Lecture 3: Infectious Disease pt 3 Flashcards
What are 3 ways we can classify bacteria?
1) Gram positive vs negative
2) Aerobic vs anerobic
3) Atypical
Differentiate between gram negative and positive organisms
1) Negative: 2 cell membranes, thin cell wall, pink
2) Positive: 1 cell membrane, thick cell wall, purple
Give some common examples of gram negative bacteria
1) E. coli
2) Pseudomonas
3) H. influenzae
4) Proteus
5) Neisseria
-N. Gonorrhea and N. Meningitides
6) Klebsiella
7) Legionella
8) Serratia
9) H. Pylori
Give some common examples of gram positive bacteria
1) Staphylococcus
-Staph aureus, staph epidermidis, staph saprophyticus
2) Streptococcus
-Group A strep (pyogenes), Group B strep (agalactiae), Strep viridans
3) Enterococcus
4) Listeria
5) Clostridium
-C. difficile, C. perfringes, C. tetani
Which are more likely to spread, gram positives or negatives?
G+ bacteria
1) Define aerobic
2) Define anaerobic
3) Define facultative anaerobe
1) Needs oxygen
2) Cannot survive with oxygen
3) Can go either way
List 4 atypical bacteria
1) Mycoplasma
2) Rickettsial species
3) Chlamydia
4) Spirochetes
What do B-lactams do? Give an example
Inhibit cell wall biosynthesis; amoxicillin, etc
True or false: Mycobacterium Tuberculosis is atypical
True
Mycobacterium Marinum:
1) Type?
2) Pathophysiology?
3) Exposure Risks?
1) Atypical
2) Causes Nodular Lymphangitis
3) Fresh and saltwater exposure
-Fish handlers, swimming in lakes and oceans
Describe Mycobacterium Marinum primary and secondary lesions
1) Primary Lesion: 2–8-week incubation
2) Secondary Lesions: Erythematous papules, nodules up lymph chain. Lesions ulcerate or form abscesses
Mycobacterium Marinum:
1) How is it diagnosed?
2) How is it treated?
1) Organisms rarely seen under microscope, so culture of biopsied tissue requires special incubation temperatures
-PPD (purified protein derivative): Usually >10mm in active cases
2) Treatment: Apply warm compresses to lesions
-Antibiotics for 2-3 months
-Clarithromycin and Rifampin
Mycobacterium Avium Complex (MAC)
1) Bacteria type?
2) Epidemiology?
3) Signs and Sx?
1) Atypical
2) Found in environment, rarely occurs if CD4 count >50
Dissemination MAC infection: 40% occurs in North American AIDS
3) Fever, fatigue, night sweats, wasting, GI upset, unilateral firm fluctuant lymphadenitis
Mycobacterium Avium Complex (MAC):
1) Labs?
2) How do you Dx? (3 things)
3) Tx?
1) Alkaline Phosphatase increased, low Hgb, blood cultures, lymph node biopsy, PPD positive only 50%
2) pulmonary symptoms+ chest xray+ Sputum
3)
1) Prophylaxis for HIV with CD4 cell count <50: Azithromycin 1200mg PO weekly
2) Management: Clarithromycin+ rifampin + ethambutol for 12 months
Rocky mountain spotted fever:
1) Etiology?
2) Epidemiology?
1) Rickettsia rickettsia
2) 6000 cases per year. Most lethal of Tick-borne illnesses. Most common April to September.
Rocky mountain spotted fever:
1) Epidemiology
2) Pathophysiology
1) 60%: North Carolina, Oklahoma, Arkansas, Tennessee, Missouri
2) Tick to human (as early as 2 hours).
-Infects endothelial cells and smooth muscle cells, Spreads through the lymphatic system.
Rocky mountain spotted fever:
1) Signs and Sx
2) What can it lead to? Do we have any immunity?
3) Rash distribution
4) How to Dx
5) Labs
1) Fever, flu-like illness, headache, erythematous, macular rash (transitions to petechiae), NV, abdominal pain.
2) Suspected life-long immunity after natural infection
Can lead to meningitis.
3) Peripheral to central spread. Can be on palms and soles. Face is spared.
4) Clinical findings. Biopsy only if needing confirmation.
5) Thrombocytopenia common
Rocky mountain spotted fever Tx
Within 5 days; Empiric Tx if Dx likely (endemic, tick bite or exposure):
-Doxycycline 100 mg PO/IV BID x 7d (ok for pregnancy)
Continue treatment x 3 days after afebrile
Lyme disease:
1) Epidemiology
2) Clinical manifestations
3) Is it reportable?
1) Spirochete Borrelia burgdorferi; spread by Ixodes scapularis “deer ticks”
-Mostly in northeast
2) Transmission via tick bite leads to early localized infection, or straight to early disseminated infection. Both can lead to late stage Lyme.
3) Yes, reportable
The “The classic “Bull’s Eye” erythema migrans (EM) rash is seen 60-80% of the time in what disease? Explain
Lyme disease
-20% of folks with Lyme won’t have this “classic rash”
Only 25% of patients with early localized disease recall a tick bite
How may Lyme manifest during the Early disseminated phase?
1) Early disseminated rash
2) Neurologic findings
-Lymphocytic meningitis, radiculopathies, cranial nerve palsies (CN7 especially). Bell’s Palsy
3) Carditis: Anything from 1st degree to 3rd degree block
List and describe a specific type of early disseminated lyme
Lyme Carditis:
-Occurs in early disseminated phase, about 1-28 weeks after infection
-About 1% of Lyme cases get Lyme Carditis
-Fairly wide range of disease, from mild to deadly
How may Lyme manifest during the “late lyme” phase?
Occurs months to years after infection:
1) Arthritis: usually 1 joint, though can be a few
-Usually the knee
-Eventually occurs in 60% of untreated patients
-Most common complication of late lyme disease
-Monoarthritis of the knee is most common
2) Chronic neurologic effects
3) Peripheral neuropathy or encephalitis
Early Localized Lyme disease:
1) How do you Dx it?
2) When will tests be positive?
1) Mostly a clinical diagnosis; Erythema migrans and exposure to an endemic area, with or without a tick exposure, is enough to make the diagnosis
2) Lyme serologies are likely to be negative this early
-About 25% of Lyme serologies will be positive at this phase
-Repeat convalescent serologies in a few weeks should be positive
How do you test for Lyme?
Validated Lyme serology testing follows a two-tiered approach:
1) ELISA first, more sensitive
-If ELISA negative, no further testing needed
2) Western Blot second, more specific.
1) What is the preferred Tx for Lyme disease?
2) What other Tx is there?
3) What is the Tx for if it’s severe (meningitis)?
1) Doxycycline 100mg BID x 10-21 days
Avoid in pregnancy and under 9
2) Amoxicillin 500mg TID x 14-21 days
3) Ceftriaxone 2g IV QD for 14-28 days
-If cardiac block might need to add a temporary pacemaker
Syphilis:
1) Etiology
2) Epidemiology
3) What type of bacteria is it?
1) Transmission by mucous membranes, non-intact skin, transfusions and vertical transmission.
2) Resurgence since HIV epidemic, 207,255 cases in 2022 in US.
3) Treponema Pallidum (Spirochetes, atypical)
Describe the signs/ Sx of primary syphilis
Solitary Chancre (95%): a painless, well demarcated ulcer
Describe the signs/ Sx of Secondary Syphilis (3)
1) Nickel and dime-size pale, pink to red discrete round papular lesions
-Distributed over trunk, flexors, palms and soles
2) Condyloma Lata (painless wart like lesions)
3) Syphilitic Alopecia (random patches)
1) How long is latent symphilis? What is it?
2) When is it infectious?
3) What may it progress to and how often?
1) Asymptomatic period (3-20 years)
2) Infectious only in pregnancy and blood transfusions
3) 1/3 will progress to tertiary syphilis
List 3 types of Tertiary Syphilis
1) Syphilitic Gumma
2) Cardiovascular Syphilis
3) Neurosyphilis
Syphilitic Gumma signs/ Sx
Granulomas and Psoriassi-like Plaques: Diffusly distributed solf ulcerative lesions with firm necrotic center
Name one manifestation of cardiovasc. syphilis
Thoracic aneurysm
Name 3 manifestations of neurosyphilis
1) Tabes Dorsalis
2) Meningitis
3) Dementia
slide 62
1) What is Tabes Dorsalis and what is it a complication of? When can it occur?
2) What can it cause?
1) Demyelination of posterior column dorsal roots and dorsal root ganglia; 20-30 years after initial infection
2) Ataxia of the legs
Lancinating pain and Paresthesias
Urinary overflow incontinence
Absent knee and ankle deep tendon reflexes
Proprioception loss
Abnormal Romberg test and ataxia
Progressive degeneration of spinal cord
Charcot’s Joints and….
Argyll-Robertson Pupil
1) What is Argyll-Robertson Pupil?
2) What is it a potential complication of?
1) “Prostitute pupil”; pupils don’t constrict when exposed to bright light, but do constrict on a near object.
2) Syphilis
1) How do you Dx syphilis if there’s a lesion?
2) What are two tests for syphilis?
3) Is syphilis reportable?
1) Darkfield examination
2) Nontreponemal tests (VDRL) and a treponemal test (T. Pallidum passive particle agglutination)
3) Yes (including congenital cases)
1) How is syphilis treated?
2) What if neurosyphilis?
3) What if there’s an allergy?
1) Benzathine Penicillin G: 2.4mu IM for one dose
2) If Neurosyphilis: high dose and for 14 days
3) If allergy: desensitize (bc there’s NO other Tx)
Chlamydia:
1) What type of bacteria is it?
2) Etiology?
3) Epidemiology?
1) Atypical
2) Chlamydia trachomatis
3) Most common bacteria STI in the United States. 2.8 million cases/year
Describe chlamydia trachomatis signs/ Sx
1) Usually asymptomatic
2) Dysuira
3) Post-coital bleeding
4) Mucopurulent discharge
5) Pelvic pain
6) Epididymitis
After 3-30 days, what can chlamydia progress to? Describe its two stages
Lymphogranuloma venereum (LGV):
1) Primary genital lesion: Small, painless papule, pustule, nodule, shallow erosion
-Secondary lesions
2) 2-6 weeks later: Inguinal syndrome
-Central necrosis
How is chlamydia trachomatis diagnosed?
Chlamydia PCR via:
1) “Dirty Urine” or swab from endocervical, urethral, vaginal, pharyngeal or rectal
-Also test for other STDs
How do you Tx chlamydia trachomatis?
1) No intercourse for 7 days after treatment
-Doxycyline PO 100mg BID x 7days
-Azithromycin PO 1g x1 (pregnant)
2) COTREAT for gonorrhea!
List 5 complications of Chlamydia trachomatis
1) Pelvic inflammatory disease (PID)
2) Chlamydia Conjunctivitis
3) Neonatal Chlamydia Pneumonia
4) Reactive Arthritis “Reiter’s Syndrome”
5) Fitz-Hugh-Curtis Syndrome
Arthritis, conjunctivitis, urethritis are all Sx of what? What can this be caused by?
1) Reactive Arthritis (Reiter’s syndrome)
2) Chlamydia
What is a type of Chlamydia conjunctivitis?
Ophthalmia Neonatorum (in babies eyes, can cause blindness)
Chlamydia trachomatis:
1) What is Fitz-Hugh-Curtis Syndrome? (a potential complication)
2) What are the symptoms?
1) Perihepatitis Syndrome
2) -Abdominal pain, vaginal discharge, fevers, dyspareunia, dysuria, prolonged menses or post-coital bleeding
AND
-Pleuritic right upper quadrant pain (bc of liver capsule inflammation)
Chlamydia trachomatis:
1) What do more severe infections need?
2) Is it reportable?
1) Admission with IV antibiotics
2) Yes
Gonorrhea:
1) Etiology & type of bacteria
2) Epidemiology
3) What other STI is it usually seen with?
1) Neisseria gonorrhoeae. Gram negative diplococci
2) 500-700,000 cases per year. Highly contagious. 50% transmission rate.
(don’t memorize numbers)
Neisseria gonorrhoeae:
1) Signs and Sx
2) How do you Dx?
3) Tx?
1) Most are asymptomatic; similar symptoms as chlamydia
-Proctitis: Usually diarrhea, painful defecation, discharge, anal itching
2) Nucleic Acid Amplification (preferred), Gram stain, culture (chocolate agar)
3) Co-treat with Chlamydia. Ceftriaxone 500mg IM x1. Resistance increasing.
Disseminated Gonorrhea:
1) Sx
2) Tx
3) Is it reportable
1) Dermatitis, Tenosynovitis, endocarditis, meningitis
-Gonococcal Arthritis: Most common joint involved is knee; if tapped, will show bacteria
2) IV course for 7 days (14 if meningitis)
Ceftriaxone 50mg/kg IV every 24 hours
3) Yes
A 6 y/o M is seen in your clinic with a 3 month history of intermittent fevers, fatigue, migratory joint pain and weight loss. 3 months ago mom reports that he had a sore throat that he stayed home from school for a week for. You notice a new systolic murmur with a thrill at the mitral area with radiation to the axilla. Left knee is mildly swollen and warm. Painless nodules are noted over his ankles and elbows.
What is your suspected diagnosis?
Acute Rheumatic fever
Acute Rheumatic Fever:
1) Etiology
2) Epidemiology
1) Streptococcus pyogenes (Gram +, aerotolerant)
-Follows untreated Streptococcal pharyngitis infection; an autoimmune reaction
2) 20 million cases a year; 3% of untreated strep pharyngitis
-Age range: typically 6-12 years
(don’t need to know numbers)
Acute Rheumatic Fever:
1) Pathophysiology
2) Clinical features
1) Pt gets beta hemolytic strep, antibodies go to attack it, but accidentally attack the mitral heart valve or joints instead
2) Carditis, arthritis, Sydenham chorea, subcutaneous nodules, erythema marginatum
RHD: permanent heart valve damage subsequent to ARF
Acute Rheumatic Fever:
1) DDx
2) How do you Dx?
1) Poststreptococcal reactive arthritis (PSRA), rheumatoid nodules, other types of chorea, erythema annulare
2) Jones criteria (2 major OR 1 major + 2 minor)
What are the major criteria for diagnosing acute rheumatic fever? (mnemonic)
J: Joints (migratory arthritis)
O: “Shape of the Heart” (Carditis)
N: Nodules (subcutaneous)
E: Erythema Marginartum
S: Sydenham’s Chorea
Acute rheumatic fever:
1) What is the most common Sx?
2) When does this Sx significantly improve?
3) Where is this Sx located?
4) How long does it occur? Who is it worse in?
1) Migratory Polyarthritis (up to 80%)
2) With aspirin or NSAIDs
3) Large joints starting with legs and moving to arms: knees and ankles, wrists and elbows, rarely spine.
4) Transient (3 days per joint, 3 weeks total); more severe in teens and young adults.
Acute Rheumatic Fever complications/ Sxs:
1) What is present in 50-60% of cases?
2) Describe this complication. When does it occur, and what can this complication then cause?
1) Carditis
2) Endocarditis (mitral valve most commonly affected); 10-20 years after carditis in 50% of patients
Mitral Stenosis can develop
Acute Rheumatic Fever complications/ Sxs:
1) What are subcutaneous nodules?
2) Where are they located?
1) Small, firm painless Nodules on extensor surfaces
2) Dorsal wrist, elbow and anterior knee most common
Acute Rheumatic Fever complications/ Sxs:
1) What are Erythema Marginatum?
2) Where is it located? How long does it last?
1) Non-pruritic pink to slightly red rings
2) Involves trunk and proximal extremities; spares the face
-Transiently appears, rapidly advances and disappears over months
Acute Rheumatic Fever complications/ Sxs:
What 4 things characterize Sydenham’s Chorea? Describe each
1) Abrupt onset of “choreoform” movements: Purposeless, nonrhythmic, involuntary; only present while awake
2) Motor Weakness
3) Emotional disturbance: Outbursts, Psychosis
4) Late finding: 8 months after initial infection; resolves over 2-3 years
Acute Rheumatic Fever: What are the minor criteria? (5)
1) Arthralgias
2) Fever
3) Elevated Sedimentation Rate (ESR)
4) Elevated C-Reactive Protein
5) Prolonged PR interval on Electrocardiogram
Acute rheumatic fever:
1) How is it managed?
2) How is the polyarthritis treated?
3) How is the carditis treated?
4) What bacteria should you treat for? How?
1) Admit for definitive dx and evaluation
2) Aspirin/NSAIDS
3) Corticosteroids
4) Penicillin VK 500mg BID x 10 days
1) What is MRSA?
2) What are risk factors for it?
3) What are the characteristics?
4) How is it Dx’d?
1) Methicillin Resistant Staphylococcus Aureus
2) Athletes, military recruits, Prison Inmates, IV drug users, DM, Hemodialysis, Prior history
3) Skin and soft tissue infections, delayed wound healing
4) Rapid MRSA assay
MRSA: Describe how you would manage it in both outpatient and inpatient settings
1) Outpatient: Avoid beta-lactam antibiotics. Avoid Fluoroquinolones due to resistance:
a) Trimethoprim-Sulfamethoxazole DS x 7 days
Or
b) Doxycyline 100mg x 7 days
Or
c) Clindamycin 300mg X 7-10 days
2) Inpatient: Vancomycin IV 12 hrs
Botulism:
1) Etiology (include sources)
2) Epidemiology
1) Botulinum toxin (Clostridium botulinum: anaerobic, spore-forming bacillus in soil/dust)
-Honey, food-borne, wounds (from soil), home-canned vegetables, smoked meats, vacuum-packed fish
2) Extremely potent (high-priority agent by CDC: bioterrorism); FB highest in Alaska natives (aged fish)
-Outbreaks: home-canned foods (fruits, veggies, fish)
Prison brew
Botulism in infants:
1) What is the most common age of infection?
2) What are the presenting S/Sx?
1) 1 week-12 months (median 3-4 months)
2) Constipation, weakness, feeding difficulties, descending (or global) hypotonia, drooling, anorexia, irritability, weak cry (ie, floppy baby syndrome)
Botulism:
1) Classic presentation
2) Key features
1) Acute onset (12-36 hrs of ingestion) of bilateral cranial neuropathies a/w symmetric descending weakness.
2) -Absence of fever
-Symmetric neurologic deficits (CN palsies like EOM impairment)
-Normal sensorium & mental status
-Normal or slow heart rate & normal BP
-Absence of sensory deficits (exception of blurred vision)
Botulism:
1) How is it Dxd?
2) How is it prevented?
3) Is it reportable?
1) Clinical; toxin in serum, stool, vomitus, & foods (state health dept. or CDC)
2) Careful home-canning
3) Yes
Botulism: Describe how you manage it (6 steps)
1) Admit & monitor for signs of respiratory failure, ICU for paralysis (~1-3 months)
2) Antitoxin within 24 hours (CDC)(skin testing)
-Intubation & mechanical ventilation for respiratory failure
3) Attempted removal of unabsorbed toxin from GI tract (no antibiotics)
4) Wounds: extensive debridement, tetanus booster,
5) Penicillin G, ID consult if complicated
6) Locate & observe others
Diphtheria:
1) Etiology
2) Epidemiology
3) S/Sx
1) Corynebacterium diphtheriae
2) Rare in US due to immunization; Ongoing epidemic in the former USSR
3) Sore throat, dysphagia, weakness, malaise, low grade fever, tachycardia, pharyngeal erythema, grey-white tenacious excaudate or “membrane” adheres to posterior pharynx. “Bull neck” appearance
Diphtheria:
1) How is it Dx’d?
2) Treated?
3) Prevented?
1) CBC. Throat culture and nasal culture: Positive for Corynebacterium organisms
2) Droplet precautions. Diphtheria antitoxin. Erythromycin x 14 days or penicillin G IM.
3) Vaccinations!
Is diphtheria reportable?
Yes
Bartonella
1) What type of bacteria is it?
2) What are 2 associated conditions?
1) Gram Negative Rod, obligate anaerobe. Several species
2) Cat Scratch Disease and Trench Fever
Bartonella: Cat Scratch Disease
1) What bacteria?
2) What % of cats are infected?
3) Describe its duration and Tx
1) Bartonella Henselae
>50% of cats are infected (thanks to fleas) and transmit the infection via biting or clawing
Self-Limited of immunocompetent host. May use antibiotics for moderate cases
Bartonella: Cat Scratch Disease (Bartonella Henselae)
1) S/Sx?
2) Tests?
3) Tx?
1) Myalgias, arthralgias, malaise, anorexia, low-grade fever, Dermatitis at cat scratch/bite then painful ipsilateral lymphadenopathy, encephalopathy, neuroretinitis
2) Serology, IgG titers
3) Azithromycin x 5 days or Bactrim (trimethoprim-sulfamethoxazole) x 10 days
Bartonella: Trench Fever (Bartonella Quintana)
1) Who does it affect most commonly?
2) S/Sx?
3) Tx?
1) Affected millions in WWI, spread by Body Lice, seen in homeless patients
2) Relapsing fever, headaches, back and leg pain, splenomegaly and sometimes rash. Can progress to endocarditis
3) Usually more than one combo of tetracyclines, aminoglycosides and macrolides
Ie: Doxycyline orally for 4 weeks plus gentamicin IV for two weeks
Tetanus:
1) Etiology (/ what type of bacteria)
2) Epidemiology
1) Clostridium tetani. Gram-positive anaerobic rod
-Neurotoxin enters via puncture wounds. Produces tetanospasmin. Blocks the release of inhibitory neurotransmitters
2) Rare due to vaccine (33 U.S. cases in 2017)
How is tetanus prevented? (2 ways, describe each)
1) Active immunization: Td & booster q10yr (or time of major injury); Tdap with each pregnancy (27-36 wks)
2) Passive immunization: TIG 250 units IM & concurrent active immunization
1) Define diarrheal illness
2) Define acute diarrheal illness
3) Define persistent diarrheal illness
4) Define chronic diarrheal illness
1) >3 loose or watery stools in 24 hours.
2 Occurs for less than 14 days, usually infectious
3) 15-30 days, usually parasitic
4) Greater than 30 and is associated with chronic disease (IBS, IBD, Celiac
Typhoid Fever:
1) Etiology (/bacteria type)
2) Epidemiology
-what % become chronic carriers?
1) Salmonella typhi. Gram Negative bacteria
2) 11-20 million cases annually. 128,00-161,000 cases of death per year
-1-5% become chronic carriers
Typhoid fever:
1) Most commonly seen in who? What’s the incubation period and what route of transmission?
2) S/Sx?
1) Children and young adults. Incubation period 5-21 days. Fecal-oral route
2) Pea-Soup diarrhea. Intractable fever, malaise, anorexia. Fever with relative bradycardia. “Rose spots”: faint pink colored macular rash that spreads from trunk to extremities. Peyer’s Patches. Delirium
Typhoid fever:
1) How to Dx?
2) Tx? (what’s your first line option and what abt if severe?)
1) Diagnosis: Stool culture, Blood culture
2) Oral rehydration and electrolyte replacement is 1st line management.
-If Severe:
Ciprofloxacin x 7-10 days
or
Azithromycin PO and Ceftriaxone IV x7-10 days
Nontyphoidal Salmonella:
1) Etiology (hint: 3 bacteria)
2) Epidemiology (including sources)
1) Salmonella bongori, Salmonella enterica, Salmonella typhimurium
2) 1 million cases per year in the US
Incubation period: 8-72 Hours
-Undercooked or raw poultry, eggs, milk, fresh produce
Contact with reptiles (esp turtles)
Nontyphoidal Salmonella:
1) Clinical manifestation
2) How to Dx? (hint: only one way)
3) Tx? What abt if severe?
1) Inflammatory diarrhea (+/- blood) with vomiting
2) Stool culture
3) Oral rehydration and electrolyte replacement
Severe: Fluroquinolones
Salmonellosis bacteremia:
1) Risk factors
2) Clinical features
3) Management
1) Older age, immunosuppression, chronic liver disease, malaria
2) Prolonged or recurrent fevers, bacteremia, local infections (bone, joints, pleura, pericardium, lungs, urinary tract, or other sites), non-typhoidal isolates most common
3) Same as for enteric fever (fluoroquinolone) including abscess drainage & debridement; HIV may require lifelong suppressive therapy (relapse common)
slide 127
Who is Kiyoshi Shiga?
Japanese Physician
1897 “Sekiri” outbreak
>91,000 Japanese people
Mortality rate >20%
Shigellosis
1) Etiology
2) Epidemiology (hint: 2 sources)
3) Is it reportable?
1) Shigella dysenteriae. S. flexneri, S. boydii, S. sonnei. Shiga toxin: neurotoxic, cytotoxic and enterotoxic
2) 188 M cases worldwide, mainly affects children in U.S
-Fecal-oral route; raw vegetables
3) Yes
Shigellosis: What are the clinical features?
1) Abrupt onset of explosive, watery diarrhea that becomes progressively bloody
2) Tenesmus
3) Abdominal pain
4) +/- systemic symptoms (fever, anorexia, malaise
Shigellosis:
1) How do you diagnose it?
2) Tx?
1) -Stool culture -> Fecal WBC/RBC
-CBC -> WBC>50,000
-Sigmoidoscopy (Punctate areas of ulceration)
2) Oral rehydration and electrolyte replacement
If Severe: Fluroquinolones
Campylobacter Enteritis:
1) Etiology (species)
2) What is it the most common cause of?
3) Who does it typically affect? What’s the incubation period?
4) What are the sources?
1) Campylobacter jejuni
2) Bacterial enteritis in the US
3) Typically affects children and young adults
4) 3 days
1) Raw or undercooked poultry; raw milk; puppies
Campylobacter Enteritis:
1) What are the clinical manifestations?
2) How is it Dx’d? (2 ways)
3) How is it Tx’d? What about if severe?
4) Is it reportable?
1) Inflammatory diarrhea with cramping periumbilical pain
-Bloody Diarrhea
2) Stool culture (Gram negative, may appear S or comma shaped) OR PCR
3) Fluid and electrolyte replacement
If severe: Azithromycin
4) Yes
You are seeing a 13 y/o female while on a medical mission trip to Syria. She has been having multiple episodes of watery diarrhea that they describe looks like rice water. She appears very dehydrated.
What does she have?
Cholera
Cholera:
1) What is the etiology?
2) What is the epidemiology?
3) What are the sources?
1) Vibrio cholerae. Produces exotoxin
2) 3 million cases & 100K deaths annually worldwide, most cases in Africa & Asia
3) Contaminated food and water, Outbreaks with poor sanitation and overcrowding
List the following for cholera:
1) Clinical Manifestations
2) Diagnosis
3) Treatment (include if severe)
1) Copious watery diarrhea. “Rice water stools”
2) Stool culture: Gram negative, comma shaped rods, PCR
3) Rehydration (lactated ringers) and electrolyte replacement.
-If severe: Tetracyclines
1) How is cholera prevented?
2) Is cholera reportable?
1) Bottled water in endemic areas, washing hands with soap.
2) Yes
Clostridiodes Difficile (C. Diff):
1) When was it first recognized?
2) What’s its epidemiology?
3) What’s its mortality?
4) What’s its pathophysiology?
1) In 1978 as “antibiotic-associated diarrhea
2) US Adults: 14 cases per 1000 persons
-Most common nosocomial infection in the US
3) 6%
4) Obligate, anaerobic, gram positive, spore-forming bacillus
-Toxins produced
What are the risk factors for C. Diff?
1) Older patients >70 years old, immunocompromised, steroid use, cystic fibrosis, obesity, female, CKD, IBD, Cirrhosis, Acid suppression (omeprazole highest risk)
-RECENT ABX USE: Broad-spectrum highest risk
-Clindamycin, fluoroquinolones, Cephalosporins
What are the symptoms of C. diff?
1) (Can be asymptomatic carriers), 20-30 stools a day, mucous and blood often present, pain,
2) Can progress to Toxic Megacolon
slide 140 labs for C. diff
Contraindications: Formed stool, recent laxative use in prior 48 hours, testing for cure in asymptomatic patients, children <12 months of age
C. Diff PCR
CBC/CMP/lactic acid
Markers of Severe infection
Hypoalbuminemia, lactic acidosis, serum creatinine >1.5. WBC >15,000.
When is imaging appropriate for C. Diff? What would you expect to see?
1) If severe abdominal pain or h/o ulcerative colitis/crohns disease
2) CT Abdomen: target sign or double halo sign.
How long should C. Diff be treated for? With what? (2 things)
1) Fidaxomicin (Dificid): Macrolid (new), very expensive ($3,000)
2) Vancomycin: HAS to be oral. Not IV; needs serum level monitoring esp in Kidney disease
How do you prevent C. Diff spore spread?
Resistant to Alcohol/ Antiseptics:
1) Chlorhexidine and Soap are effective
2) Contact Isolation of the patient
