Showing posts with label infections. Show all posts
Showing posts with label infections. Show all posts
Friday, November 12, 2010
ENTAMOEBA HISTOLYTICA
Microbiology
Enteric protozoan
Cyst: 5-20 micrometer with one to four nuclei
Trophozoite (ameba): 12-60 micrometer with a single nucleus, a centrally located nucleolus with a uniformly distributed peripheral chromatin
Many strains, differentiated by isoenzyme analysis
Epidemiology
10% of the world is infected
50,000-100,000 E. histolytica-associated deaths per year (third leading parasitic cause of death in the world)
Endemic in Mexico, India, West and South Africa and portions of Central and South America
Vast majority (90%) of patients remain asymptomatic
High risk factors for invasive diseases in North America:
recent immigration, institutionalization and homosexuality
Transmission by fecal-oral route
Clinical syndromes
Intestinal:
Asymptomatic colonization
Acute amebic colitis
Fulminant colitis
Ameboma
Extraintestinal
Hepatic abscess
Pleuropulmonary
Peritonea
Pericardial
brain abscesses
Diagnosis
Serology (generally positive after 7 days)
Cyst and parasite in stool (rapid examination after special coloration: modify Kinouyn: as trophozoites die rapidly)
Comments on treatment
Surgical drainage if abscess
Asymptomatic cyst passer:
recommended: Paromomycin or Iodoquinol
alternative: diloxanide furoate
Diarrhea
recommended: Metronidazole and (Paromomycin or Iodoquinol)
alternative: (tinidazol or ornidazole) and (Paromomycin or Iodoquinol)
Extraintestinal infection:
Metronidazole and Iodoquinol
HELICOBACTER PYLORI AND PEPTIC ULCER
Microbiology
Formerly Campylobacter pylori
Spiral-shaped gram-negative bacillus
Ability to survive the acidic pH of gastric fluids
Epidemiology
Implicated as a cause of duodenal and gastric ulcers
Infection increasing with age
Natural reservoir in humans
Transmission is fecal-oral
Clinical syndromes
Duodenal and gastric ulcers
Dyspepsia (non-ulcer)
Gastric carcinoma
Diagnosis
Urease test (breath test)
Culture
Gastric biopsy
Serology
Comments on treatment
Susceptible in vitro to a variety of antimicrobial agents: Tetracycline, Metronidazole, Amoxicillin and Clarithromycin
Resistance to these antibiotics has been described (associated with treatment failures)
Recommended: see Ulcer, Gastric & Duodenal for more details
Amoxicillin and Clarithromycin and (omeprazole or lansoprazole)
Alternative:
bismuth and Tetracycline and Metronidazole and omeprazole
Hepatitis-B
Microbiology
Outmoded designation: serum hepatitis, due to its historically recognized route of percutaneous transmission (interesting to note that most of the patients with "serum hepatitis" were not actually infected with HBV)
Partially double-stranded DNA virus member of the hepadnavirus family (hepatotropic DNA viruses)
Reverse-transcriptase activity associated with the viral DNA
HBSag
product of the S gene of HBV
major surface protein
several subtypes
anti-HBs is the protective antibody
extremely large production during an infection (500µg/ml or 10 trillions particles per ml)
HBcAg
core antigen
product of the C gene
HBeAg
soluble nucleocapsid protein
reliable marker of replication and infectivity
Epidemiology
Virus found in every body fluid of infected individuals (saliva, tears, CSF, seminal fluid, ascites, breast milk, gastric fluid, synovial fluid, pleural fluid, urine and even (rarely) feces)
Low infectivity with oral ingestion of the agent
Sexual and perinatal transmission are important routes
Carrier state in human (more than 200 millions in the world) is the main reservoir
Prevalence is 0.1 and 0.5% in normal population but as high as 20% in some high risk groups
Higher risk groups:
Down's syndrome
leprosy
leukemia
Hodgkin's
polyarteritis
IVDU
hemodialysis patients
spouse of acutely infected persons
sexually promiscuous people
people who required repeated transfusions (low risk with present-day blood products with screening
Clinical syndromes
Subclinical
Fulminant acute hepatitis
Chronic persistent hepatitis
Chronic active hepatitis
Hepatocellular carcinoma
Diagnosis
Serology
Comments on treatment
Acute: no therapy recommended
Chronic
recommended: interferon-alfa (2a or 2b) (4-6 months of treatment. 33% will respond)
alternative: lamivudine (duration not established)
Prevention (after transplantation for HBV-induced cirrhosis
HIV-AIDS
Microbiology
One of the four known pathogenic human retroviruses and a member of the Lentiviruses
Two recognized subtypes of HIV:
HIV-1 causes AIDS worldwide
HIV-2 produces an AIDS-like illness but appears to be less pathologic
Each virion has 2 identical copies of a single-stranded viral RNA genome
Goes through reverse transcription (RNA into double-stranded DNA)
Contains three essential genes for viral replication: gag (Group-specific AntiGen), pol (polymerase) and env (envelop)
Epidemiology
HIV is now the leading cause of death of men aged 25-40, the sixth leading cause of death of adolescent males 15-24 years of age, and the fourth leading cause of death in women 25-44 years of age.
By the year 2000, the World Health Organization estimates that there will be 40 million HIV-infected individuals worldwide.
Male homosexuality continues to be the most common mode of transmission, but I.V. drug use and heterosexual transmission continues to rise
HIV in women continues to rise
Minorities account for a disproportionate amount of AIDS
Clinical syndromes
Category A:
Asymptomatic HIV infection
Persistent generalized lymphadenopathy (PGL)
Acute (primary) HIV illness
Category B
Symptomatic, not A or C conditions
Examples include but not limited to:
Bacillary angiomatosis
Candidiasis, vulvovaginal: persistent >1 month, poorly responsive to therapy
Candidiasis, oropharyngeal
Cervical dysplasia, severe, or carcinoma in situ
Constitutional symptoms (eg, fever >38.5°C or diarrhea >1 month)
NB: attributed to HIV infection or have a clinical course or management complicated by HIV
Category C
Candidiasis: esophageal, trachea, bronchi
Coccidioidomycosis, extrapulmonary
Cryptococcosis, extrapulmonary
Cervical cancer, invasive
Cryptosporidiosis, chronic intestinal (>1 month)
CMV retinitis, or other than liver, spleen, nodes
HIV encephalopathy
Herpes simplex with mucocutaneous ulcer >1 month, bronchitis, pneumonia
Histoplasmosis: disseminated, extrapulmonary
Isosporiasis, chronic (>1 month)
Kaposi's sarcoma
Lymphoma: Burkitt's, immunoblastic, primary in brain
M. avium or M. kansasii, extrapulmonary
M. tuberculosis: pulmonary or extrapulmonary
Mycobacterium, other species disseminated or extrapulmonary
Pneumocystis carinii pneumonia
Pneumonia: recurrent (>2 episodes in 1 year)
Progressive multifocal leukoencephalopathy
Salmonella bacteremia, recurrent
Toxoplasmosis, cerebral
Wasting syndrome due to HIV
Diagnosis
Serology (ELISA and Western Blot)
PCR
CD4 counts
Comments on treatment
For more info see: AIDS
Primary:
PI (protease inhibitors) + 2 NRTIs (nucleoside reverse-transcriptase inhibitors)
Indinavir + ZDV + 3TC
Nelfinavir + d4T + ddI
(Sequinavir ± ritonavir) + [(ZDV + DDC) or (d4T + 3TC)
Alternative :
2 NRTIs (ZDV, ddI, DDC, d4T, 3TC) + NNRTI (delavirdine , nevirapine, efavirenz)
[(ZDV + 3TC) or (d4T + ddI) or (ZDV + DDC) or (d4T + 3TC)] +(efavirenz or delavirdine or nevirapine)
Sunday, October 31, 2010
Upper urinary tract infection
Presentation
The patient has some combination of urinary frequency, urgency, dysuria, flank pain, nausea, fever, and chills. On physical examination, there is tenderness elicited by percussing the costovertebral angle over the kidneys. The urinalysis may help establish the diagnosis with tubular casts of white cells.
What to do:
Examine urine for presence of gram-positive cocci (presumptively enterococci) or the more usual gram- negative rods, and send for culture and sensitivity.
If the patient appears toxic, with a high fever or white count, nausea or vomiting to prevent adequate oral medicatication and hydration, or if the patient is pregnant or there is any sign of urinary obstruction or developing sepsis, he or she should be admitted to the hospital for intravenous antibiotics.
For stable, otherwise healthy patients, start with a first dose of intravenous antibiotics in the ED (ampicillin 1000mg plus gentamicin 80mg, ceftriaxone 1000-2000mg, ofloxacin 200-400mg or ciprofloxacin 200-400mg), then discharge home on oral hydration and two weeks of oral antibiotics (trimethoprim 160mg plus sulfamethoxazole 800mg bid, ciprofloxacin 500mg bid, norfloxacin 400mg bid or ofloxacin 400mg bid x 14d).
Instruct the patient to return to the ED for re-evaluation in 24-48 hours, and sooner if symptoms worsen. Most patients improve on this regimen, but the others will require hospital admission if they are not improving in two days.
What not to do:
Do not lose the patient to followup. Although lower UTIs often resolve without treatment, upper UTIs inadequately treated can lead to renal damage or sepsis.
Do not miss an infection above a ureteral stone or obstruction. Crampy, colicky pain or hematuria with the symptoms above calls for an excretory urogram (IVP). Antibiotics and hydration alone may not cure an infected obstruction.
Discussion
Although oral antibiotics are usually sufficient treatment for upper UTIs, there is a significant incidence of renal damage and sepsis as sequelae, mandating good followup or admission when necessary. By the same token, lower UTIs can ascend into upper UTIs, or it can be difficult to decide the level of a given UTI, in which case it should be treated as an upper UTI.
Studies have shown tat a 14 day course of oral therapy is highly effective for the woman with clinical evidence of pyelonephritis without sepsis, nausea or vomiting. Quinolones such as ofloxacin (Floxin), ciprofloxacin (Cipro) and norfloxacin (Noroxin) are highly effective and probably the drugs of choice in this setting, except for pregnant women, for whom they are contraindicated. Trimethoprim-sulfamethoxazole (Bactrim, Septra) could also be used, although resistance of 5% to 15% of pathogens may be a more important factor in the selection of therapy for pyelonephritis than for cyctitis.
The patient has some combination of urinary frequency, urgency, dysuria, flank pain, nausea, fever, and chills. On physical examination, there is tenderness elicited by percussing the costovertebral angle over the kidneys. The urinalysis may help establish the diagnosis with tubular casts of white cells.
What to do:
Examine urine for presence of gram-positive cocci (presumptively enterococci) or the more usual gram- negative rods, and send for culture and sensitivity.
If the patient appears toxic, with a high fever or white count, nausea or vomiting to prevent adequate oral medicatication and hydration, or if the patient is pregnant or there is any sign of urinary obstruction or developing sepsis, he or she should be admitted to the hospital for intravenous antibiotics.
For stable, otherwise healthy patients, start with a first dose of intravenous antibiotics in the ED (ampicillin 1000mg plus gentamicin 80mg, ceftriaxone 1000-2000mg, ofloxacin 200-400mg or ciprofloxacin 200-400mg), then discharge home on oral hydration and two weeks of oral antibiotics (trimethoprim 160mg plus sulfamethoxazole 800mg bid, ciprofloxacin 500mg bid, norfloxacin 400mg bid or ofloxacin 400mg bid x 14d).
Instruct the patient to return to the ED for re-evaluation in 24-48 hours, and sooner if symptoms worsen. Most patients improve on this regimen, but the others will require hospital admission if they are not improving in two days.
What not to do:
Do not lose the patient to followup. Although lower UTIs often resolve without treatment, upper UTIs inadequately treated can lead to renal damage or sepsis.
Do not miss an infection above a ureteral stone or obstruction. Crampy, colicky pain or hematuria with the symptoms above calls for an excretory urogram (IVP). Antibiotics and hydration alone may not cure an infected obstruction.
Discussion
Although oral antibiotics are usually sufficient treatment for upper UTIs, there is a significant incidence of renal damage and sepsis as sequelae, mandating good followup or admission when necessary. By the same token, lower UTIs can ascend into upper UTIs, or it can be difficult to decide the level of a given UTI, in which case it should be treated as an upper UTI.
Studies have shown tat a 14 day course of oral therapy is highly effective for the woman with clinical evidence of pyelonephritis without sepsis, nausea or vomiting. Quinolones such as ofloxacin (Floxin), ciprofloxacin (Cipro) and norfloxacin (Noroxin) are highly effective and probably the drugs of choice in this setting, except for pregnant women, for whom they are contraindicated. Trimethoprim-sulfamethoxazole (Bactrim, Septra) could also be used, although resistance of 5% to 15% of pathogens may be a more important factor in the selection of therapy for pyelonephritis than for cyctitis.
Lower urinary tract infection
Presentation
The patient (usually female) complains of urinary frequency and urgency, internal dysuria, and suprapubic pain. There may have been some antecedent trauma (sexual intercourse) to inoculate the bladder, and there may be blood in the urine (hemorrhagic cystitis). Usually, there is no labial irritation, external dysuria or vaginal discharge (which would suggest vaginitis); and no fever, chills, nausea, flank pain, or costovertebral angle tenderness (which would suggest an upper urinary tract infection.)
What to do:
If available in the ED, dip stick for white cells or obtain a urinalysis or Gram stain a sample of urine. The presence of any white cells or bacteria in a clean specimen on microscopic examination confirms the infection. A positive nitrite on dip stick is helpful, but a negative does not rule out infection because many bacteria do not produce nitrites.
If the clinical picture is clearly that of an uncomplicated lower UTI, give trimethoprim 160mg plus sulfamethoxazole 800mg (Bactrim DS or Septra DS) one tablet bid for three days or a 3 day regimen of a quinolone such as ciprofloxacin (Cipro) 250mg bid, norfloxacin (Noroxin) 400mg bid or ofloxacin (Floxin) 200mg bid. Single dose treatment with two TMP/SMX DS tablets is also effective in the young healthy female, but does have a higher early recurrence rate. Instruct the patient to drink plenty of liquids (such as cranberry juice) but do not push fluids when treating children or males.
Extend therapy to 7 days and obtain cultures when treating a patient who is unreliable, pregnant, diabetic, symptomatic more than 5 days, older than 50 or younger than 16. Also extend treatment and obtain cultures on all male patients and those with an indwelling urinary catheter, renal disease, obstructive urinary tract lesions, recurrent infection or other significant medical problems.
If there are no bacteria or few white cells, no hematuria or suprapubic pain, gradual onset over 7-10 days, and a new sexual partner, the dysuria may be caused by a chlamydia or ureaplasma urethritis. Perform a pelvic exam and obtain samples for culture and microscopic examination. Ask the patient about the use of spermicides or douches, which may irritate the periurethral tissue and cause dysuria.
If there is external dysuria, vaginal discharge, odor, itching and no frequency or urgency, then evaluate for vaginitis with a pelvic examination.
If the dysuria is severe, you may also prescribe phenazopyradine (Pyridium) 200mg tid for 2 days only, to act as a surface anesthetic in the bladder. Warn the patient that it will stain her urine (and perhaps clothes) orange.
Arrange for followup in 2 days if the symptoms have not completely resolved. If necessary, urine culture and a longer course of antibiotics can be undertaken then.
What not to do:
Do not undertake expensive urine cultures for every lower urinary tract infection of recent onset in nonpregnant, normally health women with no history of recent UTI or antibiotic use.
Do not follow the single-dose or 3 day regimens for a possible upper urinary tract infection.
Do not rely on gross inspection of the urine sample. Cloudiness is usually caused by crystals and odors result from diet or medication.
Do not require a follow up visit or culture after therapy unless symptoms persist or recur.
Discussion
Lower UTI or cystitis is a superficial bacterial infection of the bladder or urethra. The majority of these infections involve Escherichia coli, Staphylococcus saprophyticus or enterococci. The urine dip stick is a reasonable screening measure that can direct therapy if results are positive. Under the microscope, in a clean sediment (free of epithelial cells) one white cell per 400x field suggests a significant pyuria, although clinicians accustomed to imperfect samples usually set a threshold of 3-5 WBCs per field. In addition, Trichomonas may be appreciated swimming in the urinary sediment, indicating a different etiology for urinary symptoms or associated vaginitis. In a straightforward lower UTI, urine culture may be reserved for cases which fail to resolve with single-dose or 3 day therapy. In complicated or doubtful cases, however, or with recurrences, a urine culture before initial treatment may be helpful.
Risk factors for UTI in women include pregnancy, sexual activity, use of diaphragms or spermicides, failure to void post coitally, and history of prior UTI. Healthy women may be expected to suffer a few episodes of lower urinary tract infection in a lifetime without indicating any major structural problem, but recurrences at short intervals suggest inadequate treatment or underlying abnormalities. Young men, however, have longer urethras and far fewer lower UTIs, and probably should be evaluated urologically after just one episode unless they have a risk factor such as an uncircumcised foreskin, HIV infection or homosexual activity and respond to initial treatment. In sexually active men, consider urethritis or prostatitis as the etiology. In men over 50 years old, there is a rapid increase in UTI due to prostate hypertrophy, obstruction and instrumentation.
References:
Valenstein PN, Koepke JA: Unnecessary microscopy in routine urinalysis. Am J Clin Pathol 1984;82:444-448.
Stamm WE, Hooton TM: Management of urinary tract infections in adults. N Eng J Med 1993;329:1328-1334.
The patient (usually female) complains of urinary frequency and urgency, internal dysuria, and suprapubic pain. There may have been some antecedent trauma (sexual intercourse) to inoculate the bladder, and there may be blood in the urine (hemorrhagic cystitis). Usually, there is no labial irritation, external dysuria or vaginal discharge (which would suggest vaginitis); and no fever, chills, nausea, flank pain, or costovertebral angle tenderness (which would suggest an upper urinary tract infection.)
What to do:
If available in the ED, dip stick for white cells or obtain a urinalysis or Gram stain a sample of urine. The presence of any white cells or bacteria in a clean specimen on microscopic examination confirms the infection. A positive nitrite on dip stick is helpful, but a negative does not rule out infection because many bacteria do not produce nitrites.
If the clinical picture is clearly that of an uncomplicated lower UTI, give trimethoprim 160mg plus sulfamethoxazole 800mg (Bactrim DS or Septra DS) one tablet bid for three days or a 3 day regimen of a quinolone such as ciprofloxacin (Cipro) 250mg bid, norfloxacin (Noroxin) 400mg bid or ofloxacin (Floxin) 200mg bid. Single dose treatment with two TMP/SMX DS tablets is also effective in the young healthy female, but does have a higher early recurrence rate. Instruct the patient to drink plenty of liquids (such as cranberry juice) but do not push fluids when treating children or males.
Extend therapy to 7 days and obtain cultures when treating a patient who is unreliable, pregnant, diabetic, symptomatic more than 5 days, older than 50 or younger than 16. Also extend treatment and obtain cultures on all male patients and those with an indwelling urinary catheter, renal disease, obstructive urinary tract lesions, recurrent infection or other significant medical problems.
If there are no bacteria or few white cells, no hematuria or suprapubic pain, gradual onset over 7-10 days, and a new sexual partner, the dysuria may be caused by a chlamydia or ureaplasma urethritis. Perform a pelvic exam and obtain samples for culture and microscopic examination. Ask the patient about the use of spermicides or douches, which may irritate the periurethral tissue and cause dysuria.
If there is external dysuria, vaginal discharge, odor, itching and no frequency or urgency, then evaluate for vaginitis with a pelvic examination.
If the dysuria is severe, you may also prescribe phenazopyradine (Pyridium) 200mg tid for 2 days only, to act as a surface anesthetic in the bladder. Warn the patient that it will stain her urine (and perhaps clothes) orange.
Arrange for followup in 2 days if the symptoms have not completely resolved. If necessary, urine culture and a longer course of antibiotics can be undertaken then.
What not to do:
Do not undertake expensive urine cultures for every lower urinary tract infection of recent onset in nonpregnant, normally health women with no history of recent UTI or antibiotic use.
Do not follow the single-dose or 3 day regimens for a possible upper urinary tract infection.
Do not rely on gross inspection of the urine sample. Cloudiness is usually caused by crystals and odors result from diet or medication.
Do not require a follow up visit or culture after therapy unless symptoms persist or recur.
Discussion
Lower UTI or cystitis is a superficial bacterial infection of the bladder or urethra. The majority of these infections involve Escherichia coli, Staphylococcus saprophyticus or enterococci. The urine dip stick is a reasonable screening measure that can direct therapy if results are positive. Under the microscope, in a clean sediment (free of epithelial cells) one white cell per 400x field suggests a significant pyuria, although clinicians accustomed to imperfect samples usually set a threshold of 3-5 WBCs per field. In addition, Trichomonas may be appreciated swimming in the urinary sediment, indicating a different etiology for urinary symptoms or associated vaginitis. In a straightforward lower UTI, urine culture may be reserved for cases which fail to resolve with single-dose or 3 day therapy. In complicated or doubtful cases, however, or with recurrences, a urine culture before initial treatment may be helpful.
Risk factors for UTI in women include pregnancy, sexual activity, use of diaphragms or spermicides, failure to void post coitally, and history of prior UTI. Healthy women may be expected to suffer a few episodes of lower urinary tract infection in a lifetime without indicating any major structural problem, but recurrences at short intervals suggest inadequate treatment or underlying abnormalities. Young men, however, have longer urethras and far fewer lower UTIs, and probably should be evaluated urologically after just one episode unless they have a risk factor such as an uncircumcised foreskin, HIV infection or homosexual activity and respond to initial treatment. In sexually active men, consider urethritis or prostatitis as the etiology. In men over 50 years old, there is a rapid increase in UTI due to prostate hypertrophy, obstruction and instrumentation.
References:
Valenstein PN, Koepke JA: Unnecessary microscopy in routine urinalysis. Am J Clin Pathol 1984;82:444-448.
Stamm WE, Hooton TM: Management of urinary tract infections in adults. N Eng J Med 1993;329:1328-1334.
Candidiasis
CAUSATIVE AGENT:-
Small, oval, thin-walled, budding cells with or without the presence of pseudohyphae
Stains gram-positive
C. albicans is identified by the ability to produce germ tubes and/or chlamydospores in cornmeal agar
All Candida species may be distinguished by sugar fermentation tests.
Epidemiology
Normal host saprophyte yeasts found commonly in the gastrointestinal tract, genitourinary tract and oropharynx
Worldwide distribution
70% of nosocomial candidal infections are due to C. albicans with the rest due to C. glabrata, C. guilliermondii, C. krusei, C. pseudotropicalis, C. stellatoidea and C. tropicalis
Fifth most common blood pathogen isolated from hospitalized patients and the fourth most common in ICU patients
Risk factors for candidiasis:
age extremes
central venous catheters
TPN
burns
exogenous hormone therapy
prosthetic devices
malnourishment
metabolic disease
concurrent infections with other pathogens
antibiotic therapy
uncontrolled diabetes mellitus
GI surgery
AIDS
mechanical disruption of epithelial surfaces
physiological impairment of epithelial barrier function
Clinical syndromes
Candiduria
Cutaneous
Disseminated
Oral candidiasis
Vulvovaginitis
Diagnosis
Diagnosis is dependent on visualization of budding yeast (with or without pseudohypha) and the presence of clinical symptoms
culture
KOH preparation
Gram's stain
Comments on treatment
Cutaneous
Requires drying
Nystatin powder or imidazole (Butoconazole, Clotrimazole, Miconazole , Tioconazole ) powder
Topical steroids initially
Paronychia may require topical imidazole up to 3 months
Oral candidiasis:
Nystatin, Fluconazole, Itraconazole, Clotrimazole.
Candiduria:
Remove predisposing factors, (ie, Foley catheter)
Recommended: Amphotericin B (conventional)
Alternative: Fluconazole
Disseminated:
Drainage or debridement
Recommended: Amphotericin B (conventional)
Alternative: Fluconazole (not effective against C. krusei or C. glabrata)
Endophthalmitis may require subtenonian or intracameral injection of Amphotericin B (conventional)
Vulvovaginitis:
Imidazole derivatives (Butoconazole, Clotrimazole, Miconazole , Tioconazole ) and triazole derivative (Terconazole) (85% to 90%) are more effective than Nystatin
Extensive vulvar inflammation usually requires topical cream
Resistant or recurrent infections: oral agents (Ketoconazole, Fluconazole or Itraconazole)
Prophylaxis: Ketoconazole and Fluconazole
Small, oval, thin-walled, budding cells with or without the presence of pseudohyphae
Stains gram-positive
C. albicans is identified by the ability to produce germ tubes and/or chlamydospores in cornmeal agar
All Candida species may be distinguished by sugar fermentation tests.
Epidemiology
Normal host saprophyte yeasts found commonly in the gastrointestinal tract, genitourinary tract and oropharynx
Worldwide distribution
70% of nosocomial candidal infections are due to C. albicans with the rest due to C. glabrata, C. guilliermondii, C. krusei, C. pseudotropicalis, C. stellatoidea and C. tropicalis
Fifth most common blood pathogen isolated from hospitalized patients and the fourth most common in ICU patients
Risk factors for candidiasis:
age extremes
central venous catheters
TPN
burns
exogenous hormone therapy
prosthetic devices
malnourishment
metabolic disease
concurrent infections with other pathogens
antibiotic therapy
uncontrolled diabetes mellitus
GI surgery
AIDS
mechanical disruption of epithelial surfaces
physiological impairment of epithelial barrier function
Clinical syndromes
Candiduria
Cutaneous
Disseminated
Oral candidiasis
Vulvovaginitis
Diagnosis
Diagnosis is dependent on visualization of budding yeast (with or without pseudohypha) and the presence of clinical symptoms
culture
KOH preparation
Gram's stain
Comments on treatment
Cutaneous
Requires drying
Nystatin powder or imidazole (Butoconazole, Clotrimazole, Miconazole , Tioconazole ) powder
Topical steroids initially
Paronychia may require topical imidazole up to 3 months
Oral candidiasis:
Nystatin, Fluconazole, Itraconazole, Clotrimazole.
Candiduria:
Remove predisposing factors, (ie, Foley catheter)
Recommended: Amphotericin B (conventional)
Alternative: Fluconazole
Disseminated:
Drainage or debridement
Recommended: Amphotericin B (conventional)
Alternative: Fluconazole (not effective against C. krusei or C. glabrata)
Endophthalmitis may require subtenonian or intracameral injection of Amphotericin B (conventional)
Vulvovaginitis:
Imidazole derivatives (Butoconazole, Clotrimazole, Miconazole , Tioconazole ) and triazole derivative (Terconazole) (85% to 90%) are more effective than Nystatin
Extensive vulvar inflammation usually requires topical cream
Resistant or recurrent infections: oral agents (Ketoconazole, Fluconazole or Itraconazole)
Prophylaxis: Ketoconazole and Fluconazole
Malaria
Organism-
Obligate intracellular parasite
Sexual reproduction in mosquitoes, asexual in humans
Only 4 species are infective to humans: P. falciparum, P. vivax, P. ovale and P. malariae
Epidemiology
Only endemic in tropical areas of the developing world
Vector (Anopheline mosquito) present worldwide
In North America, transmission occurs after the influx of many infected persons (ex: refuges from endemic areas)
Transmission can also occur by blood products, among IV drug users (IVDU) who shares needles and congenitally
Clinical syndromes
Initial infection is very non-specific, "flu-like"
P. falciparum infection in more fulminant than the other and is often resistant to chloroquine and is a medical emergency
Diagnosis
Blood smear
Comments on treatment
Prevention
screen, nets and DEET
Chloroquine sensitive (Haiti/Dominical Republic, Central America West and North of the Panama canal and parts of the Middle East): chloroquine phosphate
Chloroquine resistant: mefloquine, doxycycline, atovaquone
Treatment
P. vivax or P. ovale
chloroquine phosphate
chloroquine-resistant P. vivax: halofantrine
P. falciparum (chloroquine sensitive) or P. malaria: chloroquine phosphate
P. falciparum (chloroquine resistant): PO treatment
quinine + doxycycline
atovaquone + provaquine
P. falciparum (chloroquine resistant): IV treatment: quinidine
Obligate intracellular parasite
Sexual reproduction in mosquitoes, asexual in humans
Only 4 species are infective to humans: P. falciparum, P. vivax, P. ovale and P. malariae
Epidemiology
Only endemic in tropical areas of the developing world
Vector (Anopheline mosquito) present worldwide
In North America, transmission occurs after the influx of many infected persons (ex: refuges from endemic areas)
Transmission can also occur by blood products, among IV drug users (IVDU) who shares needles and congenitally
Clinical syndromes
Initial infection is very non-specific, "flu-like"
P. falciparum infection in more fulminant than the other and is often resistant to chloroquine and is a medical emergency
Diagnosis
Blood smear
Comments on treatment
Prevention
screen, nets and DEET
Chloroquine sensitive (Haiti/Dominical Republic, Central America West and North of the Panama canal and parts of the Middle East): chloroquine phosphate
Chloroquine resistant: mefloquine, doxycycline, atovaquone
Treatment
P. vivax or P. ovale
chloroquine phosphate
chloroquine-resistant P. vivax: halofantrine
P. falciparum (chloroquine sensitive) or P. malaria: chloroquine phosphate
P. falciparum (chloroquine resistant): PO treatment
quinine + doxycycline
atovaquone + provaquine
P. falciparum (chloroquine resistant): IV treatment: quinidine
Conjunctivitis
Presentation
The patient complains of a red eye, a sensation of fullness, burning, itching, or scratching, and perhaps a gritty or foreign body sensat ion and tearing or purulent discharge and crusting or mattering. Examination discloses generalized injection of the conjunctiva, thinning out towards the cornea (localized inflammation suggests some other diagnosis such as a foreign body, episcleritis, or a viral or bacterial ulcer). Vision and pupillary reactions should be normal and the cornea and anterior chamber should be clear. Any discomfort should be temporarily relieved by instilling topical anesthetic solution. Deep pain, photophobia, decreased vision and injection more pronnounced around the limbus (ciliary flush) suggest more serious involvement of the cornea and iris.
Different symptoms suggest different etiologies. Tearing, preauricular lymphadenopathy and upper respiratory symptoms suggest a viral conjunctivitis. Pain upon awakening with lid crusting and a copious purulent exudate suggests a bacterial conjunctivitis. Few symptoms upon awakening but discomfort worsening during the day suggests a dry eye. Little conjunctival injection with a seasonal recurrence of chemosis and itching, and cobblestone hypertrophy of the tarsal conjunctiva suggests allergic (vernal) conjunctivitis. Physical and chemical conjunctivitis, caused by particles, solutions, vapors, natural or occupational irritants that inflame the conjunctiva, should be evident from the history.
What to do:
Instill proparcaine anesthetic drops (Alcaine, Ophthaine) to allow for a more comfortable exam and to help determine if the patient's discomfort is limited to the conjunctiva and cornea or, if there is no pain relief, that the pain comes from deeper eye structures.
Examine the eye, including visual acuity, inspection for foreign bodies, pupillary reaction fundoscopy, estimation of intraocular pressure by palpation of the globe above the tarsal plate, slit lamp examination (when available), and fluorescein and ultraviolet or cobalt blue light to assess the corneal epithelium.
Ask about and look for any rash, arthritis, or mucous membrane involvement which could point to Stevens-Johnson syndrome, Kawasaki's, Reiter's, or some other syndrome that can present with conjunctivitis.
For bacterial conjunctivitis, start the patient on warm compresses and seven days of topical antibiotics such as erythromycin, sulfacetamide, tobramycin or gentamycin ointment (which transiently blurs vision) every 4 hours, or solutions such as sulfacetamide 10%, tobramycin 0.3% or ciprofloxacin every 2 hours, with oral analgesics as needed. If it is unclear whether the problem is viral or bacterial, it is safest to treat it as bacterial.
For viral and chemical conjunctivitis, use cold compresses and weak topical vasoconstrictors such as naphazoline 0.1% (Naphcon) every 3-4 hours, unless the patient has a shallow anterior chamber that would be prone to acute angle- closure glaucoma with mydriatics.
For allergic conjunctivitis, use cold compresses and topical decongestant- antihistamine combinations such as drops of naphazoline with pheniramine (Naphcon A) or naphazoline with antazoline (Vasocon A) every 3-4 hours. Topical corticosteroid drops provide dramatic relief, but prolonged use increases the risk of opportunistic viral, fungal and bacterial corneal ulceration, cataract formation and glaucoma. If a severe contact dermatitis is suspected, then a short course of oral prednisone would be indicated.
If the problem is dry eyes (keratoconjunctivitis sicca) use methylcellulose (Dacriose) artificial tear drops.
Have the patient follow up with the ophthalmologist if the infection does not clearly resolve in 2 days. Obtain early consultation there is any involvement of cornea or iris.
What not to do:
Do not forget to wash your hands and equipment after examining the patient, or you may spread herpes simplex or epidemic keratoconjunctivitis to yourself and other patients. Also, do not forget to instruct the patient on the importance of hand washing and separation of towels and pillows for ten days after the onset of symptoms.
Do not patch an affected eye, as this interferes with the cleansing function of tear flow.
Do not give steroids without arranging for ophthalmologic consultation, and never give steroids if a herpes simplex infection is suspected.
Discussion
Warm compresses are soothing for all types of conjunctivitis, but antibiotic drops and ointments should be reserved for when bacterial infection is likely. Neomycin-containing ointments and drops should probably be avoided, because allergic sensitization to this antibiotic is common. Any corneal ulceration requires ophthalmological consultation. Most viral and bacterial conjunctivitis will resolve spontaneously, with the possible exception of staphylococcus, meningiococcus, and gonococcus infections, which can produce destructive sequelae without treatment.
Most bacterial conjunctivitis is caused by Streptococcus pneumoniae, Haemophilus aegyptus and Staphylococcus aureus. Routine conjunctival cultures are seldom of value, but you should Gram stain and culture a copious purulent exudate. Neisseria gonorrhoeae infection confirmed by Gram-negative intracellular diplococci on Gram stain requires immediate ophthalmologic consultation. Corneal ulceration, scarring and blindness can occur in a matter of hours. Chlamydial conjunctivitis will usually present with l
The patient complains of a red eye, a sensation of fullness, burning, itching, or scratching, and perhaps a gritty or foreign body sensat ion and tearing or purulent discharge and crusting or mattering. Examination discloses generalized injection of the conjunctiva, thinning out towards the cornea (localized inflammation suggests some other diagnosis such as a foreign body, episcleritis, or a viral or bacterial ulcer). Vision and pupillary reactions should be normal and the cornea and anterior chamber should be clear. Any discomfort should be temporarily relieved by instilling topical anesthetic solution. Deep pain, photophobia, decreased vision and injection more pronnounced around the limbus (ciliary flush) suggest more serious involvement of the cornea and iris.
Different symptoms suggest different etiologies. Tearing, preauricular lymphadenopathy and upper respiratory symptoms suggest a viral conjunctivitis. Pain upon awakening with lid crusting and a copious purulent exudate suggests a bacterial conjunctivitis. Few symptoms upon awakening but discomfort worsening during the day suggests a dry eye. Little conjunctival injection with a seasonal recurrence of chemosis and itching, and cobblestone hypertrophy of the tarsal conjunctiva suggests allergic (vernal) conjunctivitis. Physical and chemical conjunctivitis, caused by particles, solutions, vapors, natural or occupational irritants that inflame the conjunctiva, should be evident from the history.
What to do:
Instill proparcaine anesthetic drops (Alcaine, Ophthaine) to allow for a more comfortable exam and to help determine if the patient's discomfort is limited to the conjunctiva and cornea or, if there is no pain relief, that the pain comes from deeper eye structures.
Examine the eye, including visual acuity, inspection for foreign bodies, pupillary reaction fundoscopy, estimation of intraocular pressure by palpation of the globe above the tarsal plate, slit lamp examination (when available), and fluorescein and ultraviolet or cobalt blue light to assess the corneal epithelium.
Ask about and look for any rash, arthritis, or mucous membrane involvement which could point to Stevens-Johnson syndrome, Kawasaki's, Reiter's, or some other syndrome that can present with conjunctivitis.
For bacterial conjunctivitis, start the patient on warm compresses and seven days of topical antibiotics such as erythromycin, sulfacetamide, tobramycin or gentamycin ointment (which transiently blurs vision) every 4 hours, or solutions such as sulfacetamide 10%, tobramycin 0.3% or ciprofloxacin every 2 hours, with oral analgesics as needed. If it is unclear whether the problem is viral or bacterial, it is safest to treat it as bacterial.
For viral and chemical conjunctivitis, use cold compresses and weak topical vasoconstrictors such as naphazoline 0.1% (Naphcon) every 3-4 hours, unless the patient has a shallow anterior chamber that would be prone to acute angle- closure glaucoma with mydriatics.
For allergic conjunctivitis, use cold compresses and topical decongestant- antihistamine combinations such as drops of naphazoline with pheniramine (Naphcon A) or naphazoline with antazoline (Vasocon A) every 3-4 hours. Topical corticosteroid drops provide dramatic relief, but prolonged use increases the risk of opportunistic viral, fungal and bacterial corneal ulceration, cataract formation and glaucoma. If a severe contact dermatitis is suspected, then a short course of oral prednisone would be indicated.
If the problem is dry eyes (keratoconjunctivitis sicca) use methylcellulose (Dacriose) artificial tear drops.
Have the patient follow up with the ophthalmologist if the infection does not clearly resolve in 2 days. Obtain early consultation there is any involvement of cornea or iris.
What not to do:
Do not forget to wash your hands and equipment after examining the patient, or you may spread herpes simplex or epidemic keratoconjunctivitis to yourself and other patients. Also, do not forget to instruct the patient on the importance of hand washing and separation of towels and pillows for ten days after the onset of symptoms.
Do not patch an affected eye, as this interferes with the cleansing function of tear flow.
Do not give steroids without arranging for ophthalmologic consultation, and never give steroids if a herpes simplex infection is suspected.
Discussion
Warm compresses are soothing for all types of conjunctivitis, but antibiotic drops and ointments should be reserved for when bacterial infection is likely. Neomycin-containing ointments and drops should probably be avoided, because allergic sensitization to this antibiotic is common. Any corneal ulceration requires ophthalmological consultation. Most viral and bacterial conjunctivitis will resolve spontaneously, with the possible exception of staphylococcus, meningiococcus, and gonococcus infections, which can produce destructive sequelae without treatment.
Most bacterial conjunctivitis is caused by Streptococcus pneumoniae, Haemophilus aegyptus and Staphylococcus aureus. Routine conjunctival cultures are seldom of value, but you should Gram stain and culture a copious purulent exudate. Neisseria gonorrhoeae infection confirmed by Gram-negative intracellular diplococci on Gram stain requires immediate ophthalmologic consultation. Corneal ulceration, scarring and blindness can occur in a matter of hours. Chlamydial conjunctivitis will usually present with l
Dengue
Microbiology
Member of the arbovirus
heterogeneous group of RNA virus
usually transmitted by hematogenous arthropods
spherical, non-enveloped
Family flavivirideae
4 types
Epidemiology
Natural virus: humans
Distribution similar to malaria: warm, humid (tropical) countries
Clinical syndromes
Dengue fever
Dengue hemorrhagic fever
Diagnosis
Serology
Comments on treatment
Supportive
No antimicrobial agents shown effective
Member of the arbovirus
heterogeneous group of RNA virus
usually transmitted by hematogenous arthropods
spherical, non-enveloped
Family flavivirideae
4 types
Epidemiology
Natural virus: humans
Distribution similar to malaria: warm, humid (tropical) countries
Clinical syndromes
Dengue fever
Dengue hemorrhagic fever
Diagnosis
Serology
Comments on treatment
Supportive
No antimicrobial agents shown effective
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