatment
Often these infections lack any specific external diagnostic signs or symptoms
Rare – 1000 cases per year in USA
Severe infections, rapid progression
Combination of expeditious surgery and antibiotics for treatment
Significant longterm morbidity
Bacteriology of Nectrotizing infections
Top 4
- staph aureus 45%
- Pseudomonas Aeruginosa 10%
- Enterococcus spp 10%
- E.coli 7%
Rarely single organism (except group A Streptococcus [GAS])
- Β-hemolytic Streptococcus, anaerobic GPC, aerobic GNR, Bacteroides
Synergy between aerobic and anaerobic organisms for the necrosis of skin, soft tissue and fascia
Diagnosis of NI’s
spontaneous vs overall frequent sites
Often lack any diagnostic external signs of necrotizing infection
- Cellulitis, small ulcer
Most frequent SPONTANEOUS site is perineum
Most frequent sites OVERALL are the limbs
- Wound, puncture, injury
Lab Risk Indicators for the Development of NI
Low sodium and high creatinine
Perineum
The perineum refers to the area between the anus and genitals, extending from either the vaginal opening to the anus or the scrotum to the anus.
Gold standard Diagnostic Modality for Nectrotizing Infection
- what are other techniques
Gold standard is tissue biopsy
Frozen section, gram stain
Necrotic areas are insensate and thus biopsy can be performed at bedside
Plain radiographs – 25%
CT scan
MRI
Surgical debridement
List specific Necrotizing Infections
Necrotizing fasciitis type I (polymicrobial) i.e. bacterial Synergistic Gangrene, Necrotizing fasciitis type II (group A streptococcal), and Clostridial myonecrosis (gas gangrene)
Bacterial Synergistic Gangrene
- which parts of the skin
- organisms
- treatment
Rare form of gangrene affecting trunk and limbs (Meleney’s ulcer)
-Affects skin and soft tissues BUT NOT FASCIA
Streptococci, S. aureus, GNR
- Slow infection
- Treatment includes antibiotics and often radical debridement
Necrotizing Fasciitis
- which skin layers
- symptoms
Aggressive necrotizing infection involving the skin, soft tissue and fascia BUT NOT INVOLVING THE MUSCLE
-Patients can be very ill with hypotension, fever, decreased level of consciousness
Management of Necrotizing Fasciitis
SUPPORTIVE
- Resuscitation
- Antibiotics
- IVIG
SURGERY
- Fascial probing
- RADICAL DEBRIDGEMENT
RECONSTRUCTION
Group A Streptococcus - GAS
- Brown Classification
- what do they produce?
Brown classified them 1919 into
a-hemolytic (partial hemolysis)
b-hemolytic (complete hemolysis)
g-hemolytic (no hemolysis)
Produce extracellular products capable of TISSUE DESTRUCTION
Notably: Exotoxin A which is a SUPERANTIGEN
- For which there is a genetic susceptibility for a more exaggerated response
Superantigens
Normal MHC II binding of antigen presenting cells to T-cells is very specific
- Antigen peptide binds to both the α- and β-chains within the antigen groove
- Leads to the activiation of 1 in 10,000 T-cells
- Superantigens bind to the antigen presenting cell outside of the normal antigen groove
- Can activate 1/5 to 1/10 T-cells leading to an exaggerated response
- Activation of T-cells leads to the release of cytokines and other inflammatory mediators
- fever, capillary leak and hypotension, rash, desquamation
Management of GAS infection
Supportive therapy
- Mechanical ventilation
- Fluid resuscitation
- Inotropic medication for hypotension
Antibiotic therapy - penicillin
Wide surgical debridement to normal tissue
- amputation
Clostridial Cellulitis
- which skin layers
- organism
- treatment
type of NI
Slow progressive infection of the soft tissues sparing the muscle
- Crepitus (gas) in subcutaneous tissues, foul-smelling exudate
- C. perfringes, sprogenes
- Wide debridement, broad spectrum Abx (penicillin-based)
Clostridial Myonecrosis
- which skin layers
- organism
- treatment
type of NI
- Rapidly progressive infection involving dermis, fascia and muscle (no inflammation)
- ”Mousy smell”, bronzing of skin
- Rapid debridement often requiring amputation
- Penicillin G mainstay of treatment
Empiric ABX Management
Pip/tazo
for pts with allergy
- Metronidazole
- Clindamycin
Adjunctive Therapy for NI
Intravenous Immunoglobulin
Pooled immunoglobulin from various donors
Binds exotoxin for Staphylococcal and Streptococcal species
- Limit inflammatory response to toxin
Studies underpowered to demonstrated true benefit
Still recommended for critically-ill patients
