Unit 5 Flashcards
HIV patients with the following should be offered primary pneumocystis prophylaxis
● CD4 count < 200 cells/mcL
● CD4 lymphocyte percentage < 14%
● Weight loss
● Oral candidiasis
Patients with a history of Pneumocystis should receive secondary prophylaxis until …
● viral load is undetectable AND
● They have maintained a CD4 count > of 200 cells/mcL while receiving ART for > 3 mo.
Pneumocystis prophylaxis meds
-Trimethoprim-sulfamethoxazole 1 double-strength tablet 3 times a week -up to- 1 tab daily
● After treatment of an infection with Pneumocystis jiroveci prophylaxis should be maintained
until CD4 count is > 200 for 3 months.
● If patient intolerant to Bactrim treat with Dapsone or Atovaquone.
Dapsone 50-100 mg daily or 100 mg 2to3 times per week (if Bactrim not tolerated)
Atovaquone 1500 mg daily with a meal
Pentamidine (IV or aerosolized)
Preexposure ART Prophylaxis (PrEP) Regimen
-Used for those at high risk for contracting HIV
-● emtricitabine/TDF (Truvada) - reduces the risk of sexual transmission of HIV among uninfected
individuals at high risk for infection, and in men who have sex with men.
● Tenofovir - reduces HIV infections among injection drug users
Post-exposure prophylaxis (PEP): Goal, when to give
-Goal of therapy is to reduce/prevent local viral replication prior to dissemination to abort infection
● Treatment should be started as soon as possible, success declines with increased length of time from
HIV exposure. Treatment not recommended to be offered > 72 hours after exposure
● Treatment should be offered with prevention counseling; focusing on how to prevent future exposures
Post-exposure prophylaxis (PEP): Regimen
Preferred regimen: tenofovir with emtricitabine (Truvada) with raltegravir
Who should get ART therapy
All HIV-infected patients should be considered for ART regardless of CD4 count. The benefit of
ART is well established in preventing progression to AIDS and associated comorbidities.
What is symptomatic HIV
Symptomatic HIV: the presence of any of the following: thrush, vaginal candidiasis, herpes zoster,
peripheral neuropathy, bacillary angiomatosis, cervical dysplasia in situ, constitutional symptoms
such as fever or diarrhea for more than 1 month, ITP, PID or listeriosis.
Goals of ART therapy
-CD4 cell counts and HIV viral load should be repeated 1-2 months after initiation or change
of ART regimen and every 3-4 months thereafter in clinically stable patients.
■ With integrase regimens 80% of patients will have undetectable HIV viral load at 1
month.
■ All patients should have undetectable HIV viral load by 3 months
■ If not, the usual problem is compliance.
Opportunistic Infections of HIV
●Pneumocystis jiroveci pneumonia*** most common
● Toxoplasma gondii encephalitis (Toxoplasmosis)
● Mycobacterium tuberculosis disease (TB)
● Disseminated MAC disease
● Non-Hodgkin lymphoma
● Cryptococcal meningitis
● Cytomegalovirus retinitis (sight threatening)
● Esophageal candidiasis
● Vaginal candidiasis
● Herpes simplex infection
● Herpes zoster
● Kaposi sarcoma
● Aspergillosis
What causes increased risk of AIDS-related
complications
Drug holidays or structured treatment interruptions have be shown to increase risk of AIDS-related
complications - the interruptions are NOT recommended
Only stop ART for toxicity
when a diagnosis of AIDS
Look up answer to this
What test is necessary for osteomyelitis diagnosis
bone biopsy
most common pathogen identified in causing Community acquired pneumonia
Strep pneumoniae
Most common cause of pneumonia is young adults and adolescents
Mycoplasma pneumoniae
Pneumocystis, candida, herpes.
know treatments
Influenza vaccine is given in which months
September and October
Most common fungal infection for HIV patients
Candida
look at pics
for herpes zoster and skin cancer
What if patient is not at goal after months of ART therapy
-ASK ABOUT MED COMPLIANCE
-Resistance testing is recommended for patient receiving ART and have suboptimal viral
suppression.
● Resistance testing is complex, many clinicians require expert interpretation of the results
● Resistance testing should NOT replace a carefully documented history of what medications the
patient has taken in the past and for how long.
● After testing and with knowledge of patient history a second-line ART regimen is constructed with 3
medications (from 2 different classes) to which the virus is not resistant.
● With the availability of new classes and new generations medications, a combination of ART can
successfully treat virtually all patients - no matter how much resistance is present.
Normal Spinal fluid analysis: cells
0–5 lymphocytes
Normal Spinal fluid analysis: glucose
45–85
Normal Spinal fluid analysis: protein
15–45
Normal Spinal fluid analysis: opening pressure
70–180 mm H 2 O
Purulent meningitis Spinal fluid analysis (numbers)
200–20,000 polymorphonuclear neutrophils
Low (< 45) glucose
High (> 50) protein
opening pressure Markedly elevated (>180)
Clinical manifestations of meningitis
fever (high > 38C), nuchal rigidity, change in mental status, Headache, N/V, photophobia, seizures coma, lethargy, Rash: petechial, purpura fulminans, myalgia, unilateral CN abnormality, Papilledema, dilated on responsive pupils, posturing decorticate/decerebrate,
Kernig & Brudzinkski- seen in later
Meningitis workup
-Stat labs, history/phyiscal
-CT BEFORE LP if pt presents with SAH, new focal neuro deficit, papilledema, seizures within one week,
AMS, CNS (tumor, stroke), age > 60, immunodeficient
-Lumbar puncture
-Empiric therapy
Empiric therapy for meningitis
- Dexamethasone 10 mg iv q 6hr x 4 days
- Selected third-generation cephalosporins (ie, cefotaxime 2gm iv q 4-6 hr and ceftriaxone
2g iv q 12) are the beta-lactams of choice in the empiric treatment of meningitis, vancomycin 15-20 mg/kg iv q 8-12 hrs should be added to cefotaxime or ceftriaxone as empiric treatment until culture and susceptibility results are available due to penicillin-resistant pneumococci - Adult > 50 add ampicillin 2 gm iv q 4 hr to cover listeria
Bacterial Endocarditis Essentials of Dx
i. Fever.
ii. Pre-existing organic heart lesion.
iii. Evidence of vegetation on echocardiography.
iv. New or changing heart murmur.
v. Evidence of systemic emboli
What is bacterial endocarditis, what is the virulent type?
-Bacterial infxn of the valvular or endocardial surface of the heart.
-Clinical presentation depends on the infecting organism and the valve/valves
infected.
-S. aureus : Virulent organism
How does a patient with endocarditis caused by more virulent organisms present
- Acute febrile illness.
- Complicated by early embolization, acute valvular regurgitation, and
myocardial abscess formation.
Less virulent strains of endocarditis
Viridian strains of streptococci, enterococci, other bacteria, yeasts, and fungi tend
to cause a more subacute presentation
Valvular Dz with endocarditis, what is it, what does it do
- Present 50% of the times.
- Alters blood flow and produces jet effects that disrupts the endothelial surface, providing a nidus (Nest. Site of origin for disease or bacteria. A place where bacteria multiplies) for attachment and infection of microorganisms to enter the bloodstream.
Predisposing Valvular Abnormalities
- Rheumatic involvement of any valve, bicuspid aortic valves, calcific or
sclerotic aortic valves, hypertrophic subaortic stenosis, mitral valve
prolapse. - Rheumatic Dz is no longer the major predisposing factor in developing
countries. - Regurgitation lesions are more susceptible than stenotic ones.
The initiating event in Native Valve Endocarditis
- colonization of the valve by bacteria that gain access to the bloodstream.
1. Transient bacteremia is common during dental, upper respiratory, urologic, and lower GI diagnostic and surgical procedures.
2. Less common in upper GI and gynecologic procedures.
Intravascular Devices role in bacterial endocarditis
-increasingly implicated as a portal of access of
microorganisms into the bloodstream.
-A large proportion of cases of S. aureus endocarditis are attributed to health-care associated bacteremia.
Native Valve Endocarditis leading causative organism
- S. aureus
- > 60% of injection drug user cases.
- 80-90% of cases: Tricuspid Valve is infected
Prosthetic Valve Endocarditis leading causative organism, early and late
- Early infxns: Occurring w/in 2 months after valve implantation; Commonly caused by staphylococci: Coagulase-Positive Organisms, Coagulase-Negative Organisms
- Late Prosthetic Valve Endocarditis: Streptococci commonly identified
signs and symptoms of bacterial endocarditis
Fever, Duration: Typically a few days to weeks, Changing regurgitant murmur (Significantly diagnostic), Cough, Dyspnea, Arthralgias/Arthritis, Diarrhea, Abdominal, Back, Flank Pain, Characteristic Peripheral Lesions, Strokes and major embolic events are present in about 25% of patients (Tend to occur before or w/in the first week of antimicrobial tx), Hematuria and Proteinuria may result from emboli or immunologically mediated glomerulonephritis causes Kidney Dysfxn.
Peripheral lesions associated with bacterial endocarditis
- Petechiae: On the palate or conjunctiva or beneath the fingernails.
- Subungual (Splinter) Hemorrhages.
- Osler Nodes: Painful, Violaceous raised lesions of the Fingers, Toes, or Feet).
- Janeway Lesions: Painful erythematous lesions of the palms or soles.
- Roth Spots: Exudative lesion in the retina. Occur in about 25% of patients.
Antibiotic Management of Bacterial Endocarditis
i. Empiric regimens while culture results are pending. Should include agents active against staphylococci, streptococci, etc enterococci.
ii. Vancomycin 1gm q12hrs IV + Ceftriaxone 2gm q24hrs provides appropriate
coverage pending definitive diagnosis.
iii. Infectious Dz Consultation: Strongly preferred/recommended.
Most common agent of CAP in AIDS/immunocompromised pts
Pneumocystitis jirovecii
Antibiotic therapy for a patient diagnosed with pneumonia caused by S. pneumoniae if no prior use of abx
- azithromycin or clarithromycin + macrolide
Antibiotic therapy for a patient diagnosed with pneumonia caused by S. pneumoniae if at risk for drug resistance, >65 years old, comorbidities, immunosuppresion
-A fluoroquinolone (levo, moxi, or gemi floxicin)
OR you can treat with:
-Combo of macrolide PLUS beta-lactam (amox or amox/clav)
- Give for a minimum of 5 days and recommended until patient is afebrile for 48-72hours
Most common sites for nosocomial infections
- Urinary tract infections caused by foley catheters are the most common
- Others are blood stream infections from central lines, surgical wounds, abscesses
- Pneumonia in intubated patients
- Those most at risk are those critically ill, hospitalized for long durations and those who have received multiple abx courses
Malarial prophylaxis when traveling to country WITHOUT drug resistant parasites
-Bug repellant, insecticides, and bed nets are the
most effective prevention
- Chemoprophylaxis is recommended for all travelers from non-endemic to endemic areas
- Chloroquine
Malarial prophylaxis when traveling to country WITH drug resistant parasites
-Bug repellant, insecticides, and bed nets are the
most effective prevention
- Mefloquine or Malarone or doxycycline are all used in resistant areas
Management of VRE
- If rectal or stool then no tx recommended
- If resistant to Vanco, often resistant to many other abx (80% will be resistant to ampicillin also)
- Potential tx agents are: Linezolid or Daptomycin
- Also mentions Quinupristin- dalfopristin (synercid) but this is only effective on rare strains and it causes myalgias, arthralgias, and venous irritation so rarely used
Pyelonephritis causative agents in hospital
E. coli., Klebsiella, enterobacter or
pseudomonas
Pyelonephritis causative agents outpatient
E. coli, K. pneumoniae, Proteus species, or s.
Saprophyticus
Antibiotic management of pyelonephritis in hospital
These will be tx w/ceftriaxone 1gm q24h OR cipro 400mg q12h OR levofloxacin 500mg q24 *all IV
If empiric tx is started while waiting on abx then should be ampicillin & gent OR cipro, levofloxacin, or bactrim**
Antibiotic management of pyelonephritis outpatient
These are tx with fluoroquinolones for 7 days (*preferred) or Bactrim for 7-14 days
Workup to Dx of osteomyelitis
ESR (high), CRP, blood cx, bone cx, bone biopsy (required for diagnosis), PCR analysis of specimens, xray, MRI best, SPECT
signs and symptoms of osteomyelitis
fever/chills, painful/tender bone (sometimes neuropathic pain if pt has vascular insufficiency)
Inpatient and outpatient treatment for osteomyelitis
- In hospitalized patients tx is IV nafcillin 2gm q4h or cefazolin 2gm q8h for MSSA
- If MRSA susp. Tx w/ vanc or dapto instead
- In outpatient 6-8 weeks of fluoroquinolones, can add rifampin if s. Aureus is the cause
Challenges to treating osteomyelitis
- Chronic osteomyelitis has high tx failure rates due to poor vascular supply, nondistensible bone tissue, and limited penetration of bone tissue.
- Inadequate treatment of bone infections results in chronicity of infection, and this possibility is increased by delaying diagnosis and treatment. Extension to adjacent bone or joints may complicate acute osteomyelitis
- Hyperbaric sometimes needed chronic, or ID specialist if multiple tx failures
- Most patients will require I & D and LONG abx tx course
Causes and Antibiotic management of intra-abdominal infections
● Intra-Abdominal sepsis (postoperative, peritonitis, cholecystitis ect): likely caused by
gram neg, anaerobic, streptococci, or clostridia.
● Tx: Piperacillin-Tazobactam 4.5Gm IV q6h OR ertapenem 1 Gm IV daily
Characteristics of fever of unknown origin
- illness at least 3 weeks
- Fever over 38.3C on several occasions,
- No Dx after 3 hospital visits or 3 days inpatient
Causes of fever of unknown origin
Infection (most common), neoplasm, autoimmune disorders, miscellaneous, undiagnosed
Management of fever of unknown origin
-Thorough history, Labs + blood cultures, CXR, CT abd/pelvis, LP, HIV testing, any other testing such as biopsies, MRIs, etc. don’t just randomly give Abx or
steroids because it may delay Dx/Tx.
● Refer if immunocompromised, rapidly declining, weight loss, recent organ transplant
Causes of a fever in a post-op patient on day one
medications given perioperatively, surgical trauma, infections that were present before surgery, necrotizing fasciitis (due to group A strep), malignant hyperthermia (from anesthesia), rapidly developing chemical pneumonitis (from aspiration of stomach contents)
Management of a fever in a post-op patient on day one
Treat the cause
Endemic regions for Histoplasma capsulatum fungus
● Central and eastern US (Ohio River and Mississippi River beds), eastern canada, Mexico, Central and
South America, Africa, and Southeast Asia
● Isolated from soil in river valleys contaminated with bird and bat droppings
Fungal infections that clinically manifests in the central nervous system
● Disseminated coccidioidomycosis can cause fungal meningitis, brain abscess, and granuloma formation.
● *Cryptococcus, Aspergillus and Candida can cause fungal cerebritis.
● *Aspergillus can cause meningeal vasculitis with vessel thrombosis and localized brain infarction
Which causative agent of malaria is most virulent and fatal
Plasmodium falciparum - responsible for nearly all severe disease
Which agent is transmitted via cat feces
Toxoplasmosis - definitive host of T gondii are cats.
Anthrax inoculation: injectional
May have similar skin lesions present with IV drug users, which may progress rapidly with systemic dissemination; NOT associated with eschar formation
Anthrax inoculation: Cutaneous
-Occurs within 2 weeks post-exposure to spores; no latency period; self-limiting in most cases, but hematogenous spread with sepsis or meningitis may occur
- Initial lesion: erythematous papule, often on exposed skin that vesiculates, ulcerates, and undergoes necrosis, progressing to purple-black painless eschar ;
pain indicates secondary staphylococcal or streptococcal infection
- Surrounding area: edematous, vesicular, not purulent
- Signs/Symptoms: regional adenopathy, fever, malaise, headache, N/V
Anthrax inoculation: inhalation
- occurs in 2 stages ~10 days post-exposure, may have latent onset 6 weeks
- Signs/Symptoms:
Initial stage - nonspecific viral symptoms like fever, malaise, headache, dyspnea, cough, congestion (nose, throat, larynx), anterior chest pain (mediastinitis);
Fulminant stage - within hours to few days; sepsis signs,hemorrhagic meningitis (delirium, obtundation, meningeal irritation)
Anthrax inoculation: Gastrointestinal
- occurs within 2-5 days post-ingestion of contaminated meat
- Initial lesion: ulcerative, produces blood-tinged or coffee-ground emesis and blood-tinged or melenic stool; bowel perforation can occur
- Signs/Symptoms: fever, diffuse abdominal pain, rebound abdominal tenderness, vomiting, constipation, diarrhea
- Oropharyngeal form: local lymphadenopathy, cervical edema, dysphagia, upper respiratory tract obstruction
Which inoculation route of Anthrax has highest mortality rate
● Inhalational anthrax is the most lethal form (>90%), higher mortality with meningeal
infection
● Fatality rates: Cutaneous <1%, GI 25-60%, Injectional 34%
Clinical manifestations of Group A beta strep infection
-Gram positive
-STREP PHARYNGITIS, SCARLET FEVER, IMPETIGO,
ERYSIPELAS, ARTHRITIS, PNEUMONIA, EMPYEMA, ENDOCARDITIS, NECROTIZING FASCIITIS, STREPTOCOCCAL TOXIC SHOCK SYNDROME
Empiric management of a patient with abdominal pain and free air on abdominal x-ray
○ Broad spectrum antibiotics to cover both gram negative aerobic and anaerobic bacteria:
● Mild-moderate disease: piperacillin-tazobactam 3.375g IV Q6H or 4.5g IV Q8H OR ticarcillin-clavulanate 3.1g IV Q6H. Alternative agents: ciprofloxacin 400mg IV Q12H or levofloxacin 750mg IV Q24H plus metronidazole 1g IV Q12H
● Severe life-threatening disease: imipenem 500mg IV Q6H or meropenem 1g IV Q8H.
Alternative agents: ampicillin plus metronidazole plus ciprofloxacin
Lab tests used to diagnose herpes simplex virus: Direct Fluorescent antibody slide tests
offer rapid, sensitive diagnosis
Lab tests used to diagnose herpes simplex virus: Viral Culture
helpful; most definitive method for diagnosis; results in 1-2 days; lesions should be sampled during vesicular or early ulcerative stage; cervical samples taken from endocervix
Lab tests used to diagnose herpes simplex virus: Pap Smear
will detect HSV-infected cells in cervical tissue from women without symptoms
Lab tests used to diagnose herpes simplex virus: Serologic Tests
IgG & IgM serum antibodies to HSV occur in 50-90% of adults; presence of IgM or four-fold or greater rise in IgG titers indicate recent infection
Lab tests used to diagnose herpes simplex virus: Western Blot/ELISA
specific HSV-2 serology can determine who is infected and potentially infectious; useful in couples in which only 1 partner reports genital herpes history
Lab tests used to diagnose herpes simplex virus: Tzanck Smear
readily available test shows multinucleated giant cells, but not highly sensitive
Lab tests used to diagnose herpes simplex virus: PCR
Test for herpes
Cause of herpes zoster
varicella-zoster virus
signs and symptoms of herpes zoster
Pain along course of nerve with grouped vesicular lesion; usually unilateral on face or trunk; regional lymphadenopathy; direct fluorescent antibody test will be positive
Prevention of herpes zoster
live Zostavax vaccine
Treatment in immunocompetent host with herpes zoster
oral acyclovir for 7 days, systemic corticosteroids
to shorten s/s, opioids, TCAs, gabapentin
Treatment in immunocompromised host with herpes zoster
acyclovir until lesions have completely healed
(2 weeks); do NOT use corticosteroids
Questions to include in a comprehensive travel history
Geography (rural vs urban, specific country visited), time of year, animal or insect
contact, unprotected sexual intercourse, ingestion of untreated water or raw foods,
historical or pre-travel immunizations, adherence to malaria ppx
Stage 1 of pertussis
Catarrhal: 1-2 week prodrome similar to common cold, followed by increased mucus production and excessive lacrimation with conjunctival infection
Stage 2 of pertussis
Paroxysmal: intense paroxysmal cough ending with gasps and inspiratory whoop. Anoxia, cyanosis, apnea, posttussive gagging/vomiting
Stage 3 of pertussis
Convalescent: lasts over 2 months as cough slowly decreases in severity
Rabies post exposure prophylaxis-when is it indicated
The decision to treat should be based on the circumstances of the bite, including the extent and
location of the wound, the biting animal, the history of prior vaccination, and the local epidemiology of rabies.
● Any contact or suspect contact with a bat, skunk, or racoon is usually deemed sufficient indication to warrant prophylaxis
● Postexposure treatment including both immune globulin and vaccination should be administered as promptly as possible when indicated
-Consultation with state and local health departments is recommended
What is Giardiasis
- A protozoan parasite capable of causing sporadic or epidemic diarrheal illness.
- Giardiasis is an important cause of waterborne and foodborne disease, daycare center outbreaks, and illness in international travelers.
Transmission and incubation of Giardiasis
- Transmission of infectious Giardia cysts to humans may occur via three routes:waterborne, foodborne , or fecal-oral transmission
- incubation period of 7 to 14 days
Signs and symptoms of Giardiasis
Diarrhea, Malaise, Foul-smelling and fatty stools (steatorrhea), Abdominal cramps and bloating, Flatulence, Nausea, Weight loss, Vomiting, Fever, Constipation, Urticaria
Tests for Giardiasis
Test the SHIT : direct immunofluorescent assays (DFA) ,
immunochromatographic assays, and enzyme-linked immunosorbent assays (ELISAs) DFA and ELISA now routinely used are 85-98% sensitive and 90-100% specific, Nucleic acid amplification assays(NAAT ).
● Serum albumin, VIt B12 and stool fat to exclude malabsorption
management of Giardiasis
● Tinidazole 2 gm single dose > 3 yrs old side effect of metallic taste, nausea , headache,
avoid booze
● Metronidazole 250 mg po TID x 5-7 days ( not during pregnancy)
● If pregnant , for 1st trimester: paromomycin ( less systemic) 25-35 mg/kg/ay in 3 doses
for 5-10 days
● typically resolve within five to seven days
Management of Malaria: Uncomplicated P. Falciparum
- Artemisinin-based Combination Therapies (ACTs) First line (artemether/artesunates),
- Quinine: Remains generally effective, but must be taken for extended duration and is poorly tolerated. Usually reserved for severe malaria
Management of Malaria Severe P. Falciparum
○ First-line: Intravenous artesunate, Intravenous quinine if, and only if, IV artesunate is not available.
○ Second line: In countries where IV treatment is not available intrarectal artemether or artesunate is effective
Stage 1 Lyme disease
Early localized stage: (incubation period 3-30 days) expanding erythema migrans
target lesion at the site of the tick bite at least 5 cm in size
Stage 2 Lyme disease
Early disseminated stage ( 3-6 weeks): multi organ system involvement cause by dissemination of the spirochete. Can include CNS sx with aseptic meningitis, arthritis, heart block
Stage 3 Lyme disease
Late stage (months to years): affects central and peripheral nervous system, cardiac, joints
Management of CA-MRSA in a wound: Outpatient
Clindamycin 300mg PO TID, trimethoprim-sulfamethoxazole PO BID, doxycycline or minocycline PO
Management of CA-MRSA in a wound: Inpatient
Vancomycin 1 gm IV BID, or cefazolin or nafcillin or oxacillin
When are prophylactic antibiotics indicated in bite wounds
○ Cat bites in any location
○ Hand bites by any animal, including humans
○ Individuals with certain comorbidities (Diabetes, Liver Disease) are at increased risk for severe complications and should receive prophylaxis even for low-risk
bites
○ Patients without functional spleens who are at increased risk for overwhelming
sepsis
● The risk for HIV transmission following a bite is low and routine postexposure prophylaxis is not routinely recommended. Each case should be evaluated individually and consideration for prophylaxis should be given to those who present within 72 hours of the incident, the source is known to be HIV infected, and the exposure risk is high
Prophylactic antibiotics in bite wounds
● Augmentin 500mg PO TID for 5-7 days is the regimen of choice
● For the PCN allergic: A combination of Clindamycin 300mg PO TID with one of the following for 5-7 days: Doxycycline 100mg PO BID, or double-strength TMP-SMZ PO BID, or a flouroquinolone (Cipro 500mg PO BID or Levofloxacin 500-750mg PO once daily)
Cause for lyme disease
Most common vector-born disease in the U.S. and is spread by the bite of infected blacklegged ticks (mice and deer ticks). Takes 24 to 48 hours for a tick to feed and transmit the Borrelia burgdorferi (spirochete) to the host.
diagnostic tests for Lyme disease
Elisa testing-inital test
Western blot-Confirmatory
Treatment for lyme disease
Doxycycline, Age <7 Amoxicillin
ABX prophylaxis for dental procedures in patients with a prosthetic heart valve
Amoxicillin 2g one time dose 30-60 minutes prior to dental work if allergic to PCN- Cephalexin
OR Clindamycin OR Azithromycin or clarithromycin
Cranial nerve most frequently affected by herpes zoster
CN V: Trigeminal Nerve involvement of geniculate ganglion - facial palsy, ear pain, vesicles on pinna and external auditory canal (Ramsay Hunt syndrome)
Clinical manifestations of botulism
The FOUR Ds
diplopia, dysarthria, dysphonia, and dysphagia
What is botulism and what is the cause
-Foodborne illness caused by Improper canning techniques, Honey ingestion before age of 1, and IV drug users contract it in wounds.
-Potentially fatal neuroparalytic syndrome caused by Clostridium botulinum
● Descending motor neuron process, no sensory component
● Neurotoxin acts at the motor end plate causing weakness which affects diaphragm causing respiratory failure
Spectrum of botulism in infants
Constipation then Poor feeding then Weak cry then
Floppy baby
Treatment for botulism
Treatment based on clinical presentation- don’t wait for test results. Treat with immunoglobulin
Signs and symptoms of Salmonellosis: Localized to the GI tract
■ Incubation period - 12-48 hours
■ Nausea/vomiting/diarrhea/abdominal cramps
■ Fever
■ Bacteremia
■ Self limiting - lasting 3-4 days
■ Colonization of GI tract persistent for months, especially in those treated with antibiotics
Signs and symptoms of Salmonellosis: systemic
Typhoid Fever
■ Incubation period - few days to several weeks
■ Prolonged fever - stepwise increasing temperature pattern
■ Myalgias
■ Headache, cough, sore throat
■ Malaise, anorexia
■ Abdominal pain, diarrhea or constipation
■ Hepatosplenomegaly
■ Rose spots on chest or abdomen (faint, maculopapular, blanching lesions)
Signs and symptoms of Salmonellosis: Localized outside of the GI tract
■ Can occur in any location usually in patients with underlying disease
■ Endocarditis, endovascular infections
■ Hepatic or splenic abscesses
■ UTI
■ Cause of gram-negative meningitis in neonates
■ Osteomyelitis in children with sickle cell disease
Signs and symptoms of Salmonellosis: untreated disease
■ Fever lasting 1-2 months
■ Main complication: GI bleeding
■ Rare complication: mental status changes, shock
Diagnostics for salmonellosis gastroenteritis
Stool culture
Diagnostics for salmonellosis Typhoid fever
■ Blood culture - likely to be positive early in course of illness
■ Urine and stool cultures - likely to be positive in 2-3 week of illness
■ Bone marrow biopsy - 90% positive
■ Serology using Widal’s test is helpful in retrospect with increase in titers
Lab results for Salmonellosis
-Neutropenia
○ Transaminitis
○ Positive cultures
Imaging for Salmonellas
○ Not routinely indicated
○ X-rays may be helpful for diagnosis of osteomyelitis
○ CT scan or US may be helpful for diagnosis of hepatic/splenic abscess, pleural involvement, or aortic aneurysm
Management of typhoid fever in Salmonellas
■ Levofloxacin or Ciprofloxacin for 7-10 days OR
■ Ceftriaxone for 7-14 days OR
■ Azithromycin for 5-17 days
■ Dexamethasone for 8 doses for patients with shock or mental status changes
Management of gastroenteritis in Salmonellas
■ Not usually indicated - self limiting
■ Prophylactic treatment for patients at high risk of developing bacteremia - patients
with hemoglobinopathies, atherosclerosis, aneurysms, prosthetic devices, and/or immunocompromised
Carrier state of Salmonellas
○ Possible in patients with typhoid fever, typically >60 years of age and with gallstones (typical
place of colonization)
○ Treatment considered for patients with persistent positive stool cultures and food handlers
○ Cipro for 4 weeks, Bactrim for 6 weeks, Amoxicillin for 6 weeks
When antimicrobial time outs should occur
48-72 hours after initiation of antibiotics. This is designed to give providers time to determine if the patient’s illness requires antibiotics, if they are on the right antibiotics, and if the antibiotics can be narrowed.
Importance of proper serum concentrations of certain ABX
To minimize toxicity and ensure proper dosage. With patient with altered renal or hepatic function, the dosage and frequency may need to be adjusted. It is best to measure levels in older adults, morbidly obese patients, or in those with altered kidney function
systemic lupus erythematous clinical manifestations
A patient is classified as having SLE if any 4 or more of 11 criteria are met
- Malar rash
- Discoid rash
- Photosensitivity
- Oral ulcers
- Arthritis (joint symptoms are present in 90% of patients)
- Serositis
- Kidney disease: > 0.5 g/day proteinuria, or ≥ 3+ dipstick proteinuria, or Cellular casts
- Neurologic disease: Seizures, or Psychosis (without other cause)
- Hematologic disorders: Hemolytic anemia, or Leukopenia (< 4000/mcL), or Lymphopenia (< 1500/mcL), or Thrombocytopenia (< 100,000/mcL)
- Immunologic abnormalities: Antibody to native DNA, or Antibody to Sm, or Antibodies to antiphospholipid antibodies based on (1) IgG or IgM anticardiolipin antibodies, (2) lupus anticoagulant, or (3) false-positive serologic test for syphilis
- Positive ANA
SLE General management
● Treatment is supportive. No cure. Since the various manifestations of SLE affect prognosis differently and
since SLE activity often waxes and wanes, drug therapy must be tailored to match disease severity.
● Patients should be cautioned against sun exposure and should apply a protective lotion to the skin while
out of doors.
SLE treatment
● Skin lesions often respond to the local administration of corticosteroids.
● Minor joint symptoms can usually be alleviated by rest and NSAIDs.
● Antimalarials (hydroxychloroquine) for rashes or joint symptoms and to reduce the incidence of severe
disease flares.
● Corticosteroids for Glomerulonephritis, hemolytic anemia, pericarditis or myocarditis, alveolar
hemorrhage, central nervous system involvement, and thrombotic thrombocytopenic purpura.
● Pulsed steroid therapy for life threatening flare ups. Immunosuppressive agents are used in cases
resistant to corticosteroids.
● Cyclophosphamide for nephritis.
● Coumadin for patients with anticardiolipin antibodies.
Giant Cell Arteritis Signs/Symptoms
headache, scalp tenderness, visual disturbances, JAW CLAUDICATION, throat pain. Occurs in patients >50 yrs with a mean onset at 79 years
Giant Cell Arteritis clinical manifestations
may have nodular, enlarged, tender, pulseless, temporal artery on exam
Giant Cell Arteritis diagnostics
ESR > 50, Elevated CRP, (+) temporal artery biopsy is gold standard
Giant Cell Arteritis management
IMMEDIATE high dose steroids (prednisone) to prevent blindness. Once blindness occurs it is irreversible. Can taper dose down after about a month
What is the concept of colonization
○ Presence and replication of micro-organisms without tissue invasion and/or damage, without
releasing toxins, and without initiating an immune response
○ Body is normally colonized by multitudes of microorganisms (normal flora)
■ Body defenses (skin, mucosa, and immune system) and normal flora are in equilibrium
(homeostasis)
○ If homeostasis is disrupted, disease/infection may occur
What is an infection
-Invasive presence and replication of micro-organisms with accompanying (some or all)
■ Local cellular injury/death
■ Secretion of toxin(s)
■ Immune response by host
How is infection made possible
Made possible by
■ Defeat of body defenses (skin, mucosa, immune system)
■ Imbalance of Normal Flora (e.g. overgrowth)
■ Increased Virulence
● Fewer microorganisms required to cause the same
○ Disease
○ Impact of disease
A culture media will grow
● Benign normal flora
● Pathogenic normal flora (Opportunistic)
● Exogenous pathogenic flora
A culture media is blind to
● Clinical picture
● Manner of collection
Proper interpretation requires consideration of what 4 things
Complete clinical picture, Manner of collection, Gram stain, Presence of other cellular evidence
Rules of antibiotic culture
-Fact: Use of any antibiotic encourages resistance
■ Selectively kills all susceptible organisms
■ Only resistant organisms survive
What spectrum of antibiotic should be used
-Unless there is high suspicion for multiple organism infection, the most narrow spectrum of
activity will be the best choice
■ Broad spectrum applies selective pressure for resistance to both normal and pathogenic
flora
■ Narrow spectrum confines selective pressure for resistance to fewer organisms
Bacterial as normal flora
know normal flora
How to read a culture
- High numbers of WBCs on gram stain suggests infection
- Dominance of epithelial cells over WBCs suggests colonization
- Gram Positive Organisms retains stain
- Gram negative organisms don’t retain stain
Staphylococcus sp.
-Gram positive cocci
■ Coag. Negative much less virulent
■ Tends to form abscesses, sticks to devices
■ Needs longer duration of tx
Streptococcus sp
-gram positive cocci
■ Group A: Causes strep throat, May develop rheumatic fever or glomerulonephritis
■ Group B: Selective for diabetics and elderly
Enterococcus sp.
gram positive organism
Corynebacterium sp.(diphtheroids)
gram positive rods
■ Essentially a-virulent, almost never causing disease
■ C. diphtheriae is exception but rare in post vaccination era
■ Normal skin flora, usually a contaminate in cultures
Bacillus sp
gram positive rods
Spore producing, more virulent
Clostridium sp
gram positive rods
Spore producing
Listeria sp.
gram positive rods
■ Not normal flora, always consider a pathogen
■ Most common in elderly, diabetics, and other immunocompromised patients.
■ May cause meningitis or sepsis
■ VERY serious infection in pregnancy
Neisseria sp.
gram negative cocci
● May be normal oropharyngeal flora (15%)
● May cause meningitis
● May be prudent to prophylactically tx those with close intimate contact (standard precautions sufficient for HCWs)
N. gonorrhoeae
- gram negative cocci
- STD
Moraxella catarrhalis
-gram negative cocci
Common agent causing ENT infections
Spirals
-gram negative cocci
■ Treponema pallidum
■ Spirochete which causes syphilis
Family Enterobacteriaceae
-gram negative rods
■ E. coli, Proteus sp., Klebsiella sp., Enterobacter sp., Serratia sp., all behave similarly
■ Normal gut flora: May be virulent opportunistic pathogen in other sites
■ May be ubiquitous on hospitalized patient
■ Common contaminant
■ Resistance is common, base treatment on susceptibility
Common agents for diarrheal diseases
-gram negative rods
■ Salmonella sp.
■ Shigella sp.: **VERY virulent , requires only 1/1000th # of organisms as Salmonella
■ Vibrio sp.
● V. cholera (prototypical watery diarrhea)
● V. vulnificus (bloody diarrhea, fatal in immune incompetence)
■ Campylobacter sp.: More common in US than V. cholera
Pseudomonas sp.
-Gram negative rods
■ Common in hospital environment: Easily acquired resistance, Difficult to treat
■ Unusual as contaminant
■ Quite virulent***
Haemophilus sp
Gram negative rods
Important cause of pneumonia, meningitis, and ENT
Legionella sp.
Gram negative rods
■ Important “atypical” cause of pneumonia (Legionnaires Disease)
■ Hx of exposure to inhalation of contaminated air conditioning
Y. pestis (Plague)
high priority agent for bioterrorism because of extreme virulence, potential for dissemination and person-to-person transmission
F. tularensis (Tularemia)
high priority agent for potential bioterrorism because of virulence and ease of dissemination
Co-morbidities that increase mortality in a patient with Vibrio vulnificus
● Cause Septic shock, larger hemorrhagic bullae, cellulitis, lymphadenitis, myositis
● Higher incidence in pts with liver dx ( cirrhosis) and immunocompromised hosts, leading cause of death r/t seafood consumption
What the presence of Corynebacterium sp. in a wound culture means
- Essentially a-virulent, almost never causing disease
- Normal skin flora, usually a contaminate in cultures
What bacteria may overgrow in the gut in a patient on multiple antibiotics
- Clostridium difficile ( C. difficile) colitis. Caused by Ampicillin, Clindamycin , 3rd gen cephalosporins, & fluoroquinolones
Likely agent responsible for a viral syndrome with GI distress
Viral gastroenteritis (stomach flu) agents: Caliciviruses ( Norovirus, Sapovirus ), Non-group A Rotavirus, Astrovirus , Adenovirus
Organism that was originally thought of as a parasite and now is classified as a fungus? What are the causes? Who is affected
● Microsporidia – the organism causes Microsporidiosis – an infection caused by single-celled,
spore-forming, intracellular protozoan.
● “Recent evidence suggests a relationship between microsporidia and fungi.” – Directly from
Ferri’s p. 831
● Usually infects: HIV/AIDS pts, children, travelers, organ transplant recipients, contact
lense-wearers, and the elderly
● Causes: chronic diarrhea, anorexia, bloating, weight loss, wasting, rhinitis, bronchitis
● Usually NO fever
What is Empiric therapy
● Treatment based on practical experience and observation, rather than on systematic logic, that
has proved to be beneficial
● Treatment begun on the basis of clinical “educated guess” in the absence of complete
information, conclusive results, or diagnostics
● Treatment given without knowledge of the cause or nature of the disorder and based on
experience rather than logic. Sometimes urgency dictates empirical treatment, as when a
dangerous infection by an unknown organism is treated with a broad-spectrum antibiotic while
the results of bacterial culture and other tests are awaited
● Typically, antibiotic coverage is targeted broadly to include resistant Gram-negative pathogens at
onset
Breaking the chain of infection: Infectious agent
the pathogen (germ) that causes disease
Breaking the chain of infection: Reservoir
includes places in the environment where the pathogen lives (this includes people, animals and insects, medical equipment, and soil and water)
Breaking the chain of infection: Portal of exit
the way the infectious agent leaves the reservoir (through open wounds, aerosols, and splatter of body fluids including coughing, sneezing, and saliva)
Breaking the chain of infection: Mode of transmission
the way the infectious agent can be passed on (through direct or indirect contact, ingestion, or inhalation)
Breaking the chain of infection: Portal of entry
the way the infectious agent can enter a new host (through broken skin, the respiratory tract, mucous membranes, and catheters and tubes)
Breaking the chain of infection: Susceptible host
can be any person (the most vulnerable of whom are receiving healthcare, are immunocompromised, or have invasive medical devices including lines, devices, and airways)
Actions to break the chain of infection
frequent hand washing, up to date on vaccines, covering coughs and sneezes, staying home when sick, following standard and contact isolation, using personal protective equipment, cleaning and disinfecting the environment, sterilizing medical instruments and
equipment, following safe injection practices, and antibiotic stewardship prevent antibiotic resistance.
Basal Cell Carcinoma: what is it
*Most common type of skin
cancer
■ Malignant tumor of skin
– arising from basal cells
Basal Cell Carcinoma signs and symptoms
▪ Occurs in fair-skinned people, in sun-exposed areas of skin (face/neck)
▪ Sun exposure before age 14 disposes a person
▪ Papule or nodule with a central scab or eroded area
▪ Nodule is waxy or “pearly” in appearance with telangiectatic vessels
▪ Papules, non-healing ulcers,scabbed lesions, or visual or scaly plaques
▪ Slow-growing
▪ Locally invasive – limited capacity to metastasize
▪ Rare in black/brown skinned people
Basal Cell Carcinoma Diagnosis
*Lesion should be biopsied, shaved, or punch-biopsied
▪ Confirmation of the diagnosis is made histologically.
▪ Boarders of lesion are translucent, elevated, and shiny with fine telangiectasias
Squamous Cell Carcinoma: what is it
*Malignant tumor of epithelial
keratinocytes (skin & mucous
membrane)
● arising in the epithelium
Squamous Cell Carcinoma signs and symptoms/ risk factors
▪ Non-healing ulcer or wart-like nodule
▪ Red, scaly, hard, nodular, crusty, or does not heal –
usually asymptomatic
▪ May develop from actinic keratosis
▪ Frequently develops on legs of women
▪ Slow growing
▪ Has the capacity to metastasize
▪ HPV is associated with increased incidence
▪ Usually caused by exogenous carcinogens
▪ Male: female = 2:1
▪ Smokers have increased risk of lip involvement
Squamous Cell Carcinoma disgnosis
*Lesion should be biopsied, shaved, or punch-biopsied
▪ Confirmation of the diagnosis is made histologically by full-thickness skin biopsy.
▪ Heaped-up edges of lesions appear fleshy rather than clear
▪ 70% on head or neck
▪ Can have lip, oral, tongue, and genital involvement (these areas also have higher risk of metastases)
Melanoma: what is it
*Leading cause of death from skin disease
● Malignant melanomas develop from benign melanocytic cells
Melanoma signs and symptoms/risk factors
▪ Tumor – characterized by dark pigmentation
▪ Flat or raised, with irregular boarders
▪ Red, black, or bluish
▪ Size > 6 mm
▪ Predisposed by blistering sun exposure and the use of sunscreen – especially in adolescence
▪ Incidence increases with proximity to equator
▪ Highest incidence: 30-50 years old
▪ Family Hx increases risk
▪ High number of nevi have greatest risk
▪ Common sites: Males = head, neck, trunk; Females = lower extremities
Melanoma: diagnosis
*Surgical biopsy is the only form of appropriate diagnostic procedure.
▪ Full-thickness total excision biopsy with 1-2 mm boarder is preferred
*NEVER curette, electrodesiccate, or shave!
▪ Must be sent to pathology
▪ Clark Staging = I: confined to epidermis; II: papillary dermis; III: interface of papillary dermis
& reticular dermis, IV: reticular dermis, V: subcutaneous fat
▪ Breslow Staging = Thin: < 0.75mm in depth,
Intermediate: 0.76-3.99 mm, Thick: > 4mm in depth
▪ Dermoscopy (shines polarized light to magnify skin lesion) – can increase accuracy in diagnosing melanoma by 10-27%
Clark Staging for melanoma
I: confined to epidermis
II: papillary dermis
III: interface of papillary dermis & reticular dermis
IV: reticular dermis, V: subcutaneous fat
Etiology of Stevens Johnson Syndrome
● Most often caused my medications, especially sulfonamides, NSAIDs, allopurinol, and
anticonvulsants (CMDT p.140)
● Drugs: phenytoin, sulfonamides, lamotrigine, sertraline, NSAIDs, tramadol, allopurinol,
B-lactam antibiotics, phenobarbital are the most common (Ferri p.1213)
● Upper respiratory tract infections: (e.g., Mycoplasma Pneumoniae) and HSV infections
have also been implicated
Clinical manifestations of Stevens Johnson Syndrome
● Sudden onset of symmetric erythematous skin lesions
● The cutaneous eruption generally occurs within 8wks of drug initiation and is generally preceded by vague, nonspecific symptoms of low-grade fever and fatigue (influenza-like symptoms) occurring 1 to 14 days before the skin lesions. Cough is often present. Fever
may be high during the active stages
● Enlarging red-purple macules or papules and bullae generally occur on the conjunctiva, mucous membranes of the mouth, nares, and genital regions. Lesions rapidly spread to
their maximum extent usually within 2 days
● Corneal ulcerations may result in blindness
● Ulcerative stomatitis results in hemorrhagic crusting
● Nikolsky sign (shearing off of epidermis with pressure on skin) can be present
● Flat, atypical target lesions or purpuric maculae may be distributed on the trunk or be widespread
● The pain from oral lesions may compromise fluid intake and result in dehydration
● Thick, mucopurulent sputum and oral lesions may interfere with breathing
Causative agents of necrotizing fasciitis
Group A streptococci ( S. pyogenes ); S. aureus, C. perfringens, Bacteroides fragilis, Vibrio vulnificus, MRSA (community-acquired)
Pharmacologic management of necrotizing fasciitis caused by Group A strep; which antimicrobial suppresses toxin production
Type II for group A strep: PCN-G 4 million units IV Q4H in pts weighing >60kg with clindamycin
600-900mg IV Q8H
- Clindamycin has added effect of suppressing toxin production
- If MRSA suspected, add vancomycin, daptomycin, or linezolid
Etiology cellulitis
● Diffuse spreading infx usually of lower leg
● Most commonly due to gram-pos cocci especially beta-hemolytic strep and staph aureus
● Most common portal of entry is toe web intertrigo with fissuring, usually a common complication of tinea pedis
● Other dz that predispose:
○ Prior episodes of cellulitis
○ Chronic edema
○ Venous insufficiency with secondary edema
○ Lymphatic obstruction
● Bacterial is almost NEVER bilateral
clinical manifestations of cellulitis
● Begins with tender small patch
● Swelling, erythema, and pain
● Expands over hours so onset to presentation usually 6-36 hours
● As lesion grows, pt becomes more ill including chills, fever, and malaise
● Lymphangitis and lymphadenopathy usually present
● If septicemia develops, hypotension can develop leading to shock
management of cellulitis
● Elevate involved limb
● Cool sterile saline dressings to remove purulence from open lesions
● Support stockings for peripheral edema
● Initial ABX: Coverage for strep, MSSA, and MRSA (in ptas with risk factors for MRSA: IV drugs, LTC
residents, athletes, men who have sex with men, prisoners)
-Erysipelas: PO: dicloxacillin, IV: cefazolin, Vanc if pcn allergic
-Staph: PO: dicloxacillin, TMP-SMZ for mild MRSA, IV: Nafcillin, Cephalosporins (except for MRSA)
-MRSA: vanc or linezolid
-H. Influenzae: PO: cefixime or cefuroxime, IV: cefuroxime or ceftriaxone
-V. vulnificus: PO: for mild cases, Doxy + cipro, IV doxy + ceftazidime or Cipro, ADMIT to ICU
- E. rhusiopathiae: Pcn
-A. hydrophilia
■ Aminoglycosides
■ Chloramphenicol
■ Complicated hospitalized pts
● daptomycin
Life threatening conditions that mimic cellulitis
Deep venous thrombosis & Necrotizing fasciitis both present with painful, red, swollen lower extremity
Best screening test for syphilis (T. palladium) in an asymptomatic patient
VDRL, or RPR both are non treponemal serologic testing
Symptoms in a female with Chlamydia
Can be asymptomatic. Low abd cramping/pain. Or purulent Vaginal discharge or irregular vag
bleeding. Endocervical bleeding can easily be induced on speculum exam due to cervical inflammation (which can also ascend up the reproductive tract and cause PID which presents with RUQ pain, cervical, uterine, adnexal tenderness)
Causes of vaginal bleeding in a non-pregnant patient
- PALM-COEIN: Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia, Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified
-Women 19-39 y.o.: pregnancy, structural lesions, anovulatory cycles, hormonal contraception,
endometrial hyperplasia
-Adolescents: Anovulation
Pregnancy testing in patients with vaginal bleeding
Urine pregnancy test: If positive, get quantitative beta human chorionic gonadotropin (β-hCG).
The following are typical although not entirely exclusive patterns:
1. Early pregnancy: follow serially every 48 hr
2. Normal pregnancy: β-hCG doubles approximately every 48 hr
3. Spontaneous abortion: β-hCG level will fall
4. Ectopic pregnancy: β-hCG level will rise inappropriately (less than expected; threshold
increase over 48 hr should be ≥66%)
5. Molar pregnancy: β-hCG level is higher than expected for gestational age
ectopic pregnancy Signs / Symptoms
abnormal menstruation. Severe, sudden onset, stabbing, intermittent pain and non-radiating. Potential abdominal distention from tubal blood leakage and mild paralytic ileus often present.
ectopic pregnancy Diagnostic
US - reliability determined by gestation, 6 weeks fetal pole. Beta-hCG of 6500 with empty uterus. Laparoscopy - choice for confirmation and removal of ectopic pregnancy.
ectopic pregnancy clinical manifestations
amenorrhea or irregular bleeding or spotting. Pelvic pain, usually adnexal.
-Adnexal mass by exam or US. Failure of beta-hCG to double in 48 hrs. No intrauterime pregnancy with
serum hCG greater than 2000.. 98% are tubal
ectopic pregnancy management
Methotrexate 50 mg/m2 IM in one or two doses — if liver and renal functions normal and 3.5 cm or less and not ruptured with no active bleeding or fetal heart tones. RUPTURED = SURGERY
pelvic inflammatory disease Signs/Symptoms-
uterine, adnexal, or cervical motion tenderness. Abnormal discharge. Chills, fever, abdominal pain, RUQ pain (fitz-Hugh and Curtis syndrome) = potential perihepatitis.
pelvic inflammatory disease clinical manifestations
Fever, elevated ESR and CRP, cervical infection with gonorrhoeae or trachomatis.
pelvic inflammatory disease Management
OP treatment: cefoxitin 2 g IM with probenecid 1 g plus doxy 100 mg bid for 14 days.
OR ceftriaxone 250 mg IM plus doxy 100mg bid x 14 days. May add metronidazole 500 mg bid 14
days can be added to the above
Most common STD in US
HPV
STD caused by a gram-negative diplococcus
Neisseria gonorrhoeae
Signs and symptoms of disseminated gonococcal infection
- Arthritis dermatitis - tenosynovitis and dermatitis skin lesions, polyarthralgias in the absence of purulent arthritis
- Purulent arthritis without skin lesion - abrupt onset of mono oligoarthritis with pain and
edema in one or more joints usually the knees, ankles and wrists
testing for disseminated gonococcal infection
Check gram stain of joint fluid for gram negative diplococcus
Treatment for disseminated gonococcal infection
longer course of the same abx (ceftriaxone/azithromycin), may need repeated surgical joint wash outs
genital herpes infection initial: Signs
management - acyclovir 400 mg 5 times a day or 800 mg 3 times a day, valacyclovir 1000 mg twice a
day, famciclovir 250 mg 3 times a day. All 7-10 days for 1st outbreak
recurrent small gouged vesicles with erythematous base. May follow minor infections, trauma,
stress, or sun exposure, regional lymph node may swell and be tender. Viral culture and direct
fluorescent antibody test POSITIVE.
genital herpes infection initial: symptoms
burning , stinging, occur on the vermilion border or lips, penile shaft, labia, perianal skin,
buttocks. Crust in about 1 week
clinical manifestations
genital herpes infection initial: management
burning , stinging, occur on the vermilion border or lips, penile shaft, labia, perianal skin, buttocks. Crust in about 1 week
subsequent genital herpes infection signs and symptoms
● Prodromal symptoms (fatigue, burning, and tingling of affected are) last 12-24 hours
● A cluster of lesions evolves w/in 24 hrs from macule to papule and then vesicles surrounded by
erythema
● Crusts shed w/in 7-10 days revealing pink surface
subsequent genital herpes infection clinical manifestations
● Generally caused by alteration in the immune system (stress, menses, local skin trauma, and
exposure to sunlight
● Most frequent location is penile shaft, glans penis and the labia
subsequent genital herpes infection management
Recurrent genital - 3 days of valacyclovir 500 mg bid, 5 days acyclovir 200mg 5 times a day. Famciclovir 125 mg bi for 5 days. OR. Valacyclovir 2 g bid for 1 day, famciclovir 1 go bid 1 day
Secondary syphilis clinical manifestations
Fevers, myalgias, arthralgias, headache, rash on trunk that spreads to extremities then to palms of hands and soles of feet. (+) condyloma lata (genital warts)
Clinical manifestations of chlamydia in males
Chlamydia: epididymitis, proctitis, arthritis, urethritis, prostatitis
Clinical manifestations of gonorrhea in males
Gonorrhea: asymptomatic or: purulent discharge, may have rectal puririts, tenesmus, and
discharge
Genital discharge is associated with BV
homogenous (similar to normal discharge), but is adherent, thin, milky white w/a stinky fish odor
Genital discharge is associated with Candidiasis
thick clumpy white (cottage cheese), vaginal tissue will be inflamed and red
Genital discharge is associated with Trich
frothy, gray or yellow-green, stinky, with “strawberry cervix” and cervical petechiae
Gonorrhea causes
Caused by N. gonorrhoeae, gram negative, intracellular, nonmotile, diplococcal bacterium
Gonorrhea signs and symptoms in females
-80% of females are Asymptomatic
-Early in females: dysuria and frequency, malodorous/mucopurulent vaginal/urethral discharge,
labial pain and swelling, lower abdominal discomfort, pharyngitis
-Later in females: fever, abnormal menses, increased dysmenorrhea, n/v, joint swelling & pain
Gonorrhea signs and symptoms in males
-Most males ARE symptomatic
-Early in males: dysuria with frequency, whitish urethral discharge, pharyngitis
-Later in males: yellow/greenish profuse, purulent urethral discharge with meatal edema and
erythema, epididymitis, lower abdominal pain
Gonorrhea clinical manifestations:
abdominal guarding w/rebound pain, may have bartholin & skene gland tenderness, enlargement, or discharge.
May have urethral discharge, vaginal will discharge or redness, cervix will be mucopurulent and
friable, adnexal tenderness and masses, uterine tenderness
Gonorrhea Diagnostics
- May do endocervical and/or throat culture, can do DNA probe test
- Co-testing for syphilis and trachomatis
- Test men at least 1 hour after voiding
Gonorrhea Management
Rocephin 250mg IM shot x 1 and EITHER Azithromycin 1gm PO single dose OR
doxycycline 100mg po BID x 7 days
Chlamydia, Signs & Symptoms in men and women Lymphogranuloma venereum (LGV)
-Acute and chronic sexually transmitted dz
cause by C. Trachomatis types L1-L3.
-In men,the initial vesicular or ulcerative lesion on the external genitalia is evanvercent and often goes unnoticed. Inguinal buboes appear 1 to 4 weeks after exposure and are often bilateral and have the tendency to fuse, soften and break down to form multiple draining sinuses with extensive scarring
-In women, genital lymph drainage is to the perirectal glands. Early anorectal manifestation are proctitis
with tenesmus with bloody purulent discharge; late manisfestation are chronic cicatrazing inflamation of
the rectal and perirectal tissue.
Chlamydial Urethritis and Cervicitis
-C. Trachomatis immunotypes D-K are isolated in about 50% of cases of nongonococcal urethritis and cervicitis.
-Coinfection with gonococci and chlamydiae is
common. Women infected with chlamydia may be asymptomatic or may have sign or symptoms of
urethritis, salpingitis or PID. The urethral and cervical discharge due to C. trachomatis tend to be less
painful , less purulent and watery compared to gonococcal infection
Diagnostics- Lymphogranuloma venereum
Positive complement fixation test
Chlamydial Urethritis and Cervicitis- Diagnosis
made by a positive nucleic amplification of urine or
vaginal swab specimen.
Management Lymphogranuloma venereum
Doxycycline( contraindicated in pregnancy)100mg PO BID for 21 days, Erythromycin, 500mg PO QID for 21 days, Azithromycin 1g PO QD for 3 weeks, may also be effective
Chlamydial Urethritis and Cervicitis management
Recommended regimens are single oral 1g dose of
azithromycin(prefered and safe in pregnancy), Doxycycline 100 mg for 7 days (contraindicated in
pregnancy or levofloxacin 500mg QD for 7 days.
Syphilis what is it
Infection by Treponema pallidium
Syphilis Symptoms
-Primary: Painless ulcer on genitalia, perianal area, rectum, pharynx, tongue, lip, elsewhere; chancre: Nontender regional lymphadenopathy
-Secondary: Rash, diffuse, condylomata lata, silvery mucoud membrane ulcers, malaise, anorexia, general lymphadenopathy, arthralgias, myalgias, HA, meningitis, cranial neuropathies II-VIII,
iritis, glomerulonephritis, hepatitis
-Tertiary/late:skin, bone & mucus membrane benign granulomatosis lesion, aortic regurg, Sz,
hemiparesis, slurred speech, tabes dorsalis
Syphilis Diagnostics
-Microscopic: *spirochetes
-Staining & PCR are not widely available
-Serologic : Nontreponemal tests detect antibodies to lipoidal antigens present in host after modification by T.Pallidium - most common, titers usually correlate with disease activity
-VRDL & RPR tests
-Lots of false positives, positive 4-6 weeks after infection or 1-3 weeks after appearance of
primary lesion
-Treponemal tests use live or killed T.Palladium as antigen to detect antibodies specific for pathogenic
treponemes
-EIA or CIA-based - reverses normal order, begins with automated treponemal antibody then VDRL or
RPR if its positive, faster & cheaper
Syphilis Management
*PCN, abstain from sex 7-10 days after tx
HIV/AIDS risk factors
● Greatest incidence in gay, bisexual, and other men who have sex with men (MSM) and in minority
and ethnic groups
● HIV disproportionately affects MSM of younger age and black and hispanic/Latino background
● Heterosexual transmission (24%) and IV drug use (9%)
HIV/AIDS complications
-The complications of HIV-related infections and neoplasms affect virtually every organ. The general
approach to the HIV-infected person with symptoms is to evaluate the organ systems involved,
aiming to diagnose treatable conditions rapidly.
-The CD4 lymphocyte count result enables the clinician to focus on the diagnoses most likely to be
seen at each stage of immunodeficiency.
When a dx of AIDS is made
- Positive HIV serology + certain infections/malignancies (Pulmonary TB, invasive cervical cancer, etc)
- Positive HIV serology + dementia and wasting (documented weight loss)
- Positive HIV serology + CD4 count below 200 OR CD4 lymphocyte percentage below 14%
