INFECTIOUS DISEASE Flashcards
Triad for Weil’s syndrome (3):
a. Jaundice
b. Hemorrhagic diathesis
c. Renal dysfunction
Coiled, thin, highly motile organisms that have hooked ends and two periplasmic flagella, with polar extrusions from the cytoplasmic membrane that are responsible for motility
Leptospira sp.
Sex predilection of leptospirosis
Men
Most important reservoir of leptospirosis
Rodents (esp. rats)
Leptopirosa serovar associated with rats as reservoir (2):
a. Icterohaemorrhagiae
b. Copenhageni
Leptopirosa serovar associated with voles as reservoir:
Grippotyphosa
Leptopirosa serovar associated with cattle as reservoir:
Hardjo
Leptopirosa serovar associated with dogs as reservoir:
Canicola
Leptopirosa serovar associated with pigs as reservoir:
Pomona
Percentage of leptospirosis that lead to severe, potentially fatal complications
~1%
An independent risk factor for leptospirosis:
Swimming in the Segama River
Phase of leptospirosis wherein organisms proliferate, cross tissue barriers, and disseminate hematogenously to all organs
Leptospiremic phase
Phase of leptospirosis when organism can be isolated from the bloodstream
Leptospiremic phase
During leptospiremic phase, organisms are able to survive in the nonimmune host by evading complement-mediated killing by binding ____:
Factor H (a strong inhibitor of the complement system)
Phase of leptospirosis where the appearance of antibodies coincides with the disappearance of leptospires from the blood
Immune phase
Phase of leptospirosis where bacteria persist in various organs, including liver, lung, kidney, heart, and brain
Immune phase
Deregulation of the expression of several transporters along the nephron in leptospirosis causes these 3:
a. Impaired sodium absorption
b. Tubular potassium wasting
c. Polyuria
Thrombocytopenia in leptospirosis is most likely due to:
Platelet consumption
The only leptospiral virulence factor shown to satisfy Koch’s molecular postulates
Loa22
Hallmarks of fatal leptospirosis (2):
a. Bleeding
b. Multiorgan failure
Incubation period of leptospirosis:
1-2 weeks (may range from 1-30 days)
During immune phase, leptospires can be cultured in the:
Urine
Milder cases of leptospirosis do not always include this phase:
Immune phase
Mild leptospirosis usually spontaneously resolve within:
7–10 days
Case–fatality rate of severe leptospirosis:
1 to 50%
Risk factor for higher mortality rates in leptospirosis (6):
a. Age >40
b. Altered mental status
c. Acute renal failure
d. Respiratory insufficiency
e. Hypotension
f. Arrhythmias
Percentage of patients with leptospirosis who have jaundice:
5-10%
Jaundice in leptospirosis is usually associated with fulminant hepatic necrosis: True/False
False
Typical electrolyte abnormalities in leptospirosis (2):
a. Hypokalemia
b. Hyponatremia
Unique feature of leptospiral nephropathy
Loss of Mg in the urine
Characteristic of renal manifestation of early leptospirosis
Nonoliguric hypokalemic renal insufficiency
Most common radiographic finding in Leptospirosis:
Patchy bilateral alveolar pattern (due to scattered alveolar hemorrhage and predominantly affects the lower lobes)
Definitive diagnosis of leptospirosis (3):
a. Isolation of organism
b. Positive PCR
c. Seroconversion or a rise in antibody titer
Microscopic agglutination test (MAT) result required for diagnosis of leptospirosis in cases with strong clinical evidence of infection:
1:200 – 1:800
Has the capacity to confirm the diagnosis of leptospirosis with a high degree of accuracy during the first 5 days of illness
PCR
DOC for severe leptospirosis
IV penicillin
Alternative drugs for severe leptospirosis (3):
a. Ceftriaxone
b. Cefotaxime
c. Doxycycline
Recommended oral drugs for mild leptospirosis (4):
a. Doxycycline
b. Azithromycin
c. Ampicillin
d. Amoxicillin
DOC for leptospirosis in areas where rickettsial diseases are coendemic (2):
a. Doxycycline
b. Azithromycin
Rare reaction that occurs within hours after the initiation of antimicrobial therapy in leptospirosis:
Jarisch-Herxheimer reaction
Adjunct therapy for pulmonary involvement associated with severe leptospirosis (2)
a. Glucocorticoids
b. Desmopressin
Dose of doxycycline in mild leptospirosis:
100 mg BID x 7 days
Dose of Amoxicillin in mild leptospirosis:
500 mg TID x 7 days
Dose of ampicillin in mild leptospirosis:
500 mg TID x 7 days
Dose of Pen G in moderate/severe leptospirosis:
1.5M u IV or IM q6hrs x 7 days
Dose of Ceftriaxone in moderate/severe leptospirosis:
2 g/day IV x 7 days
Dose of cefotaxime in moderate/severe leptospirosis:
1g IV q6hrs x 7 days
Dose of doxycycline in moderate/severe leptospirosis:
LD 200 mg IV, then 100 mg IV q12h
The protypic lesion of IE
Vegetation
Analogous process of IE in AV shunts, AA shunts (i.e. PDA) or coarctation of the aorta
Infective endarteritis
A hectically febrile illness that rapidly damages cardiac structures, seeds to intracardiac sites
Acute Endocarditis
Has indolent course and causes structural cardiac damage only slowly, and rarely metastasizes
Subacute Endocarditis
Predisposing factors for IE (4):
Congenital heart disease
Illicit IV drug use
Degenerative valve disease
Intracardiac devices
Most common organisms causing IE (3):
Viridans streptococci
Staphylococci
HACEK organisms
What are HACEK organisms?
Haemophilus species Aggregatibacter species Cardiobacterium hominis Eikenella corrodens Kingella kingae
Primary portals for IE (3):
oral cavity
skin
upper respiratory tract
Organism from GIT, associated with polyps and colonic tumors, that can cause IE:
Streptococcus gallolyticus subspecies gallolyticus (formerly S. bovis biotype 1)
How many percent of IE have negative blood cultures
5-15%
Causes an indolent, culture-negative, afebrile form of endocarditis
Tropheryma whipplei
Early prosthetic valve endocarditis arises within how many months after valve surgery?
2 months
Delayed onset prosthetic valve endocarditis arises within how many months after valve surgery?
2-12 months
Late prosthetic valve endocarditis arises within how many months after valve surgery?
> 12 months
How many percent of coagulase-negative staphylococcus strain causing PVE are resitant to methicillin?
At least 68-85%
Most common cause of cardiovascular ICD endocarditis (2):
S. aureus
CoNS
Most commonly affected valve in injection drug-use-associated endocarditis? And the most common cause?
Tricuspid valve, S. aureus
Endocarditis with uninfected vegetations seen in patients with malignancy and chronic diseases
Marantic endocarditis
Adherence of gram positive bacteria in IE is facilitated by:
Fibronectin-binding proteins
Adherence of S. aureus in IE is facilitated by:
Clumping factor
Adherence of Enterococcus faecalis in IE is facilitated by (3):
Fibrinogen-binding surface proteins (Fss2)
Collagen-binding surface protein (Ace)
Ebp pili
Adherence of streptococcus in IE is facilitated by:
Glucans or FimA
Organisms deep in vegetations are metabolically active and relatively susceptible to killing by antimicrobial agents
Inactive, resistant to killing
How many % of IE patients will have CHF?
30-40%
Cause of CHF in IE (2):
Valve dysfunction Intracardiac fistulae (occasionally)
How many % of IE patients will have MI?
2%, due to emboli to a coronary artery
Classic nonsuppurative peripheral manifestation of IE that is related to prolonged infection
Janeway lesions
Arterial emboli in IE is increased in: (3)
S. aureus endocarditis
Mobile vegetations >10 mm in diameter
Infection involving the mitral valve (esp anterior leaflet)
How many % of IE patients will have cerebrovascular emboli?
15-35%
Endocarditis of which side will more likely cause cerebrovascular emboli?
Left-sided endocarditis
Focal dilations of arteries occurring at points in the artery wall that have been weakened by infection in the vasa vasorum or where septic emboli have lodged
Mycotic aneurysms
The diagnosis of infective endocarditis is established with certainty only when
vegetations are examined histologically and microbiologically
A highly sensitive and specific diagnostic schem for IE
Modified Duke Criteria
Clinical diagnosis of definite endocarditis based on Modified Duke Criteria
two major criteria, or one major criterion and three minor criteria, or of five minor criteria
Diagnosis of endocarditis is rejected if (3):
Alternative diagnosis is established
Symptoms resolve and do not recur with ≤4 days of antibiotic therapy
Surgery or autopsy after ≤4 days of antimicrobial therapy yields no histologic evidence of endocarditis
Possible IE
One major and one minor criterion
Three minor criteria
Modified Duke Critera: Major criteria (2)
Positive blood culture
o Typical microorganism for IE in 2 separate blood culture
o Persistently positive blood culture, defined as recovery of microorganism consistent with IE from blood cultures drawn > 12 h apart, or all of 3 or a majority of >/= 4 separate blood culture with 1st and last drawn at least 1 h apart
o Single positive blood culture for Coxiella burnetti or phase I IgG antibody titer of >1:800
Evidence of endocardial involvement
o Positive echocardiogram
o New valvular regurgitation
Positive echochardiogram findings of IE (3):
Oscillating intracardiac mass on valve or supporting structures or in path of regurgitant jets or in implanted material, in the absence of an alternative anatomic explanation
Abscess
New partial dehiscence of prosthetic valve
Minor criteria of Modified Duke Criteria (5)
Predisposing heart conditions or injection drug use
Fever≥ 38C
Vascular phenomena
Immunologic phenomena
Microbiologic evidence (positive blood culture not meeting major criteria, or serologic evidence)
Vascular phenomenon included in the modified duke criteria (6)
Major arterial emboli Septic pulmonary infarcts Mycotic aneurysm Intracranial hemorrhage Conjunctival hemorrhages Janeway lesions
Immunologic phenomena included in the modified duke criteria (4)
Glomerulonephritis
Osler’s nodes
Roth’s spots
Rheumatoid factor
How to obtain blood cultures for IE?
Three 2-bottle blood culture sets, separated from one another by at least 2 h, should be obtained from different venipuncture sites over 24 h
Treatment of Candida endocarditis
Amphotericin B (3–5 mg/kg IV qd) plus flucytosine (25 mg/kg PO q6h)
Empirical therapy for culture-negative endocarditis injection drug user or health care-assocaited NVE
Vancomycin plus gentamicin or cefepime
Empirical therapy for NVE with subacute presentation
Vancomycin plus ceftriaxone
Empirical therapy for blood culture-pending PVE
Vancomyci, gentamicin and cefepime if prothetic valve has been in place for ≤1 year
Similar to NVE if prosthetic valves in place for >1 year
Duration of antibiotic therapy if with CIED endocarditis and bacteremia that persist even after removal
4- to 6-week course
Duration of antibiotic therapy for generator pocket infection without bacteremia
10- to 14-day course
Anticoagulation must be given for IE. True or false
False. Patients with IE are at risk for emboli, for hemorrhagic transformation of embolic strokes, and for intracerebral hemorrhage from septic arteritis or ruptured mycotic aneurysms
The most common indications for surgery in IE (2)
Intracardiac complications
CHF
Indications of surgery in IE (5):
Congestive Heart Failure Perivalvular Infection Uncontrolled Infection Prevention of Septic emboli CIED Endocarditis
Most commonly affected valve in the perivalvular infection complication of IE
Aortic valve
Test of choice to detect perivalvular abscesses
TEE with color Doppler
In CIED endocarditis, when can you reimplant CIED if necessary?
At a new site 10-14 days of antimicrobial therapy
If surgical indication is not urgent, cardiac surgery should be delayed for _______ after a large nonhemorrhagic embolic infarction and ______ after a cerebral hemorrhage
2-3 weeks
4 weeks
Extracardiac complications of IE (2):
Splenic abscess
Mycotic aneurysm
Salmonella sp. that are restricted to human hosts, causing enteric (typhoid) fever (2)
Salmonella typhi and paratyphi
Salmonella:
Gram negative or positive?
Spore forming or not?
Aerobe or unaerobe?
Gram negative bacilli, non-spore-forming, facultatively anaerobic bacilli
Family of Salmonella
Enterobacteriaceae
Salmonella produce what gas on sugar fermentation? Salmonella that does not form this gas?
H2S
Salmonella typhi
Serogroup of salmonella that cause ~99% of infections in humans and other warm-blooded animals
O-antigen serogroups
Infectious dose of salmonella
200 CFU to 106 CFU
Characterized by infiltration of mononuclear cells into the small bowel mucosa
Enteric fever
infectous disease that is characterized by massive PMN leukocyte infiltration into both the large and small bowel mucosa
NTS gastroenteritis
Etiologic agents of enteric fever
S. Typhi and S. Paratyphi serotypes A, B and C
Incubation period of enteric fever
average of 10-14 days but ranges from 5-21 days
Which is milder, S. parathyphi or typhi?
Paratyphi
Rash of typhoid fever and found in how any percentage?
Rose spots – 30%
Faint, salmon-colored, blanching, maculopapular rash primarily in the trunk and chest, and evident at the end of the 1st week of typhoid fever
Rose spots
ECG findings in typhoid fever seen in <50% of cases
Relative bradycardia at the peak of high fever
Disease that has neuropsychiatric symptoms of “muttering delirium” or “coma vigil”, and picking at bedclothes or imaginary objects
Typhoid fever
Up to ____ of untreated salmonellosis will excrete S. Typhi in the feces for up ______, and _____ will be a chronic carrier up to ____.
10% - 3 months
2-5% - >1 year
Concomittant infection with this organism is a risk factor for chronic asymptomatic carriage of Salmonella
S. haematobium
Chronic asymptomatic carriage of salmonella will increase risk of what cancer
Gallbladder CA
In salmonellosis, if blood, bone marrow, and intestinal secretions are all cultured, the yield is
> 90%
Serologic test for typhoid fever for febrile agglutinins
Widal serologic tests
Most effective class of agents for drug-susceptible typhoid fever
Fluoroquinolones
Preferred fluoroquinolones for typhoid fever
Ciprofloxacin
Treatment for DSC Typhoid fever (3)
Ceftriaxone
Azithromycin
High dose ciprofloxacin
Treatment for MDR salmonellosis
Ceftriaxone
Cefotaxime
Cefixime
Treatment of complicated enteric fever and duration of treatment
IV 3rd gen cephalosporin or fluoroquinolone up to at least 10 days or for 5 days after fever resolution
Glucocorticoid used for enteric fever (include dose and indication)
Dexamethasone initial dose of 3 mg/kg then 8 doses of 1 mg/kg every 6 h
severe enteric fever
Treatment of chronic salmonella carriage and duration of treatment
Oral ciprofloxacin or other fluoroquinolones x 4 weeks
2 typhoid vaccines
Ty21a – oral live attenuated S. Typhi vaccine
Vi CPS – parenteral vaccine consisting of purified Vi polysaccharide from the bacterial capsule
DOC for MDR – nontyphoidal salmonellosis (2)
extended spectrum cephalosporins and fluoroquinolones
An illness that mimics inflammatory bowel disease that is seen in NT salmonellosis
Pseudoappendicitis
Antibiotics is not usually recommended in NT salmonellosis. Why?
may prolong fecal carriage
Bacteremia is most common in what organism causing NTS (2)?
Salmonella Choleraesuis and Salmonella Dublin
Suspected in elderly patients with prolonged fever and back, chest or abdominal pain developing after an episode of gastroenteritis
NTS Arteritis
Preemptive antibiotic treatment for NTS is given only to these populations (6)
- Neonates (up to 3 mos of age)
- > 50 years of age
- Athersosclerosis
- Immunosuppressed
- Cardiac valvular or endovascular abnormalities
- Significant joint disease
Treatment for NTS endocarditis and arteritis with duration:
- 6 weeks IV β-lactam antyibiotic (ceftriaxone or ampicillin)
- May also be given with IV ciprofloxacin
2 forms of Rabies
- Encephalitic
* Paralytic
Genus of rabies virus
Lyssavirus
Rabies virus is what kind of virus? DNA or RNA?
Single-stranded RNA virus, nonsegmented
Incubation period of rabies
20-90 days
In muscles, rabies bind to what receptor?
nicotinic Acetylcholine receptor on postsynaptic membranes at NMJ
Rabies virus spread centripetally along peripheral nerves toward the spinal cord or brainstem via _______. Virus then enters the CNS and rapidly disseminates to other regions of the CNS via ______ along neuroanatomic connections
retrograde fast axonal transport
fast axonal transport
T or F: Rabies virus prominently infect astrocytes
False. Neurons. Astrocytes infection is unusual
Pathologic changes in rabies include mononuclear inflammatory infiltration in the leptomeninges, perivascular regions, and parenchyma, including the microglial nodules called
Babes nodules
Most characteristic pathologic finding in rabies
Negri bodies
Eosinophilic cytoplasmic inclusions in brain neurons composed of rabies virus proteins and viral RNA
Negri bodies
T or F: neuronal death is responsible for the clinical disease in rabies
False. Neuronal dysfunction
Earliest specific neurologic symptoms that strongly suggest rabies (3):
- Paresthesias near the site of the exposure
- Pain near the site of the exposure
- Pruritus near the site of the exposure
Encephalitic (furious) form and paralytic form are seen in how many percent of rabies patients respectively
80%
20%
T or F: Episodes of hyperexcitability in rabies are typically followed by periods of complete lucidity that become shorter as the disease progresses
True
Early brainstem involvement in rabies present as
Hydrophobia
Aerophobia
T or F: Paralytic forms of rabies generally survive a few days shorter than those with encephalitic rabies
False. Longer.
Highly sensitive and specific test for rabies (2)
RT-PCR
Direct fluorescent antibody (DFA) testing (can be performed quickly)
Difference between rabies encephalitis and other acute encephalitis
Early brainstem involvement with preservation of consciousness
T or F: rabies has 100% mortality rate
False. Aggressive management with supportive care in critical care units has resulted in the survival of more than 15 patients with rabies. But is an almost uniformly fatal disease.
T or F: Rabies is nearly always preventable after recognized exposures with appropriate postexposure therapy during the early incubation period
True
Active immunization of rabies
Four 1 mL doses of rabies vaccine given IM in the deltoid area or anterolateral aspect of the thigh (children) at day 0, 3, 7, 14 (5th dose on Day 28 no longer recommended)
T or F: Rabies vaccine is contraindicated in pregnancy
False
Who should receive the passive immunization of rabies?
To all previously unvaccinated persons
When should rabies Ig be administered
Should be administered within 7 days after the 1st vaccine dose
Dose of Rabies Ig
20 iu/kg, or 40iu/kg (purified ERIG) infiltrated at the site of bite then the remaining dose given IM at distant site; If exposure is through mucous membrane, entire dose must be given as IM
T or F: Rabies Ig may be given at the same site as the vaccine
False. Not same site
Preexposure rabies vaccination is given at how many doses?
3 doses. Day 0, 7, and 21 or 28
When a previously immunized individual is exposed to rabies, when will you give booster dose?
2 doses. Day 0 and 3.
most common and frequent infections in humans
Respiratory virus infection
mark the transition between the upper and lower respiratory tracts
Vocal cords
Parts of lower respiratory tract (5)
- Trachea
- Bronchi
- Bronchioles
- Alveolar spaces
- Lung tissue
Upper respiratory tract • Sinuses • Middle-ear spaces • Eustachian tubes • Conjunctiva • Nasopharynx • Oropharynx • Larynx
Principal types of cells in the major airways (3)
- Cilated or nonciliated epithelial cells
- Goblet cells
- Clara cells
Wheezing is the constriction of lumen size of smooth muscles at the level of
Bronchioles
With narrowest lumen diameter of the airways
Bronchioles
Difficulty in inspiration associated with barky cough
Croup
Inflammation or infection of the larynx, trachea, and bronchi
Most common viral causes of serious lower respiratory tract disease (3)
- Influenza viruses
- RSV
- Human metapneumovirus
Most common cause of common colds
Rhinoviruses
Most common virus isolated in immunosuppressed patients with pneumonia during bronchoalveolar lavage
Cytomegalovirus
Influenza virus belong to what family?
Orthomyxoviridae
Influenza infection has high rate of complication with bacterial superinfection, most commonly with (2)
S. aureus and S. pneumoniae
Describe influenza virus
A single-stranded, segmented, negative-sense, RNA genome virus
Influenza virus that is most virulent for humans
Influenza A
Influenza that is composed of hemagglutinins and neuraminidase
Influenza A
Influenza that infect humans almost exclusively
Influenza B
A process that can make the zoonotic viruses (e.g avian or swine) more fit for replications in humans
Reassortment
RSV is from what genus and family?
Genus: Pneumovirus
Family: paramyxoviridae
Single-stranded, negative-sense, non-segmented, RNA virus that is one of the most common viral causes of severe lower respiratory tract illness in the elderly and in children
RSV
Infection with this virus early in life have strong association with subsequent asthma
RSV
Measles virus is from what genus and family?
Genus: Morbilivirus
Family: paramyxoviridae
Most contagious respiratory virus infection of humans
Measles virus
Clinical manifestations of measles (4)
- ≥ 3 days of high fever
- 3 Cs: cough, coryza and conjunctivitis
- Diffuse maculopapular rash appears within days of fever onset
- Koplik’s spots
Typical mucosal lesions in the mouth that appear briefly in measles
Koplik’s spots
Coxsackievirus belong to what family?
Picornaviridae
Enterovirus A
Causes hand-foot-and-mouth disease and herpangina
Coxsackievirus
Clinical syndrome of ulcers or small vesicles on the palate that often involves the tonsillar fossa associated with fever, difficulty swallowing, and throat pain
Herpangina
Clinical manifestation of epidemic pleurodynia
Acute illness characterized by sharp chest pain and fever
Epidemic herpangina is caused by
Echovirus 11
Describe structure of rhinovirus
Single-stranded, positive-sense RNA virus
Icosahedral and non-enveloped
Describe structure of adenovirus
Double-stranded DNA virus, non-segmented, <100 nm in diameter, non-enveloped, icosahedral morphology
Common in stressful or crowded living conditions and was first recognized among military recruits during WWII
Adenovirus
Most often associated with adenovirus types 4 and 7
When was the epidemic of SARS-CoV
Nov 2002 to July 2003
Mortality rate of SARS-CoV
10%
Mortality rate of MERS-Cov
35%
MERS-CoV may have emerged from what animals?
Bats
Herpes that mostly affects the oral cavity
HSV-1
Describe the structure of polyomaviruses
Small, double-stranded, DNA viruses, non-enveloped, icosahedral
Respiratory virus that may be oncogenic
Polyomavirus
Polyomavirus that can infect the respiratory system, kidney, or brain
JC virus
Polyomavirus that causes mild respiratory infection or pneumonia
BK virus
Major determinant of risk for symptomatic disease during respiratory virus infection
Age
T or F: Primary infection of respiratory virus is usually more severe than reinfection
True
Gold standard for diagnosing a respiratory viral infection
Virus isolation
Most sensitive and specific test for respiratory viral infection
RT-PCR
Neuraminidase inhibitors act on what influenza type
A and B
Neuraminidase inhibitors
Oseltamivir
Zanamivir
Peramivir
Laninamivir
Neuraminidase inhibitors that may cause bronchospasm in asthma and COPD
Zanamivir
Adamantanes are used for treatment of what influenza?
Influenza A
Nucleoside antimetabolite prodrug that is used as treatment for RSV infection
Ribavirin
Caused by point mutations in the H and N molecules of influenza
Antigenic drift
This is the reason why there is a need to produce new vaccines yearly
Antigenic drift
Reassortment of 2 viruses during co-infection of one individual or animal that may cause a pandemic
Antigenic shift
Most common cause of contact transmission of viruses
Poor hand hygiene
The basic level of infection control that is used in the care of all patients at all times
Standard precaution
The second level of infection control that is used and may require a single room for the patient when possible
Contact precaution
Range of large-particle droplets during transmission of virus
3 ft
T or F. Acute bacterial infection of joints typically involve multiple joints
False. single or a few joints only
Immunologic reaction of joints during course of endocarditis, rheumatic fever, disseminated neisserial infection, and acute hepatitis B
Acute polyarticular arthritis
Cell count in normal synovial fluid
<180 cells per microliter
Predominant cell in normal synovial fluid
mononuclear
Cell count in synovial fluid during acute bacterial infection
Cell count of 25,000 – 250,000/uL
> 90% neutrophils
Cell count in synovial fluid of crystal-induced, rheumatoid, and noninfectious inflammation
<30,000-50,000/uL
Cell count in synovial fluid during mycobacterial and fungal infection
10,000 – 30,000/uL
50-70% neutrophils and the remainder lymphocytes
Mode of transmission of acute bacterial arthritis
o Hematogenous infection
o Direct inoculation
Most mode of transmission of acute bacterial arthritis
Hematogenous route
Most common bacteria isolated in acute bacterial arthritis in young adults and adolescents
N. gonorrheae
Most common nongonococcal bacteria isolated in acute bacterial arthritis in adults
S. aureus
Most common bacteria isolated in acute bacterial arthritis that is post-surgical or trauma-induced
S. aureus
Penetration of a sharp object through a shoe will cause an arthritis in the foot caused by what organism
Pseudomonas aeruginosa
Highest incidence of infective arthritis occurs in patients with
Rheumatoid arthritis
Most common cause of infectious arthritis among patients with rheumatoid arthritis
S. aureus
Infectious arthritis that is most often seen in primary iimmunoglobulin deficiency
Mycoplasmal arthritis
treatment of mycoplasmal arthritis (2)
tetracycline and IV immunoglobulin
Most commonly involved joint in the acute bacterial arthritis
Knee
Most commonly involved joints in the acute bacterial arthritis among IV drug users (3)
Spine, sacroiliac joints, and sternoclavicular joints
On plain radiograph, this indicates advanced infection with poor prognosis
Narrowing of the joint space and bony erosions
T or F: Men are more likely to develop disseminated gonococcal infection (DGI) and arthritis than women
False. Women are more likely, especially during menses and pregnancy
Small number of papules that progress to hemorrhagic pustules in the trunk and extensor surfaces of the distal extremities associated with migratory arthritis and tenoxynovitis of the knees, hands, wrists, feet and ankles
Disseminated Gonococcal Infection
T or F. In true gonococcal septic arthritis, blood culture is almost always negative
True
Agar used to isolate organism in gonococcal arthritis
Thayer-Martin agar
This supports a clinical diagnosis of the disseminated gonococcal syndrome if cultures are negative
Dramatic alleviation of symptoms within 12-24 h after the initiation of appropriate antibiotic therapy
Treatment for gonococcal arthritis
Ceftriaxone 1g IV or IM every 24 h
Once local and systemic signs are clearly resolving, 7-day course of therapy can be completed with an oral fluoroquinolone such as ciprofloxacin 500 mg BID and Amoxicillin 500 mg TID
Aside from treating the gonococcal arthritis with ceftriaxone or ciprofloxaciin, what other antibiotic will you give and for what reason?
Azithromycin 1g single dose
they should be treated for Chlamydia trachomatis infection also
Cause of lyme disease
Borrelia burgdorferi
Lyme diseaseis transmitted by
Ixodes tick
Antibiotic treatment of lyme disease (3)
Oral doxycycline 100 mg BID for 28 days
Oral amoxicillin 500 mg TID for 28 days
IV ceftriaxone 2g/day for 2-4 weeks
Periarticular swelling and immobilization of the involved limbs complicate osteochondritis of long bones in congenital syphilis
Parrot’s pseudoparalysis
Late joint manifestation of congenital syphilis caused by painless synovitis with effusions of large joints
Clutton’s joint
Joint deformity that result from sensory loss due to tabes dorsalis
Charcot joint
in tertiary syphilis
Most common presentation of mycobacterial arthritis
Chronic granulomatous monoarthritis
Unusual syndrome which is a reactive symmetric form of polyarthritis that affects persons with visceral or disseminated tuberculosis
Poncet’s disease
Most common cause of fungal arthritis (3)
Coccidioids immitis
Blastomyces dermatitidis
Histoplasma capsulatum
Treatment of fungal arthritis
amphotericin (IV and intraarticular)
T or F. In management of infections of prosthetic joints, prosthesis must be always replaced
False.
Prosthesis may not be removed if:
o In cases of streptococci or pneumococci
o Lack of radiologic evidence of loosening of the prosthesis
o Antibiotic therapy must be initiated within several days of the onset of infection
o Joint should be drained vigorously by open arthrotomy or arthroscopically
Therapy that has a high cure rate with retention of prosthesis in infections of prosthetic joints
Oral rifampin plus another antibiotic
Trematodes are also known as
flatworms
Trematodes belong to what phylum?
Platyhelminthes
All the trematodes are hermophriditic except for
Shistosomes
Definitive host of trematodes
mammal / humans
Infective stage of Schistosoma
Cercariae
Cercariae of the schistosomes penetrate intact human skin within a few minutes after attaching to the skin then transform to
shistosomula
Where does the schisosomes mature to adult males and females
portal vein
Final location of adult schistosomes (2)
mesenteric or pelvic venous plexus
Interval from schistosome cercarial penetration to sexual maturation and egg production
Prepatent period
5-7 weeks
Free-swimming larval stage of schistosomes
miracidium
Life cycle of schistosomes that penetrate the host snail then undergoes asexual multiplication
miracidium
The only stage of the schistosome that is detected in humans
egg
Schistosome egg that has terminal spine
S. haematobium eggs
Schistosome egg that has lateral spine
S. mansoni eggs
Schistosome egg that is smaller, rounder, with a small lateral spine or knob
S. japonicum eggs
Body forms a groove or gynecophoric canal in which the mature adult female is held
Male schistosome
Compared to male schistosome, female worm is
Longer, thinner, and rounded
Humans are the most important definitive hosts for these schistosomes (3)
S. mansoni,
S. haematobium,
S. intercalatum
Zoonotic schistosomes
S. japonicum and S. mekongi
The most important of the neglected tropical diseases and is second only to malaria in public health impact
• Schistosomiasis
T or F: Most manifestations of schistosomiasis are due to immunologic reactions to worms retained in host tissues
False. Eggs
Egg, and not the adult worms, induce the organ-specific morbidity
Schistosome species that cause hepatosplenomegaly (2)
S. mansoni
S. japonicum
Schistosome egg-induced granulomatous response leads to this severe periportal fibrosis
Symmers clay pipestem fibrosis
S. haematobium has predilection to what veins
urogenital plexus
This schistosome can cause intense egg-induced tissue inflammation leading to bladder wall thickening and development of masses and pseudopolyps
S. haematobium
Swimmer’s itch is caused by
Schistosomes
Cause of swimmer’s itch
cercarial penetration of the skin
causes severe form of cercarial dermatitis
Avian schistosomes
Cannot complete development in humans and die in the skin leading to inflammatory allergic reaction
Treatment of cercarial dermatitis
Systemic or topical antihistamines or glucocorticoids
to reduce symptom only
Acute schistosomiasis is also known as
Katayama fever
Onset of katayama fever is how many weeks/months after exposure?
2 weeks to 3 months
Symptoms of Katayama fever (6)
o Fever o Myalgia o General malaise and fatigue o Headache o Nonproductive cough o Abdominal tenderness or pain
Liver is enlarged (especially the left lobe) smooth, and firm with no hepatic fibrosis on USD is manifestation of what infection?
Hepatosplenic Schistosomiasis
Early inflammatory hepatosplenomegaly
Left hypochondrial mass with discomfort and anorexia, and with USD of typical periportal fibrosis and dilation of the portal vein is manifestation of what infection?
Hepatosplenic schistosomiasis
Late hepatosplenic disease with periportal or Symmers fibrosis
Most severe complication of hepatosplenic schistosomiasis
hematemesis
Characteristic sign of active stage of urogenital schistosomiasis
Painless, terminal hematuria
Manifests as nocturia, urinary retention, dribbling, and incontinence, and with cystoscopic findings of “sandy patches”
Chronic stage of urogenital schistosomiasis
Schistosome that is classified as definitely carcinogenic to humans (group 1 carcinogen) and what cancer does to cause?
S. haematobium
May cause squamous cell carcinoma of the urinary bladder
Schistosomes that can end up in the spinal venous plexus (2) and the condition that they cause
S. mansoni and S. haematobium
transverse myelitis
Schistosome that causes granulomatous lesions in the brain
S. japonicum
Rectal biopsies can detect what schistosomes (2)
S. mansoni and S. haematobium
Serology that is used by CDC to detect schistosomiasis
Falcon assay screening test / enzyme-linked immunosorbent assay (FAST-ELISA)
Use S. mansoni adult microsomal antigen
Drug of choice for all forms of schistosomiasis
Praziquantel
Cornerstone of management and control
Praziquantel mass administration programs
Most important liver flukes causing human infections (4)
o Opistorchis viverrini and Opistorchis felineus
o Clonorchis sinensis
o Fasciola hepatica
o Fasciola gigantica
1st and 2nd intermediate hose of opistorchiasis and clonorchiasis
host snail
fresh water fish
Infective stage of opistorchiasis and clonorchiasis
metacercariae
Tretamatodes that may cause cholangiocarcinoma
Opistorchiasis
Clorchis sinensis
2nd intermediate host of Fasciola hepatica
None
metacercariae adhere directly to aquatic plans such as watercress
Intestinal fluke
Fasciolopsis buski
Lung fluke
Paragonimus westermani
2 intermediates host of paragonimus
o Freshwater snail
o Freshwater crustacean
Infective stage of paragonimus westermani
metacercariae
2 DOC for trematode infection
o Praziquantel
o Triclabendazole
Based on RITM guidelines, what is Stage I, II and III of tetanus based on incubation period
I - > 14 days
II - > 10-14 days
III - <10 days
Based on RITM guidelines, what is Stage I, II and III of tetanus based on period of onset
I - > 6 days
II - > 3-6 days
III - <3 days
Based on RITM guidelines, what is Stage I, II and III of tetanus based on trismus
I - mild
II - moderate
III - severe
An acute illness with muscle spasms or hypertonia in the absence of a more likely diagnosis than tetanus
Probable tetanus
an illness occurring in a child who has the normal ability to suck and cry in the first 2 days of life but who loses this ability between days 3 and 28 of life and becomes rigid and has spasms
Neonatal tetanus
Maternal tetanus occus during pregnancy or within _____ after the conclusion of pregnancy (whether with birth, miscarriage, or abortion) – WHO
6 weeks
Describe C. tetani in terms of:
aerobic vs anaerobic
gram + vs -
spore-forming vs non-spore-forming
coccus vs bacilli
an anaerobic, gram-positive, spore-forming rod whose spores are highly resilient and can survive readily in the environment throughout the world
In______% of cases of tetanus, no puncture entry wound is found.
20–30%
the most common infection sites of tetanus in adults
Superficial abrasions to the limbs
Difference between tetanospasmin and botulinum toxin in terms of transport to CNS
Tetanospasmin undergoes retrograde transport into the CNS (unlike the botulinum toxin) and thus produces clinical effects different from the botulinum toxin
Botulinum toxins remain at the NMJ
Aim of management of tetanus infection (2)
o Neutralize remaining unbound toxin
o Support vital functions
In generalized tetatnus,, which part is affected first most often?
muscles of the face and jaw
Milder form of tetanus
Localized tetanus
Difference between incubation period and period of onset in tetanus
o Incubation period – time from wound to first symptom
o Period of onset – time from first symptom to first generalized spasm
T or F. In tetanus, shorter incubation period and/or period of onset has worse outcome
True
The most common cause of death in tetanus without ventilatory support
Respiratory failure
Labile BP with rapid fluctuations from high to low accompanied by tachycardia in tetanus is caused by
autonomic dysfunction
Aside from labile BP, autonomic involvement of tetanus is evidenced by (4)
Gastrointestinal stasis
Sweating
Increased tracheal secretions
Acute (often high-output) renal failure
Level of serum anti-tetanus IgG (measured by standard ELISA) that is protective and do not support the diagnosis of tetanus
> 0.1 IU/mL
Preferred antibiotic therapy for tetanus (with dose)
Metronidazole 400 mg rectally or 500 mg IV every 6 h for 7 days
Alternative antibiotic for tetanus (with dose)
Penicillin 100,000–200,000 IU/kg per day
Theoretically, this drug may exacerbate spasms and in one study was associated with increased mortality in tetanus
Penicillin
Preparation of choice of tetanus antitoxin (with dose)
Human tetanus immune globulin (TIG)
Single IM dose (3000–5000 IU) is given with a portion injected around the wound
Dose of equine antitoxin for tetanus
10,000–20,000 U is administered IM as a single dose or as divided doses
These drugs used in tetanus to control spasm by sedation (2)
Benzodiazepines
Propofol infusion
T or F: In treating the cardiovascular instability in tetanus, long-acting drug are preferred
False. Short-acting drugs that allow rapid titration are preferred.
Longer-acting drugs such as β antagonists may cause hypotensive cardiac arrest
Recovery from tetanus may take up to
4–6 weeks
How do you give the “Catch-up” schedules for tetanus vaccination?
3-dose primary course with 4 weeks between doses followed by 2 boosters 6 months apart
For persons who have received a complete primary course of tetanus vaccine in childhood but no further boosters, how many doses should you give?
Two doses at least 4 weeks apart are recommended
T or F. Patients with incomplete or unknown tetanus vaccination or last booster given > 10 years of earlier must be vaccinated but may not be given with TIG.
False. Must also be given passive immunization with TIG
WHO recommendation for prevention of maternal and neonatal tetanus
Administration of two doses of tetanus toxoid at least 4 weeks apart to previously unimmunized pregnant women
In high-risk areas: more intensive approach. All women of childbearing age must receive a primary course along with education on safe delivery and postnatal practices
Factors associated with a poor prognosis in adult tetanus in terms of: Age incubation period time from onset to admission entry site period of onset heart rate SBP spasms temperatur
Age >70 years Incubation period <7 days Short time from first symptom to admission Puerperal, IV, postsurgery, burn entry site Period of onset <48 h Heart rate >140 beats/min Systolic blood pressure >140 mmHg Severe disease or spasms Temperature >38.5°C
Vibrio cholerae need ____ bacteria to cause disease
10^5-10^8
Produces an adherence protein called colonization factor antigen necessary for colonization of the upper small intestine by the organism prior to production of enterotoxin
Enterotoxigenic E. coli
3 exotoxins causing vomiting/diarrhea
Enterotoxins
Cytotoxins
Neurotoxins
Prototypical enterotoxin
Cholera toxin
Exotoxin that cause watery diarrhea by acting directly on secretory mechanisms in the intestinal mucosa
Enterotoxins
Part of cholera toxin that contains the enzymatic activity of the toxin
A subunit
Part of cholera toxin that binds holotoxin to the enterocyte surface receptor (GM1)
B subunits
Cholera toxin causes diarrhea by
Increasing Cl secretion and decreasing Na absorption causing loss of fluid
Exotoxin that cause inflammatory diarrhea
Cytotoxins
Cause destruction of mucosal cells
This exotoxin produce syndrome of dysentery, with bloody stools containing inflammatory cells
Cytotoxins
Shigella dysenteriae type 1 and Shiga toxin producing E. coli strains
More than 99% of the normal colonic microbiota is made up of
anaerobic bacteria
T or F. Neutralization of gastric acid with antacids, PPIs, or H2 blockers increase risk of enteric colonization
True
The major mechanism for clearance of bacteria from the proximal small intestine
Normal peristalsis
Opiates can cause increased frequency of bacterial overgrowth and infection of the small bowel with enteric pathogens by
Impairing intestinal motility
As well as other antimotility drugs, anatomic abnormalities, or hypomotility states
Blood group with increased susceptibility to disease due to V. cholerae, Shigella, E. coli O157, and norovirus
O Blood Group
marker of fecal leukocytes
Fecal lactoferrin
HUS syndrome follows infection with (3)
Shiga toxin-producing bacteria
Shigella dysebteriae type 1 and enterohemorrhagic E. coli
GBS is commonly associated with what infection Shigella dysebteriae type 1 and enterohemorrhagic E. coli
Campylobacter infection
most common travel-related infectious illness
Traveler’s diarrhea
Single most important cause of Traveler’s diarrhea
Enterotoxigenic strains of E. coli
Enteroaggregative strain is also common
Traveler’s diarrhea that is associated with cruise ship is often caused by
Novovirus
Traveler’s diarrhea that is common among hikers and campers who drink from fresh water streams
Giardia lamblia
Most common etiologic agent associated with outbreaks of AGE
Novovirus
Predominant cause of nosocomial diarrhea among adults
C. difficile
Caused more than ½ of cases of significant diarrheal illness in elderly patients in chronic-care institutions
C. difficile
Identified as a cause of antibiotic-associated hemorrhagic colitis
Klebsiella oxytoca
Most morbidity and mortality from enteric pathogens occurs at what age
< 5 years of age
Bacteria that cause disease by enterotoxin elaborated outside the host (2)
S. aureus and B. cereus
Incubation period and duration for bacterial disease caused by an enterotoxin elaborated outside the host
1-6 h
<12 h
Outbreaks following picnics where potato salad, mayonnaise, and cream pastries have been served is commonly caused by
Staphylococcal food poisoning
2 forms of B. cereus food poisoning
Emetic
Diarrhea
Emetic form of B. cereus food poisoning is mediated by what toxin
staphylococcal type of enterotoxin (shorter incubation)
Diarrheal form of B. cereus food poisoning is mediated by what toxin
enterotoxin resembling E. coli heat-labile toxin (longer incubation period)
(8-16 )
Heat-resistant spores of this bacteria is found in inadequately cooked meat, poultry, or legumes
Clostridium perfringens
T or F. All food poisoning has bacterial cause.
False. Not all food poisoning has bacterial cause.
Other causes:
Capsaicin
Toxins from fish and shellfish
Mainstay of treatment of acute infectious diarrheal diseases
Adequate rehydration
Per L water of ORS consists (4)
- 2.6 g NaCl
- 2.9 g trisodium citrate
- 1.5 g KCl
- 13.5 g glucose (or 27 g sucrose)
T or F. Bloody diarrhea should be treated empirically with an antimicrobial agent
True. fluoroquinolone or macrolide
But, Enterohemorrhagic E. coli should NOT be treated with antimicrobial agents because it will increase by 20-fold the risk for HUS and renal failure
Treatment of Campylobacter infection
Macrolide such as erythromycin or azithromycin
Enterohemorrhagic E. coli should NOT be treated with antimicrobial agents because it will increase by 20-fold the risk for
HUS and renal failure
Malaria is transmitted by the bite of
infected female Anopheles mosquitoes
Most important of the parasitic diseases of humans
Malaria
Almost all malaria deaths are caused by what sp
falciparum malaria
Female anopheles mosquito inoculates this life stage of malaria to humans during blood meal
Sporozoites
Asexual reproduction of malaria occurs in
Liver
intrahepatic or preerythrocytic schizogony
During asexual reproduction of malaria, sporozoites produce
10,000->30,000 merozoites
Stage of malaria that invade the RBC
Merozoites
Once at the RBC, the malarial stage is called
Trophozoites
When malaria reach densities of__________, symptomatic stage begins
~50/μL of blood (~100 million parasites)
Dormant form of malaria parasite
hypnozoites
A proportion of intrahepatic forms of these plasmodium sp do not divide immediately but remain inert for a period of 2 weeks to ≥1 year (2)
P. vivax and P. ovale
Hypnozoites - cause of the relapses in these species
Blood group antigens that plays an important role in invasion of malaria
Duffy blood group antigens – Fya or Fyb
Duffy-negative FyFy phenotype – generally resistant to P. vivax malaria
By the end of the intraerythrocytic life cycle, the plasmodium has consumed 2/3 of the RBC’s hemoglobin and has grown to occupy most of the cell. This is then called
Schizont
When plasmodium-infected RBC ruptures, it release
6-30 daughter merozoite
Malaria disease in human beings is caused by (2)
- Direct effects of asexual parasite (RBC invasion and destruction)
- Host’s reaction
Sexual form of malaria
Gametocytes
Life stage of malaria that are ingested by biting female anopheles mosquito
Gametocytes
Malarial morphology: usually only ring-form, banana-shaped gametocytes
Falciparum
Malarial morphology: irregularly shaped large rings and trophozoites, enlarged erythrocytes and Schuffner’s dots
P. vivax
Malarial morphology: infected erythrocytes, enlarged and oval with tufted ends; Schuffner’s dots
P. ovale
Malarial morphology: band or rectangular forms of trophozoites
P. malariae
Pigment colors of the malarial species
Falciparum – black
Vivax – yellow-brown
Ovale – dark brown
Malariae – brown-black
Malaria sp that may have relapse
Vivax and ovale
Endemicity of malaria in Hypoendemic, Mesoendemic, Hyperendemic and Holoendemic
- Hypoendemic - <10%
- Mesoendemic – 11-50%
- Hyperendemic – 51-75%
- Holoendemic – >75%
Characteristic of malarial transmission seen in hyper- and holoendemic areas
Stable transmission
constant, frequent, year-round infection
Characteristic of malarial transmission seen in hypoendemic areas
Unstable tansmission
Transmission is low, erratic, or focal
Full protective immunity is not acquired
Malaria can behave like an epidemic disease
High mortality rates among all age group
Principal determinants of epidemiology of malaria (3)
- Number / density of anopheline mosquito
- Human-biting habits of anopheline mosquito
- Longevity of anopheline mosquito
Number of sporozoite-positive mosquito bites per person per year is also called
Entomologic inoculation rate
Most common measure of malaria transmission
Entomologic inoculation rate
Effect of malaria to RBC
Alters the RBC membrane
RBCs become more irregular in shape, more antigenic, and less deformable
Processes that are central to pathogenesis of P. falciparum infections (3)
Cytoadherence
Resetting
Agglutination
This pathogenetic process of malaria refers to attachment to receptors on venular and capillary endothelium mediated by strain-specific erythrocyte membrane adhesive protein (PfEMP1)
Cytoadherence
This pathogenetic process of malaria refers when infected RBCs adhere to uninfected RBCs
Resetting
This pathogenetic process of malaria refers when infected RBCs adhere to other parasitized erythrocyte
Agglutination
Plasmodium sp with marked predilection for young RBCs (2)
P. vivax and P. ovale
Plasmodium sp with predilection to old RBCs
P. malariae
Plasmodium sp that can invade RBCs of all ages (2)
P. falciparum
P. knowlesi
Process when spleen removes damaged ring-form malarial parasites
Pitting
Spleen returns the once-infected RBC to the circulation shortened survival
Rupture of schizont – happens to those cells escaping splenic removal
This host response to malaria is defined by accelerated removal of both parasitized and uninfected RBCs
Augmented splenic immunologic and filtrative clearance
Genetic disorders that confer protection against death from falciparum malaria (5)
- Thalassemias
- Sickle cell disease
- Hemoglobins C and E
- Hereditary ovalocytosis
- G6PD deficiency
Reason why thalassemia patients are protected against malarial death
α- thalassemia have frequent malaria in early years of life, hence, protection from severe disease
Reason why sickle cell disease patients are protected against malarial death
HbA/S RBCs impair parasite growth at low oxygen tensions
6-fold reduction in the risk from of dying from severe falciparum malaria
Reason why hereditary ovalocytosis patients are protected against malarial death
Rigid RBCs resist merozoite invation
state of plasmodium infection without illness
Premunition
Fever spikes, chills, and rigors at regular intervals is characteristic of
Malaria
Classic malarial paroxysms
Generalized seizure occur to this malaria type
falciparum malaria
Herald the development of encephalopathy in cerebral malaria
If malaria is appropriately and promptly treated, mortality rate is
< 0.1%
Once vital-organ dysfunction occurs or total proportion of RBC infected by malaria increases to ____________, mortality risk rises steeply
> 2% (>10^12 parasites in adult)
A characteristic and ominous feature of cerebral malaria caused by falciparum
Coma
Death rate: ~20% among adults and 15% among children
Cerebral malaria manifest as what type of encephalopathy
diffuse symmetric encephalopathy
Primitive reflexes that are common in cerebral malaria (2)
Bruxism and pout reflex
Other primitive reflexes are absent
Hypoglycemia in malaria may be compounded by these antimalarial treatment
Quinine and quinidine
Powerful stimulant of pancreatic insulin, causes hyperinsulinemic hypoglycemia
Conditions that compounds acidosis in adults and children with malaria
Renal impairment – adult
Ketoacidosis – children
Best biochemical prognosticators in severe malaria (2)
Serum bicarbonate or lactate
Mortality rate of noncardiogenic pulmonary edema in severe malaria
> 80%
Renal impairment in malaria manifests as
acute tubular necrosis
Description of anemia in malaria
Normocytic, normochromic
Acute hemolytic anemia with massive hemoglobinuria seen in malaria
Blackwater fever
- Hemoglobinuria may contribute to renal injury
- May be seen in patients with G6PD deficiency
Antimalarial treatment that may have sudden hemolysis many days after treatment
Artesunate
Due to synchronous loss of once-parasitized “pitted” RBCs
T or F: Pregnant mothers in areas with stable malarial transmission are prone to severe infections
False.
In areas with stable transmission, pregnant mothers remain asymptomatic despite intense accumulation of parasitized erythrocytes in the placental microcirculation
In areas with unstable transmission, pregnant women are prone to severe infections
T or F. Incubation period of transfusion malaria is longer
False. Incubation period is short – because there is no preerythrocytic stage
Clinical features of hyperreactive malarial splenomegaly (3)
- Abdominal mass
- Dragging sensation in the abdomen
- Perisplenitis
Chronic or repeated infections with P. malariae (or other malarial species) may cause soluble immune complex injury to the renal glomeruli leading to nephrotic syndrome. This condition is called
Quartan malarial nephropathy
Histology of quartan malarial nephropathy (2)
Focal or segmental glomerulonephritis
Splitting of capillary basement membrane
Diagnosis of malaria is obtained by
demonstration of asexual forms of parasite in stained PBS
Preferred Romanowsky stains used in malaria detection
Giemsa at pH 7.2
Other stains:
• Field’s
• Wright’s
• Leishman’s
Diagnostic stain of malaria that is fixed and density of parasitemia is expressed by number of parasitized RBC per 1000 RBCs
Thin blood smears
Diagnostic stain of malaria that is not fixed and number of parasites per unit volume is calculated from the total leukocyte count then converted to number of parasitized RBCs per microliter
Thick blood smear
First-line treatment for uncomplicated falciparum malaria in malaria-endemic areas
Artemisinin-based combination therapy (ACT)
Remains an effective treatment for P. vivax, P. ovale, and P. malariae
Chloroquine
Tinnitus, high-tone hearing loss, nausea, vomiting, dysphoria, postural hypotension are manifestations of this ADR of antimalarial drugs. What is this ADR and what are the antimalarial drugs that may cause it?
cinchonism
Quinine and quinidine
Antimalarial drug that has the ADR of agranulocytosis and hepatotoxicity
Amodiaquine
Antimalarial drug that is contraindicated in G6PD patients
Primaquine
May actually be used by with lower dose
Antimalarial drug that eradicates hepatic forms of P. vivax and P. ovale; kills all stages of P. falciparum gametocyte development; kills developing liver stages of all species
Primaquine
Drug of choice for all patients with severe malaria
Parenteral artesunate
If unavailable, may use artemether, quinine or quinidine
T or F. Fluid management of malaria is similar to that of sepsis
False.
Fluid boluses are potentially dangerous un severe malaria
In severe malaria, this antimalarial drug must be avoided because it can increase risk of post-malaria neurologic syndrome
Mefloquine
Artemisinin derivatives (3)
- Artesunate
- Artemether
- Dihydroartemisinin
Used for radical treatment of malaria
Primaquine
Antimalarial drug that has adverse neuropsychiatric reaction
Mefloquine
These antimalarial drugs exacerbate the orthostatic hypotension associated with malaria
Quinolines (chloroquine, mefloquine, and quinine)
If the level of malarialparasitemia does not fall below ___ of the admission value in 72 h or if parasitemia has not cleared by____, drug resistance is likely and the regimen should be changed
25%
7 days
Treatment of acute renal failure in malaria
Renal replacement therapy
Hemofiltration or hemodialysis
Suspected when condition of any patient suddenly deteriorates for no obvious reason during antimalarial treatment
Sepsis
Used in mass treatment of malaria for focal elimination of falciparum malaria
slowly eliminated antimalarials such as dihydroartemisinin-piperaquine
Peak feeding times of anopheles
dusk to dawn
Chemoprophylaxis for malaria (3).
Atovaquone-proguanil (Malarone)
Doxycycline
Mefloquine
Other drugs may also be used
Once-daily chemoprophylaxis for malaria that is effective in ALL types of malaria including MDR falciparum malaria
Atovaquone-proguanil (Malarone)
Only drug advised for pregnant women traveling to areas with drug-resistant malaria
Mefloquine
- Choloroquine and proguanil – safe, but recommended in very few regions only
- Doxycycline – safe until 15 weeks of pregnancy
Duration of malarial chemoprophylaxis for travelers.
Antimalarial drugs 2 days to 2 weeks before departure, continued for 4 weeks after leaving an endemic area
Exceptions: Atovaquone-proguanil or primaquine – discontinued 1 week after departure from endemic area
Have a “dewdrop” appearance and develop in crops randomly about the trunk, extremities, and face over 3–4 days
Varicella
Occurs in a single dermatome and appearance of vesicles is preceded by pain for several days
Herpes zoster
HSV found on or around the lips
HSV-1
HSV found on the genitals
HSV-2
Herpes infection in head and neck of young wrestlers
Herpes gladiatorum
Herpes infection in the digits of health care workers
Herpetic whitlow
Hands-foot-mouth disease is caused by
Coxsackievirus A16
A painful, vesicular, localized S. aureus or group A streptococcal infection of the pulps of the distal digits of the hands.
Blistering dactylitis
Infection caused by a toxin (exfoliatin) from phage group II S. aureus
Staphylococcal scalded-skin syndrome (SSSS)
Impetigo contagiosa is caused by
S. pyogenes
Bullous impetigo is caused by
S. aureus
most common cause of localized folliculitis
S. aureus
Inflammation of sweat glands that mimic infection of hair follicles, particularly in the axillae
Hidradinitis suppurativa
Hot-tub folliculitis is caused by
Pseudomonas aeruginosa
Cat-scratch disease and Bacillary angiomatosis are caysed by
Bartonella henselae
Raised serpiginous or linear eruptions caused by burrowing larvae of dog or cat hookworms (Ancylostoma braziliense)
Cutaneous larva migrans
This is transmitted mostly in persons bitten by Simulium flies in Africa that may cause blindness
Onchocerca volvulus
Begins as a pruritic papule then develops within days into an ulcer with surrounding vesicles and edema and then into an enlarging ulcer with a black eschar. They may also cause chronic nonhealing ulcers with an overlying dirty gray membrane.
Cutaneous anthrax
Painful ulcerated lesions on the genitals
Chancroid
Ulcerated painless lesions on the genitals
Primary syphilis
Cause of erysipelas
S. pyogenes
An abrupt onset of fiery-red swelling of the face or extremities associated with intense pain
Erysipelas
Desquamation of the involved skin occurs 5–10 days into the illness
Treatment of erysipelas
Penicillin
Most common cause of purulent cellulitis
S. aureus
Most common cause of nonpurulent cellulitis
S. pyogenes
More rapidly spreading, diffuse process that is frequently associated with lymphangitis and fever
Elevated serum IgE is seen in patients with
Job syndrome
Cellulitis acquired by cat bites is caused by
Pasteurella multocida
P. aeruginosa causes three types of soft tissue infection, which are
Ecthyma gangrenosum in neutropenic patients
Hot-tub folliculitis
Cellulitis following penetrating injury
Necrotizing fasciitis is caused by
group A Streptococcus or mixed aerobic–anaerobic bacteria
Necrotizing fasciitis associated with gas gangrene is caused by
Clostridium perfringens
Necrotizing fasciitis may also be caused by strains of MRSA that produce this toxin
Panton-Valentine leukocidin (PVL) toxin
Massive swelling of the scrotum and penis with extension into the perineum or the abdominal wall and the legs
Fournier’s gangrene
Most common cause of pyomyositis
S. aureus
Gas gangrene of the uterus is caused by
Clostridium sordellii
Uniformly fatal and death ensues rapidly
Primary treatment of animal bite (prophylaxis or early infection)
Amoxicillin–clavulanate (875/125 mg PO bid)
Alternative: Doxycycline (100 mg PO bid)
Primary treatment of animal bite with established infection
Ampicillin–sulbactam (1.5–3 g IV q6h)
Alternative: Clindamycin (600–900 mg IV q8h) plus Ciprofloxacin (400 mg IV q12h) or cefoxitin (2 g IV q6h)
Primary treatment of herpex simplex infection
Acyclovir (400 mg PO tid for 10 days)
Alternative: Famciclovir (250 mg PO tid for 5–10 days) or valacyclovir (1000 mg PO bid for 10 days)
Primary treatment of herpex zoster infection
Acyclovir (800 mg PO 5 times daily for 7–10 days)
Alternative: Famciclovir (500 mg PO tid for 7–10 days) or valacyclovir (1000 mg PO tid for 7 days)
Primary treatment of Cellulitis (staphylococcal or streptococcalb,c)
Nafcillin or oxacillin (2 g IV q4–6h)
Alternative: Cefazolin (1–2 g q8h) or ampicillin/sulbactam (1.5–3 g IV q6h) or erythromycin (0.5–1 g IV q6h) or clindamycin (600–900 mg IV q8h)
Primary treatment of MRSA skin infection
Vancomycin (1 g IV q12h)
Alternative: Linezolid (600 mg IV q12h)
Primary treatment of Necrotizing fasciitis (group A streptococcal)
Clindamycin (600–900 mg IV q6–8h) plus penicillin G (4 million units IV q4h)
Alternative: Clindamycin (600–900 mg IV q6–8h) plus a cephalosporin (first- or second-generation)
Primary treatment of Necrotizing fasciitis (mixed aerobes and anaerobes)
Ampicillin (2 g IV q4h) plus clindamycin (600–900 mg IV q6–8h) plus ciprofloxacin (400 mg IV q6–8h)
Alternative: Vancomycin (1 g IV q6h) plus metronidazole (500 mg IV q6h) plus ciprofloxacin (400 mg IV q6–8h)
Primary treatment for gas gangrene
Clindamycin (600–900 mg IV q6–8h) plus penicillin G (4 million units IV q4–6h)
Alternative: Clindamycin (600–900 mg IV q6–8h) plus cefoxitin (2 g IV q6h)
Infections are associated with relative bradycardia. Patients have a lower heart rate than might be expected for a given body temperature. What do you call this sign?
Faget’s sign
For every 1°C (1.8°F) increase in core temperature, the heart rate typically rises by
15–20 beats/min
Indirect measures of acute-phase response
Erythrocyte sedimentation rate (ESR)
Changes relatively slowly, and its measurement more often than weekly usually is not useful
Direct measures of acute-phase response
C-reactive protein (CRP)
Change rapidly, and daily measurements can be useful
Specific situations that might prompt an infectious disease consult include (4)
Difficult-to-diagnose patients with presumed infections
Patients who are not responding to treatment as expected
Patients with a complicated medical history (e.g., organ transplant recipients, patients immunosuppressed due to autoimmune or inflammatory conditions)
Patients with “exotic” diseases
Prolonged febrile illnesses without an established etiology despite intensive evaluation and diagnostic testing
FUO
Old definition of FUO: An illness of _____ duration with fever of _______ on ____ occasions and an uncertain diagnosis despite ____ of inpatient evaluation
> 3 weeks
≥38.3°C (≥101°F)
Two
1 week
New definition of FUO
Fever ≥38.3°C (≥101°F) on at least two occasions
Illness duration of ≥3 weeks
No known immunocompromised state
Diagnosis that remains uncertain after a thorough history-taking, physical examination, and obligatory investigations
Most common infectious cause of FUO
TB
Most common solid tumor that causes fever (6)
Breast Colon Hepatocellular Lung Pancreatic Renal cell carcinoma
T or F. FUO is far more often caused by an atypical presentation of a rather common disease than by a very rare disease
True
A sterile thrombotic disease that occurs as a paraneoplastic phenomenon, especially with adenocarcinomas
Marantic endocarditis
Uncommon disorder but can often be diagnosed easily in a patient with FUO who presents with urticaria, bone pain, and monoclonal gammopathy
Schnitzler syndrome
Most common diagnosis of FUO among the neoplasms
Malignant lymphoma
T or F. All drugs can cause fever, even that commencing after long-term use
True
Fever artificially induced by the patient
Factitious fever
For example, by IV injection of contaminated water
More common among young women in health care professions
The most common infectious disease associated with FUO in elderly patients
Tuberculosis
Most common diseases with an atypical manifestation of FUO in elderly (2)
giant cell arteritis and polymyalgia rheumatica
T or F. In conducting diagnostic tests for FUO, antibiotic and glucocorticoid treatment should still be continued as treatment of possible diseases
False. Before further diagnostic tests are initiated, antibiotic and glucocorticoid treatment, which can mask many diseases, should be stopped
Which is a preferred obligatory test in FUO, abdominal ultrasound or CT?
Ultrasound
If fever persists beyond ___ after discontinuation of suspected drug, it is unlikely that this drug is the cause of fever
72
Noninvasive method allowing delineation of foci in all parts of the body on the basis of functional changes in tissues
Scintigraphy
CT and MRI routinely provide information on only part of the body, while scintigraphy readily allows whole-body imaging
In FUO, if no diagnosis is reached despite scintigraphic and PDC-driven histologic investigations or culture, what is the next step?
Second-stage screening diagnostic tests
Screening abdominal and chest CT
Bone marrow aspiration
Temporal artery biopsy
Liver biopsy
In FUO, when is empiric antibiotic indicated? (2)
Hemodynamic instability or neutropenia
Highly effective in preventing attacks of familial Mediterranean fever but is not always effective once an attack is well under way
Colchicine
NSAIDs has dramatic response in FUO of what disease?
adult-onset Still’s disease
A key cytokine in local and systemic inflammation and the febrile response
Interleukin (IL) 1
A recombinant form of the naturally occurring IL-1 receptor antagonist (IL-1Ra) and blocks the activity of both IL-1α and IL-1β
Anakinra
Accounts for most FUO-related deaths
Malignancy
Non-Hodgkin’s lymphoma carries a disproportionately high death toll
In nonmalignant FUO, fatality rates are very low
Body temperature is controlled by the
Hypothalamus
Normal core body temperature
36.5–37.5°C
Mean oral temperature
36.8° ± 0.4°C
Low levels at 6 am (max is 37.2°C)
Higher levels at 4-6 pm (max is 37.7°C)
Rectal temperatures
generally 0.4°C (0.7°F) higher than oral
Oral: 36.8° ± 0.4°C
Fever that most commonly occurs in patients with central nervous system (CNS) hemorrhages
Hyperpyrexia
>41.5°C
Can develop in patients with severe infections
Uncontrolled increase in body temperature that exceeds the body’s ability to lose heat
Hyperthermia (heat stroke)
T or F. Hyperthermia responds to antipyretics
False. Does not involve pyrogenic molecules
Can be rapidly fatal and characteristically does not respond to antipyretics
Pyrogenic products of gram-positive organisms that are also called superantigens
Enterotoxins
Pyrogenic cytokines (4)
IL-1, IL-6, tumor necrosis factor (TNF), and ciliary neurotropic factor
the primary cell types that produce pyrogenic cytokines (2)
Myeloid and endothelial cells
Distinct receptors for microbial products that are located on the hypothalamic endothelium and are similar in many ways to IL-1 receptors.
Toll-like receptors
Fever lasting 3–10 days is followed by afebrile periods of 3–10 days and are classic for Hodgkin’s disease and other lymphomas
Pel-Ebstein pattern
fevers occur every 21 days and accompany the neutropenia
Cyclic neutropenia
Relapsing fever
Borrelia infection
Blocks IL-1 activity and are useful in recurrent fever of autoimmune and autoinflammatory diseases (2)
Anakinra or Canakinumab
T or F. Acitaminophen is more effective than aspirin in reducing fever in humans
False. Oral aspirin and acetaminophen are equally effective in reducing fever in humans
Aspirin increases the risk of this condition in children
Reye’s syndrome
Difference of sepsis, severe sepsis and septic shock
- Sepsis is a systemic inflammatory response to infection
- Severe sepsis – sepsis is complicated by acute organ dysfunction
- Septic shock – sepsis complicated by hypotension despite adequate fluid resuscitation along with perfusion abnormalities
a dysregulated host response to infection that leads to acute organ dysfunction
Sepsis
Septic shock criteria includes sepsis plus (2) (despite adequate resuscitation):
- Need for vasopressor to elevate MAP to ≥65mmHg
* Serum lactate concentration >2.0 mmol/L
Most common source of sepsis
Pneumonia
2nd most common source of sepsis
Intraabdominal and GU infections
Most common gram positive isolates in sepsis (2)
S. aureus and S. pneumoniae
Gram positive > gram negative
Most common gram negative isolates in sepsis (3)
E. coli, Klebsiella species, and P. aeruginosa
Structures conserved across microbial species recognized by the receptors which will lead to upregulation of inflammatory gene transcripton and initiation of innate immunity
Pathogen-associated molecular patterns (PAMP)
Lipid A moiety of LPS – common PAMP
Endogenous molecules released from the injured cells also recognized by the receptors that leads to inflammation
Damaged-associated molecular patterns (DAMPs)
Examples:
• High-mobility group protein B1
• S100 proteins
• Extracellular RNA, DNA and histones
6-organ framework that assess primary physiologic manifestations of organ dysfunction
SOFA score
24 points
Hypoxemia and bilateral infiltrates of noncardiac origin that arise within 7 days of the suspected infection
ARDS
According to Berlin criteria, mild, moderate and severe ARDS is defined as
- Mild – PaO2/FiO2 – 201-300 mmHg
- Moderate – PaO2/FiO2 – 101-200 mmHg
- Severe – PaO2/FiO2 – ≤100 mmHg
Difference between hydrostatic edema and ARDS
Hydrostatic edema has elevated pulmonary capillary wedge pressure > 18 mmHg
Findings in sepsis in terms of: HR RR SBP O2 sat WBC
HR > 90 bpm RR > 20 cpm SBP ≤100 mmHg O2 sat ≤90% WBC < 4000/μL or > 12,000/μL
Quick SOFA (qSOFA) score parameters (3)
- Systolic hypotension ≤100 mmHg
- Tachypnea ≥22 cpm
- Altered mentation
Score of ≥ 2 points – sepsis
Marker of tissue hypoperfusion in sepsis
Arterial lactate
Hyperlactemia and delayed lactate clearance – greater incidence of organ failure and death in sepsis
For every 1-h delay among patients with sepsis, a ____ increase in the odds of in-hospital death is reported
3-7%
Initial management bundle for sepsis (4)
- Early administration of appropriate broad-spectrum antibiotics
- Collection of blood for culture before antibiotic administration
- Measurement of serum lactate levels
- Cardiorespiratory resuscitation
Initial management bundle of sepsis must be completed within ___ of presentation
3 h
Management bundle of sepsis must be completed within
6 h
Management bundle for sepsis
- IV fluid bolus
- Treatment with vasopressors for persistent hypotension or shock
- Re-measurement of serum lactate levels
Recommended as first line fluids for sepsis resuscitation
Crystalloids
Primary goal of supportive treatment of sepsis
To improve delivery of oxygen to the tissues as quickly as possible
Most widely used fluids in critically ill patients
Colloids
First choice vasopressors in septic shock
Norepinephrine
Trial that compared norepinephrine and dopamine and showed no difference observed in 28-day mortality, but arrhythmias are significantly higher with dopamine
SOAP II trial
Indications of mechanical ventilatory support in sepsis (4)
- Significant hypoxemia (PaO2 < 60 mmHg or SaO2 < 90%
- Hypoventilation – rising PaCO2
- Increased work of breathing
- Inadequate or unsustainable compensation for metabolic acidosis (pH < 7.2)
T or F. Most meta-analyses report no change in mortality but an increase in shock reversal with glucocorticoid treatment
True
International CPG suggest against the use of IV hydrocortisone to treat septic shock. If to be used, may give a dose of 200 mg/day
Mortality rates for septic shock
~20%
Rate of hospital re-admission within 90 days in sepsis
> 40%
In patients with septic shock requiring vasopressors, the recommended target mean arterial pressure is
65 mmHg.
______ should be used with the intent of reducing the norepinephrine dose.
Vasopressin
In the management of sepsis, red blood cell transfusion is recommended only when the hemoglobin concentration decreases to _______ in the absence of acute myocardial infarction, severe hypoxemia, or acute hemorrhage.
<7.0 g/dL
A protocol-based approach to blood glucose management should be used in ICU patients with sepsis, with insulin dosing initiated when two consecutive blood glucose levels are
> 180 mg/dL
Cause of acute rheumatic fever
infection of the upper respiratory tract with group A streptococci
The potential role of skin infection and of groups C and G streptococci is currently being investigated
The most common cause of heart disease in children in developing countries
RHD
A major cause of mortality and morbidity in adults
Peak age of ARF
age 5–14 years
Initial episodes become less common in older adolescents and young adults and are rare in persons aged >30 years
Peak age of RHD
25-40 years
More common in females
Serotypes of group A strep that is associated with ARF
M-serotypes
It is now thought that any strain has the potential to cause ARF
Human leukocyte antigen (HLA) class II alleles associated with susceptibility to ARF
HLA-DR7 and HLA-DR4
Human leukocyte antigen (HLA) class II alleles associated with protection against ARF
HLA-DR5, HLA-DR6, HLA-DR51, HLA-DR52, and HLA-DQ
The most widely accepted theory of rheumatic fever pathogenesis
Molecular mimicry
Alternative hypothesis: initial damage is due to streptococcal invasion of epithelial surfaces, with binding of M protein to type IV collagen allowing it to become immunogenic
Latent period between the precipitating group A streptococcal infection and the appearance of the clinical features of ARF
~3 weeks (1–5 weeks)
Chorea and Indolent carditis – prolonged latent period of 6 months
Most common clinical features of ARF
- Polyarthritis – 60-75%
- Carditis – 50-60%
Other features:
• Chorea - <2 – 30%
• Erythema marginatum – rare; <5%
• Subcutaneous nodules – rare; <5%
Hallmark of rheumatic carditis
Valvular damage
Valve that is almost always affected in RHD
Mitral valve
Aortic valve – often affected together with mitral valve
The characteristic manifestation of rheumatic carditis in previously unaffected individuals
Mitral regurgitation
May be accompanied by aortic regurgitation
Stenosis – may occur over ensuing years due to recurrent episodes
The most common form of joint involvement in ARF
Arthritis
Objective evidence of inflammation, with hot, swollen, red, and/or tender joints
Characteristic of arthritis in ARF
Polyarthritis
Migratory
Large joints
Asymmetric
Treatment of joint disease in ARF
- Salicylates
- NSAIDs
Joint involvement that persists for more than 1-2 days after starting salicylates is unlikely to be due to ARF
Chorea of ARF
Sydenham’s chorea
Found mainly in females
Characteristic of chorea in ARF
darting movements of the tongue
Affect particularly the head and upper limbs
Associated emotional lability or obsessive-compulsive traits
Usually resolve within 6 weeks but sometimes may take up to 6 months
Essential in making the diagnosis of ARF
Evidence of a preceding group A streptococcal infection
Most common serologic tests for ARF
- Antistreptolysin O (ASO) titer
2. Anti-DNAse B (ADB) titer
Criteria for diagnosis of ARF
Jones criteria
T or F. There is no treatment for ARF that has been proven to alter the likelihood of developing, or the severity of, RHD
True
Drug of choice for ARF
Penicillin
- Phenoxymethyl penicillin, 500 mg (250 mg for children ≤27 kg) PO twice daily
- Amoxicillin, 50 mg/kg (maximum, 1 g) daily, for 10 days
- Benzathine penicillin G of 1.2 million units (600,000 units for children ≤27 kg) IM single dose
DOC for the treatment of arthritis, arthralgia, and fever, once the diagnosis of ARF is confirmed
Aspirin 50–60 mg/kg per day, up to a maximum of 80–100 mg/kg per day (4–8 g/d in adults) in 4–5 divided doses
Fever, joint manifestations, and elevated acute- phase reactants sometimes recur up to 3 weeks after the medication is discontinued. This Does not indicate a recurrence and can be managed by recommencing salicylates for a brief period
Alternative drug: Naproxen
Glucocorticoid is used by some clinicians in ARF as treatment of
Carditis
Prednisone or prednisolone 1–2 mg/kg per day (maximum, 80 mg), usually for a few days or up to a maximum of 3 weeks
T or F. Long term bed rest is a cornerstone in the management of ARF
False. No longer widely practiced.
Should be prescribed as needed while arthritis and arthralgia are present and for patients with heart failure. Gradual mobilization can commence as tolerated once symptoms resolve
Management of chorea in ARF
- Provide a calm environment – in milder cases
- Carbamazepine or sodium valproate – in severe cases
- Corticosteroids – in severe or refractory cases
- IVIg – in small studies
Medications to control the abnormal movements do not alter the duration or outcome of chorea
Untreated, ARF lasts on average of
12 weeks
In ARF, Echocardiogram should be performed after _____ to determine if there has been progression of carditis
1 month
The mainstay of controlling ARF and RHD
Secondary prevention
Secondary prevention in ARF and RHD
Long-term penicillin prophylaxis
Patients with ARF are at dramatically higher risk than the general population of developing a further episode of ARF after a group A streptococcal infection
The best secondary prophylaxis for ARF or RHD
Benzathine penicillin G 1.2 million units, or 600,000 units if ≤27 kg delivered every 4 weeks. Can be given every 3 weeks, or even every 2 weeks, to persons considered to be at particularly high risk
Other drugs – less effective
Oral penicillin V 250 mg twice daily
Erythromycin 250 mg BID
According to the World Heart Federation Criteria for Echocardiographic Diagnosis of Rheumatic Heart Disease (RHD) in Individuals <20Years of Age, definite RHD is defined as (4)
(A) Pathologic MR and at least two morphologic features of RHD of the mitral valve
(B) MS mean gradient ≥4 mmHg (note: congenital MV anomalies must be excluded)
(C) Pathologic AR and at least two morphologic features of RHD of the AV (note: bicuspid AV and dilated aortic root must be excluded)
(D) Borderline disease of both the MV and AV
According to the World Heart Federation Criteria for Echocardiographic Diagnosis of Rheumatic Heart Disease (RHD) in Individuals <20Years of Age, borderline RHD is defined as (4)
- At least two morphologic features of RHD of the MV without pathologic MR or MS
- Pathologic MR
- Pathologic AR
Diagnosis of ARF based on Jones criteria is when the criteria fulfilled are
- 2 major
- 1 major + 2 minor
- 3 minor
Jones major criteria (5)
- Carditis
- Arthritis
- Chorea
- Erythema marginatum
- SC nodules
American Heart Association Recommendations for Duration of Secondary Prophylaxis for patients with Rheumatic fever without carditis
For 5 years after the last attack or 21 years of age (whichever is longer)
American Heart Association Recommendations for Duration of Secondary Prophylaxis for patients with Rheumatic fever with carditis but no residual valvular disease
For 10 years after the last attack, or 21 years of age (whichever is longer)
American Heart Association Recommendations for Duration of Secondary Prophylaxis for patients with rheumatic fever with persistent valvular disease, evident clinically or on echocardiography
For 10 years after the last attack, or 40 years of age (whichever is longer); sometimes lifelong prophylaxis
A flat lesion that is due to bleeding into the skin that is <3 mm in diameter
Petechiae
A flat lesion that is due to bleeding into the skin that is >3 mm in diameter
Ecchymoses
A necrotic lesion covered with a black crust
Eschar
Discrete lesions that become confluent as rash spreads from hairline downward, usually sparing palms and soles; lasts ≥3 days
Rubeola (measles)
Nonspecific because they also develop in infectious mononucleosis, scarlet fever, and Zika virus infection
Palatal petechiase seen in Rubella
Forschheimer spots
Bright-red “slapped-cheeks” appearance followed by lacy reticular rash that waxes and wanes over 3 weeks; rarely, papular-purpuric “gloves-and- socks” syndrome on hands and feet
Erythema infectiosum (fifth disease)
Also known as 6th disease
Roseola
Exanthem subitum
Exanthem subitum is caused by
Human herpesvirus 6
Maculopapular eruption appearing in axillae, spreading to trunk and later to extremities; usually spares face, palms, soles; evolves from blanchable macules to confluent eruption with petechiae
Epidemic typhus
Cause of Epidemic typhus
Rickettsia prowazekii
Cause of endemic typhus
Rickettsia typhi
Headache; musculoskeletal pain (“breakbone fever”); leukopenia; occasionally biphasic (“saddleback”) fever are symptoms of
Dengue
Cause of erythema marginatum
Group A streptococcus
Transient 2- to 5-mm erythematous papules appearing at height of fever on trunk, proximal extremities; lesions evanescent.. Other clinical manifestations are High spiking fever, polyarthritis, splenomegaly; erythrocyte sedimentation rate, >100 mm/h
Still’s disease
Eastern African trypanosomiasis is caused by
T. brucei rhodesiense
Western African trypanosomiasis is caused by
T. brucei gambiense
African trypanosomiasis is transmitted by what vector
Tsetse fly
Winterbottom’s sign is seen in
Western African trypanosoiasis
Posterior cervical lymphadenopathy in Western African trypanosoiasis
Winterbottom’s sign
Erythema multiforme is caused by (3)
- Herpes simplex virus
- Mycoplasma pneumoniae
- Drug intake
Rat-bite fever
Haverhill fever
Rat-bite fever is caused by
Streptobacillus moniliformis
Scarlet fever is caused by
Group A streptococcus
Diffuse blanchable erythemabeginning on face and spreading to trunk and extremities; circumoral pallor; “sandpaper” texture to skin; accentuation of linear erythema in skin folds (Pastia’s lines); enanthem of white evolving
into red “strawberry” tongue; desquamation in second week
Scarlet fever (second disease)
Rash similar to scarlet fever (scarlatiniform) or EM; fissuring of lips, strawberry tongue; conjunctivitis; edema of hands, feet; desquamation later in disease
Kawasaki disease
Streptococcal toxic shock syndrome is caused by
Group A streptococcus
Macules (2–3 mm) evolving into papules, then vesicles (sometimes umbilicated), on an erythematous base (“dewdrops on a rose petal”); pustules then forming and crusting; lesions appearing in crops; may involve scalp, mouth; intensely pruritic
Varicella
Difference of variola (smallpox) from varicella (2)
- Skin lesions in any given area are at same stage of development
- Prominent distribution of lesions on face and extremities (including palms, soles)
Indurated plaque evolving into hemorrhagic bulla or pustule that sloughs, resulting in eschar formation; erythematous halo; most common in axillary, groin, perianal regions
Ecthyma gangrenosum
Large, violaceous, nonulcerative subcutaneous nodules that are exquisitely tender; usually on lower legs but also on upper extremities
Erythema nodosum (septal panniculitis)
Tender red or blue edematous nodules giving impression of vesiculation; usually on face, neck, upper extremities; when on lower extremities, may mimic erythema nodosum
Sweet syndrome (acute febrile neutrophilic dermatosis)
Palpable purpuric lesions appearing in crops on legs or other dependent areas; may become vesicular or ulcerative
Cutaneous small-vessel vasculitis
1- to 2-mm white or bluish lesions with an erythematous halo on the buccal mucosa
Koplik’s spots
Pathognomonic for measles
Koplik’s spots
Generally seen during the first 2 days of symptoms
Postauricular and suboccipital adenopathy and arthritis are usually seen in
Rubella
Cause of erythema infectiosum (fifth disease)
human parvovirus B19
Consists of 2- to 3-mm rose-pink macules and papules that coalesce only rarely, occur initially on the trunk and sometimes on the extremities (sparing the face), and fade within 2 days
Exanthem subitum (roseola)
Rash of Lyme disease
Erythema migrans
Rash of acute rheumatic fever
Erythema marginatum
Target lesions (central erythema surrounded by area of clearing and another rim of erythema) up to 2 cm; symmetric on knees, elbows, palms, soles; spreads centripetally; papular, sometimes vesicular; when extensive and involving mucous membranes, termed EM major
Erythema multiforme
Accentuated petechiae in body folds seen in scarlet fever
Pastia’s lines
In the exfoliative stage of this disease, the skin can be induced to form bullae with light lateral pressure (Nikolsky’s sign)
Staphylococcal scalded-skin syndrome
The skin can be induced to form bullae with light lateral pressure. This is called
Nikolsky’s sign
Disseminated candidiasis is often due to
Candida tropicalis
In immunocompromised hosts, nodular lesions often represent
disseminated infection
Triad of disseminated candidiasis
- Fever
- Myalgias
- Eruptive nodules
Distinctive, sparse, countable hemorrhagic pustules, usually located near joints
Disseminated gonococcemia
