98 terms

Infectious Disease


Terms in this set (...)

Causes of Abdominal Pain
1. Peritoneal irritation (emergent surgical crisis)
2. Mechanical destruction (bowel obstruction)
3. Vascular lesions (mesenteric infarct)
4. Abdominal wall conditions (caused by trauma usually)
5. Distention (lots of abdominal gas)
6. Inflammation of a viscus (itis of ileum, stomach, etc.)
7. Pain referred from extra-abdominal sources (cardiopulmonary, pelvic)
8. Metabolic - adrenal insuffiency
9. Neurologic/psychiatric
10. Toxic - heavy metal poisoning
acute abdomen
mixed intestinal flora
diagnosis is clinical
Tx: acute surgical intervention, drainage, abx
Intra-abdominal abscess
perforation and localization
symptoms: vague abdominal pain, fever due to infection, night sweats, chills,
sites: LRQ most common, LLQ (gravitational pull)
Mixed intestinal flora especially anaerobes - enteric gram negative, enterococci, streptococci

Symptoms may be masked in seriously ill patients
anaerobic bacteria
Organisms that will not grow in presence of O2 - doesn't mean O2 destroys them, but can't use it as a resource

Anaerobic infections are a mixture of multiple different bacterial species (strict anaerobes with staph or strep or enteric)

Anaerobes are NF that invade a new area with trauma and reduced blood flow/O2 supply allows rapid growth

Slow progression
Clues to anaerobic infection
Insidious onset of disease (slow progression)
contiguous to mucosal surfaces
Foul smell
Severe tissue necrosis
Gas in tissue
Tx: debreedment, IV antibiotics
Peptic Ulcer Disease
Epigastric abdominal pain, usually postprandial (1-2 hrs after eating)
etiology: Helicobacter pylori (95%) or NSAID use
Helicobacter pylori
Vibronaceae family
Was once thought to be Campylobacter, but is Urease positive (protects it in gastric environment)
Most people exposed in childhood
Lives under the mucosa in the stomach where it isn't exposed to the acidic environment
Hepatitis symptoms
Inflammation of the liver
low grade fever
Dark urine, clay colored stools
Jaundice from excess bilirubin
RUQ tenderness
Infectious causes of hepatitis
Hepatitis virus A through G
Gonorrhea, Chlamydia
Non-infectious causes of Hepatitis
Hepatitis A
Transmitted fecal-to-oral or contaminated water
Usually OUTBREAJS associated
Excreted 1-2 weeks before symptoms appear
50-70% prevalance
Usually mild, NEVER CHRONIC
Can become Fulminant Hepatitis (very bad)
Dx: IgM for acute
No treatment but gamma globulin
During viral process and shedding, develop IgM early response, then IgG as you're getting better - IgGs persist for life
Hepatitis B
Parenteral/sexual transmission
Contagious when blood test shows positive s-antigen/e-antigen
Most ppl have no symptoms, few chronic sequelae
May lead to cirrhosis or hepatoma (liver cancer)
20% get sick, 5% have sequela
Acute Hep B (DNA virus) has surface entity that is antigenic, Core that hosts the DNA
Hep B graph/testing
Hep C
Parenteral/sexual transmission
Contagiousness is poorly defined
Most without symptoms, but sequelae is COMMON
Most common cause of cirrhosis and hepatoma in the US
Dx: antibody test confirmed or PCR
Tx: Ribaviron and Interferon
Hep D
Incomplete virion that partners with Hep B
Can get Fuminant Hepatitis - aweful
Parenterally acquired - blood, IV drug use, sexual
Hep E
Same as A in the US, but in the rest of the world
Hep G
no apparent disease
Diarrhea definition
Change in frequency and consistency or both
Usually loose or watery with increased frequency
Need to ask pt their experience
Acute causes of diarrhea
Infections (bacterial or viral)
Medications - side effect
Ischemia - excess water or fecal contents
Diverticulitis - inflammatory process, proteins available in the bowel lumen
Graft vs. host disease - transplant pt on immunosuppressants
Chronic causes of diarrhea
uncommon to be infection, long list, everything on the list for abdominal pain could cause diarrhea
Infectios Diarrhea facts
Very common
Usually minor consequences in the US
Most common infection in underdeveloped world
Most common cause of death among children worldwide - malnourished children die from diarrhea
Pathogenic mechanisms of diarrhea
Small intestine pulls nutrients out, 15 L of water moves through, so a diarrheal illness means water absorption is blocked to some extent

Toxin production
Preformed Toxin
Toxin production Pathogenic Mechanism for Diarrhea
Largest volume of watery stool
Toxin blocks water reabsorption by blocking cAMP, cGMP
Annoying, but not terribly dangerous
Includes viral disease
Invasion Mediated Pathogenic Mechanism for Diarrhea
Enters and migrates through mucosa, destroys surface mucosal layer, much worse than toxins
Small volume watery diarrhea
Tenesmus (urge to go, but don't really need to)
Preformed Toxin Pathogenesis of Diarrhea
Mediated Gastric Enteritis
Eat a toxin from an organism and get sick right away
Nausea, vomitting
Abdominal pain soon after ingestion (upper abdomen)
Commonly Staph aureus, Clostridium perfringens, or Bacillus cereus
Food in summer sun, multiple ppl get sick at same time after eating same food
Absorbed into small intestines, blocks water absorption
Worldwide, Winter
30-60% of severe infantile diarrhea - can cause death
Usually age 6-24 months
Clinically: fever, vomitting, diarrhea, resp symptoms, dehydration, electrolyte change -> need IV fluids!
4-7 day course
Treat with fluids
Direct human-to-human spread, fecal-oral contamination, food and water supplies contaminated
Common in day care centers
Older children and adults
also called Calicivirus
Worldwide, Winter
Fecal-oral, water, shellfish
Incubation 24-48 hours
2-3 days fever, vomiting, diarrhea, cramps, HA, myalgia
Common in cruise ships, dormitories, hard to contain and eradicate
Enteric organisms that live in intestines
>30 genera, > 100 species, multiple biogroups
99% clinical isolates are in 12 genera, 25 species
80-95% isolates in general hospital are:
E.coli, Klebsiella pneumoniae, Proteus mirabilis
Also Salmonella and Shigella
E. coli
Most common cause of travelers diarrhea
Enterotoxigenic - most common form - toxin mediated
Eat food with this, E.coli gets to intestines, end up with diarrhea
Enterohemorrhagic- shiga-like toxin
More serious illness, toxins break down cell membrane, blood in stool, more painful, toxin can damage RBCs and kidneys
Hemolytic-urea syndrome
Hemolysis (break down RBCs, anemia), renal failure
Seen predominantly in children
Ubiquitous pathogens found in humans, livestock, mammals, reptiles, birds, and insects.
Invasion of lymphoid tissue in intestinal mucosa
Gastrointestinsal - related to improper food handling, poultry products including eggs are the most common vehicles of infection
50,000 reported cases annually
Summer/Fall peak incidence
Attach rates higher <5 or >70
S. typhimurium and S. enteriditis major cause of disease
Salmonella symptoms
Begin 24-48 hours post ingestion - migrates to Peyer's patches in lymphoid tissue
Nausea, vomiting, cramping
Large volume diarrhea
Diarrhea persists 3-4 days, resolves spontaneously
High fever present in 50% of patients
Infecting dose is >105 bacilli
Severe disease, dysentery
Non-lactose fermenter
Invades intestinal mucosa
4 species based on differences in O antigens
Shigella dystenteriae - most severe, rare in US
Sheigella flexneri
Shigella boydii
Shigella sonnei
Shigella Epidemiology
Never commensal (never NF) in human GI tract
Not destroyed by stomach acid, low inoculum disease
Highly adapted to humans
Important factors in transmission:
Feces, Food, Fingers, and Flies
<200 organisms cause disease
Largely daycare centers in the US, pediatric disease
Worldwide epidemics have high mortality
Shigella Clinical Manifestations
Classic bacterial dysentery
Abdominal cramps, tenesmus, fever (102-103), blood mucoid small volume stools
Vibrio cholera
Curved gram negative bacilli
facultative anaerobes
Polar flagella, very motile
Generally associated with water sources
Generally associated with GI disease, some skin and soft tissue infections
Single most common cause of bacterial diarrhea in US
Curved bacilli
Fastidious growth requirements: reduced O2, 42 degrees, selective media, doesn't compete well with enterics, incubate 3 days for growth

Food and water, POULTRY, pets, fecal-oral spread, high inoculum (we ingest often and don't get sick)
Clinical Manifestation Campylobacter
Rapid onset
Fever, constitutional symptoms, aches, pains
Abdominal pain, may mimic appendicitis
Diarrhea - profuse and water, smelly! may be bloody
May have relapsing episodes
Lasts 4-5 days, often feel better then relapse a few days later
Invades mucosa and releases toxins
Clostridium difficile
Most often acquired by sick people in hospitals, now spreading to community acquired as well
GI tract organism, but only some strains make toxin
Spore forming
Associated with antibiotic use pseudomembranous colitis
Toxin-mediated: gets into mucosa, blocks water absorption, protein gets into mucosal wall
Subacute diarrheal syndrome - bloody or watery
Transmission from food products, cysts ingested, may invade
Trophozoite in intestine, tries to ingest cell membrane, can invade biliary tract and get into liver
Diagnosis: fecal sample, serology
Transmission: person-to-person, water, food
Common in day care, families, surface water
Outdoor activities at risk
Subacute diarrhea with malabsorption
Bloating, discomfort, sulfur tasting
Transmission by food and water (raspberries)
Swimming pool outbreaks
Usually self-limited diarrhea
Chronic, untreatable diarrhea in immunocompromised
Dx: acid-fast or direct stain flourescent antibody
No good antimicrobial to treat
Discomfort with Urination
Consider: location and phase of urination
Dysuria, urethral discharge, inflammation in the urethra

Usually an STI, could be from trauma, could be from skin infection (staph or yeast) but unlikely.
Dysuria, perineal pain, acute or chronic presentation
(prostate based)
(uncomplicated or lower UTI)
normal anatomy
suprapubic pain
little to no fever
usually superficial, no real serious slinical consequences
(complicated or upper UTI)
structural or functional abnormalities
fever, chills, adbominal pain, flank pain, +/- cystitis symps
Much more serious, systemic element
not always cystitis --> pyelo
Usually Pyelo comes from the blood

Could be from structural or functional abnormalities, obstruction, or reflux of urine so it backflows - common with pregnancy
Cystitis Statistics
1 in 3 women will have a UTI
7 million office, 1 million ER visits
300,000 hospital stays
1.6 billion US cost
Very little preventive measures
UTI patient categories
neonate: structural disease, anatomical, significant concern (more common in males)
young child: hygeine (females with wiping) or urine retention not enough voiding (boys and girls)
adolescents: first sexual experience, STDs (more women)
Adult females: uncomplicated, pregnancy, can be recurrent, usually cystitis, not pyelo, more dangerous in pregnancy
Adult males: prostatitis, epididymitis, orchitis
Elderly: catheterized (acute or chronic), marker for patients not doing well as they age
UTI Prevalence Rates
Neonates - 1% full term, 3% premature
Children <2 - 5% febrile chile, males 2.8:1 over females
School age: 5%, 1/3 asymptomatic with recurrance
Female adults: 25-35% have at least 1 episode, 25-44% recur within 6 months
Male adults: very low prevelance
UTI Prevalence in Elderly
Elderly: females 6-33% males 5-20%
nursing home residents - more frequent, UTIs are most
frequent cause of sepsis in the elderly
UTI Prevalance in Catheterized patients
Catheterized: 100% eventually become bacteriuric
Usually a polymicrobial infection
Sometimes an unusual organism is isolated
Flora changes rapidly
Account for 40% of hospital aquired infections
Important reservoir for multi-drug resistant strains
UTI Routes of Infection
Hematogenous (mainly in neonates)
UTI Factors to consider
Human host factors (age, gender, complications)
Virulence factors of the organism
Does the patient have a catheter?
Is there an obstruction?
Is the patient immunocompromised?
Is there anything else anatomic that we should know about this patient?
Virulence Factors for UTI bugs
O groups of E. coli
High amount of K antigen
Adherence properties unique strains
Resistance to serum bactericidal activity
Hemolysis production
Aerobactin production
Female Host Factors to consider with UTIs
Short urethra
Sexual activity
Urethral and vaginal colonization
Immune hyperresponsiveness
Low levels of secretory IgA
ABO blood group nonsecretor status
Urine Screening
Patient with Pyuria: test has 90% sensitivity
Patient with Bacteruria: 85-90% sensitivity
Patient with Leukocyte esterase: 75-95% sensitivity
Nitrate: 60-80% sensitivity
Indications for Culturing in UTI suspected patients
UTI in past 3 weeks
Symptoms > 7 days
Recent hospitalization or urologic procedure
Male Patient
General UTI Management
Treat with antibiotics only if there is evidence of infection
Asymptomatic infections - don't treat unless two successive cultures yield the same organism
Symptomatic indivuduals treat with or without culture
Common UTI organisms
Community acquired: E. coli (80%)
Children: Enterobacteriaceae
Diabetics: Klebsiella, Group B Strep, Enterococcus, E. coli
Spinal cord injury patients: E. coli, Psuedomas, Proteus
Enterobacteriaceae family
> 30 genera, > 100 species
multiple biogroups and unnamed enteric groups
99% of clinical isolates belong to 12 genera and 25 species

80-95% of all isolates in the general hospital will be E. coli, Klebsiella pneumoniae, or Proteus mirabilis
Enterobacteriaceae Epidemiology
Inhabitants of lower GI tract
Survive readily in nature - free living where there is water and minimal energy sources available
Hospitalized patients typically have increased colonization with these organisms
Gram Positive Cocci
Live in the GI tract
Possess Lancefiled Group D antigens as if they were streptococci
Grow in high NaCl concentrations and in the presence of bile salts
Most strains are alpha-hemolytic or non-hemolytic, 5% beta
Two most important species:
Enterococcus faecalis, Enterococcus faecium
Clinical Syndromes of E. faecalis and faecium
UTI (nosocomial)
Spontaneous peritonitis
Bacteremia (nosocomial)
Bacterial Resistance and E. faecalis and faecium
Naturally resistant to:
Semisynthetic penicillin

Acquired resistance to:
High level resistance to Aminoglycosides
Dysuria, urethral discharge
Inflammation in women, not necessarily sexually transmitted, but usually
Not an inflammatory process - bacterial overgrowth with uncommon vaginal flora
Ulcers vs. individualized lesions/warts
Ulcers = syphilis or chancroid
lesions/warts = Molluscum contagiousum, folliculitis, HPV
Gonorrhea syndromes
5 Colony Types, T1 and T2 are pathogens - have pili on surface, attach to uroepithelial cells

Urethritis with purulent discharge, vaginitis, cervicitis, PID, Fitz-Hugh-Curtis syndrome (perihepatitis), disseminated infection with arthritis, tenovitis, rash
Could get proctitis, pharyngitis
Gonorrheal complications
Future risk for PID in women
5-10% have disseminated gonorrhea, more likely to have disease during menstruation
Tuboovarian abscess - fallopian tube cilia are destroyed via PID, so bacteria can build up and become an abscess
Diagnostic tests for Gonorrhea
Gram stain for symptomatic men
Cutlure required in most states for ID and susceptibilities
Rapid Detection:
1. EIA flurorescent antibody test (older technology)
2. DNA probe - rapid, only for genital specimens
3. LCR - highest sensitivity and specificity on genital specimens; voided urine men is still 90%, voided urine women not as good
4. PCR - not yet approved
Chlamydia Clinical Manifestations
Same as Gonorrhea
pts with dysuria, urethral/cervical discharge, pelvic pain
Pts with sexual contacts
Victims of assault
Diastnostic tests for Chlamydia
Lekocyte esterase useful screeing in males - urine dip stick
Cell Culture: no swabs with wooden shafts, multiple cell lines, sensitivity 70-90%, tedious and difficult, necessary in legal situations
EIA - simple and rapid, may get false negs
DFA - small volume rapid tests
DNA probe: rapid, high volumes, false positive
Amplication - by far the best test!!
better sensitivity - only for genital samples!
Most common viral STD in the US
Commonly acquired early in sexual experience
Most often spontaneously eliminated.
Wart strains 6, 10
Cancer strains 16, 18
Vaccine effective if given prior to exposure
Herpes Simplex Virus
Genital Herpes - recurrent outbreaks usually occur in some spot, 30% have reoccurence.
Immunocompromised have more outberaks over time.
Clustered Vesicles with pain
Can be shed during clinical outbreaks.
More frequent outbreaks = more frequent shedding.
Treatment can be acute or ongoing suppresive.
<5 per year, treat ind. episode.
>5 per year, stay on acyclovir, shedding all the time.
Syphilis facts/transmission/most likely susceptible
Treponema pallidum
A major worldwide STD
Associated with lower socioeconomic status
Humans only host
Spread by direct contact with lesions
More common with male sex
30% transmission rate
6,000 to 7,000 cases in U.S. each year (mini-outbreak in SLC right now)
Syphilis Natural History
1. Primary
Occurs 3-4 weeks following exposure
Consists of a hard chancre. A single, shallow ulcer with raised edges that is usually soft and painless. Has a well described margin and an ulcerated center. Ulcer lasts 1-5 weeks and heals.
2. Secondary
6-8 weeks following exposure
Generalized rash and systemic flu-like illness. Papulosquamous rash with discrete lesions with scale surface. INCLUDES THE PALMS AND SOLES. May also have hair loss, mucous patches in mouth and genitals. Resolves after 1-2 weeks.
3. Early Latent Syphilis
Lasts up to four year with no symptoms, but tests would be positive.
4. Late (tertiary) syphilis
No longer contagious.
Occurs 4-20 years after initial exposure.
Only 1/3 of untreated patients will get this.
Late benign disease: Gummas - tissue breakdown, ulcerating lesions, devascularizing
Cardiovascular disease: inflammation of major arteries, aortitis, aortic dissection, rupture
Central Nervous System disease: slowly progressive meningitis, peripheral sensory neuropathy (tabes dorsalis) or dementia
Congenital Syphilis
Early: Mother to fetus after 4th month of gestation
baby may be stillborn or have fulimant disease with osteochondritis, hepatosplenomegaly, lymphadenopathy, high mortality rate in 2 years

Late: Transmitted later in pregnancy or smaller innoculum
60% subclinical
Possible: joint disease, deafness, Hutchinson teeth, Mulberry molars, bone abnormalities
Diagnosing Syphilis
Direct exam: wet prep from the chancre viewed with a darkfield microscop shows spirochetes
Nontreponemal serologic tests - RPR which can show quantity over time(titer)
Trponemal serologic tests: IgG (ESA) test used by bigger hospitals - more specific, but still some false positives
Tests don't turn positive until 4-6 weeks post infection, so by secondary disease all tests are positive.
Haemophilus ducreyi
Cause of STD Chancroid
Painful, irregular ulcer with ragged edges
Not common in US, but occasional outbreaks
Pathophysiology of Bacteremia
Entry of organisms from focus of infection into lymphatics, then blood
Cytokine release results in clinical manifestations of "sepsis"
Organisms quickly cleared from blood
Infection is not of the bloodstream in most cases
Transient Bacteremia
Lasts minutes to hours
Associated with manipulation of colonized/infected material
dental, GU, GI
May be initial manifestation of focal infection such as pneumonia, osteomyelitis, meningitis, arthritis
Intermittent bacteremia
Periodic seeding from undrained or inadequately treated focus
Continuous bacteremia
Intravascular infections such as endocarditis, vascular access infection, septic thrombophlebitis
Risk factors for increased mortality with positive cultures
Advanced Age
Hospital acquired infection
Multiple underlying disease processes
Clinical Importance of blood cultures
Diagnosis: positive blood culture confirms or establishes etiologic diagnosis
Prognosis: Failure of host defenses to control infection at primary location; failure to identify/treat focus of infection; individual organism important
Diagnostic Strategy for Blood Cultures
Sterile technique
Three sticks, at least 30 minutes apart, three different locations
Most Common Endocarditis Organisms
Staph aureus
Coagulase Negative Staph
E. coli and other Enterobacteriaceae
Endocarditis - definition, location
Infection of the endocardial surface, most often one or more heart valves
May be in septal defects, arteriovenous shunts, abnormal surfaces of the aorta
Acute infection: severe disease, rapid progression to death in 6 weeks
Subacute: indolent with progression to death in longer time
Endocarditis presentation
Not a common disease
Usually considered when evidence of infection is present, but no obvious focal site
Can present in multiple different ways and with nonspecific symptoms, so is considered in many workups
Would be universally fatal if not treated with antibiotics; even with , many have long term consequences or death
Pathogenesis of Endocarditis
1. Bacteria must be circulating in blood: transient bacteremia happens all the time, events that manipulate colonized tissue (dental procedures, etc.) or IV drug use
2. Bacteria must be static in blood at site of turbulence: abnormal or damaged tissue usually
3. Changes in flow can create alterations or damage to endothelial surface, attachment becomes easier
4. Changes in flow cause fibrin and platelet clots promote bacterial attachment
5. Some bacteria have surface characteristics that make them more likely to attach
6. Complex of fibrin, platelets and bacteria are a nidus for continued deposition of material that becomes vegetation
7. vegetation damages heart valve
8. Vegetation may disoldge and embolize to other parts of the body, causing secondary infection
Endocarditis active ongoing infection
Causes an immune response with formation of large numbers of antibodies. These will often attach to antigen and create immune complexes.

Immune complexes can lead to additional clinical symptoms and destruction of other organ systems
Kidneys (glomerulonephritis)
Skin (vasculitis)
Endocarditis Common Orgs
Staph aureus - especially in IVDUs or prosthetic valves
Streptococci veridans after dental procedures
Enterococci after UT procedures or prosthetic valves
Coag neg Staph with prosthetic valves
HACEK group
Gram neg bacteria within 2 months after prosthetic valve replacement or in older adults with UT abnormalities
Clinical Manifestations Endocarditis
Acute onset over a few days or chronic illness with mild but gradually increasing symptoms over weeks

May have a specific history of a procedure associated with bacteremia

May have a history of a valvular or other predisposing intravascular disease

May be an IV drug user
Symptoms/Signs Endocarditis
heart murmur
changing murmur
embolic event
skin manifestations - petechiae, janeway, osler nodes, splinter hemorrhages
weight loss
night sweats
mycotic aneurysm,
Duke criteria
A way of stratifying patients relative liklihood of endocarditis
Complications of endocarditis
Major embolic events such as central nervous system stroke
Secondary central nervous system infections like brain abscess, meningitis, subdural empyema
Valvular insufficiency
Heart failure
Diagnosis endocarditis
Obtain a good histort for predisposing factors and symptoms
Perform a careful exam for skin, eye lesions and listening for murmurs
Obtain blood cultures: 3 separate venipunctures at least 30 minutes apart
Consider an echocardiogram
Consider serology for unusal organism like Coxiella burnetti
Approach to management endocarditis
Antibiotic for etiologic organism
Treat cardiac compromise (failure, arrhythmias) as needed
Surgery may be necessary to repair/replace valve or eliminate infection