INFECTIOUS DISEASE (6%) Flashcards
TRICHOMONIASIS
Trichomoniasis is a common cause of vaginitis.
most common non-viral STD worldwide
It is a common sexually transmitted infection, and is caused by the single-celled protozoan PARASITE** - Trichomonas vaginalis
⦁ Bacteria = Trichomonas vaginalis (T. vaginalis)
⦁ PEAR SHAPED FLAGELLATED PROTOZOA
⦁ sexually transmitted
Produces mechanical stress on host cells and then ingests cell fragments after cell death.
Trichomoniasis is primarily an infection of the UROGENITAL TRACT
MC site of infection = urethra and vagina in women
SYMPTOMS ⦁ vulvar pruritus* ⦁ vulvovaginal erythema ⦁ itching* ⦁ burning* ⦁ dysuria* ⦁ dyspareunia* ⦁ post-coital bleeding
⦁ MALODOROUS VAGINAL DISCHARGE
- copious, malodorous discharge
- FROTHY YELLOW-GREEN DISCHARGE***
- discharge is worse with menses
⦁ STRAWBERRY CERVIX*** (cervical petechiae)
Vaginal pH > 5
(normal vaginal pH = 3.8 - 4.5)
DIAGNOSIS
⦁ wet mount = mobile protozoa (trichomonads) = “CORKSCREW” motility - FLAGELLA **
⦁ elevated WBC count
⦁ vaginal pH 5-6
⦁ UA = positive for WBCs
** MOBILE WET PREP **
TREATMENT
⦁ Metronidazole (Flagyl)
- either 2g oral x 1 dose or 500mg bid oral x 7 days
- safe to use in pregnancy!
⦁ Tinidazole
** MUST TREAT PARTNER **
COMPLICATIONS
- perinatal complications
- increased HIV transmission
PNEUMOCYSTIS
Pneumocystis jirovecii (formerly carinii) = YEAST-LIKE FUNGUS - but doesn’t respond to antifungals***
- need to give antibiotics to treat, despite the fact that it is a fungal infection
TRANSMISSION
⦁ inhalation
** PCP ** (or PJP) = Pneumocystis Pneumonia =
MC opportunistic infection in HIV - especially if CD4 is < 200
pneumonia secondary to Pneumocystis Jiroveci (PJP)
PCP generally occurs in immunocompromised patients, including HIV patients with a CD4 count less than 200 cells/mL
- may also occur in transplant patients / other immunocompromised people
Once a patient’s CD4 count is less than 200 cells/mL, daily prophylaxis should be initiated with trimethoprim-sulfamethoxazole (Bactrim) to prevent PCP.
SYMPTOMS ⦁ fever* ⦁ dyspnea on exertion ⦁ non-productive, dry cough* ⦁ O2 desaturation with ambulation****** - symptoms progress over 2-3 weeks
Patients with PCP often present with a cough, unexplained fever, shortness of breath, and hypoxia out of proportion to the clinical picture.
DIAGNOSIS
⦁ XRAY = ** bilateral diffuse interstitial infiltrates * - or may be normal
⦁ Elevated LDH (lactate dehydrogenase)
⦁ Bronchoalveolar lavage or induced sputum* = definitive diagnosis ***
Chest X-ray classically shows BILATERAL DIFFUSE INTERSTITIAL INFILTRATES, but a negative chest X-ray can be seen in up to 20% of patients.
** BAT WING APPEARANCE ON CXR **
⦁ Bronchoscopy - bronchoalveolar lavage
Since the organism cannot be grown in the laboratory, diagnosis depends on other means. Most often, diagnosis is confirmed through bronchoscopy with a bronchoalvelolar lavage.
⦁ Elevated Lactate Dehydrogenase (> 200)
A classic finding in patients with PCP is an elevated lactate dehydrogenase.
TREATMENT
⦁ BACTRIM x 21 days = drug of choice
- ** add PREDNISONE if hypoxic (PaO2 < 70 mmHg) or if A-a gradient > 35 mmHg (alveolar arterial gradient)
- If sulfa allergy = Dapsone-Trimethropim, etc.
PROPHYLAXIS
- BACTRIM - as soon as CD4 falls < 200
Treatment, which should be initiated upon early suspicion and before diagnosis, is with trimethoprim-sulfamethoxazole.
TOXOPLASMOSIS
In a patient with AIDS, BACTRIM is given prophylactically at a CD4 count < 100 cells/μL to prevent infection with toxoplasmosis gondii
INFLUENZA
- the VIRUS that causes the “FLU”
- one of the most common infectious diseases
3 types of Influenza ⦁ Type A = 8 RNA segments = MC TYPE ⦁ Type B = 8 RNA segments ⦁ Type C = 7 RNA segments - each influenza type has slightly different genome and proteins
Influenza = virus family ORTHOMYXOVIRUS
Influenza viruses have a single stranded, linear, negative sense RNA structure.
MC TYPE OF INFLUENZA VIRUS = TYPE A
- most severe type - because it is constantly mutating its H and N glycoproteins - allows daughter viruses to form that are slightly different than original - can therefore avoid already formed antibodies and infect persons who became immune to previous strains
= GENETIC DRIFT = why people can get influenza year after year, or get 2 different strains in 1 year
ANTIGENIC SHIFT = virus that circulates among animals will mutate to a form that is now contractible by humans. This happens when an animal is infected by 2 different flu strains at once: 1 being a type that only infects that animal, and the other being a type that can only affect humans. RNA segments mix and now allow for new transmission. ex: Spanish Flu
TYPE A INFLUENZA
- can be further divided into subtypes - based on 2 glycoproteins displayed on envelope surface
⦁ Hemagglutinin - H protein = 3 variants
⦁ Neuraminidase - N protein = 2 variants
- can have H1N1, H1N2, H2N1, H2N2, H3N1, H3N2
MC Influenza A types to infect humans = H3N2 + H1N1
- can infect other animals as well
TYPE B INFLUENZA
- less common
- only infects humans
- doesn’t mutate as often as type A
- only has a few types of H and N proteins on its surface (hemagglutinin + neuraminidase)
TYPE C INFLUENZA
- only has 1 species
- least common type of influenza
- least likely to mutate
- can infect both humans and pigs
- causes only MILD illness in children
- Instead has F protein (hemagglutinin esterase - Fusion protein)
INFLUENZA TRANSMISSION
⦁ person sneezes or coughs = RESPIRATORY DROPLETS - can spread up to 6 feet away
- can land in eyes / mouth / nose or be inhaled by someone else
- virus can live on surfaces for a few hours - be transmitted by touching surfaces / objects
MC in fall / winter
PATHOPHYSIOLOGY
⦁ hemagglutinin protein binds to sialic acid sugars on surface of epithelial cells of upper respiratory tract
⦁ once bound, the cell swallows the virus - endocytosis
⦁ RNA (negative sense) is transcribed by RNA polymerase into positive sense mRNA before it can be translated into proteins + assembled into new viruses
⦁ viruses leave the endothelial cells - neuraminidase protein cleaves sialic acid sugars in epithelial cell membrane, releasing newly created viruses from the cell
The influenza virus surface protein HEMAGLUTTININ promotes its ENTRY into cells.
The influenza virus surface protein NEURAMINIDASE promotes VIRION RELEASE from infected cells.
SYMPTOMS OF INFLUENZA - start 1-4 days after infection - usually abrupt onset + wide range of symptoms ⦁ Fever ⦁ Headache ⦁ Rhinorrhea ⦁ Sore throat ⦁ Cough ⦁ Muscle aches = MC in legs / lumbosacral area ⦁ Fatigue / malaise ⦁ Chills ⦁ Diaphoresis
- most of these symptoms improve after 1 week
- the cough often persists for up to 2 weeks
COMPLICATIONS ⦁ Acute otitis media ⦁ Bronchiolitis ⦁ Croup ⦁ Sinusitis ⦁ Pneumonia
** STAPH, STREP, and H. FLU are the MC species causing bacterial superinfection in flu patients **
The MC complication of influenza in young patients = otitis media
HIGHEST GROUP OF COMPLICATIONS ⦁ children < 6 months (can't get flu shot) ⦁ pregnant women ⦁ adults > 65 ⦁ chronic medical conditions
young children = more likely to have neurologic complications, such as ENCEPHALITIS and FEBRILE SEIZURES
REYE’S SYNDROME
- condition where, after taking ASPIRIN after fighting off a VIRAL infection like the flu or chickenpox, a child develops ENCEPHALOPATHY and LIVER DISEASE
CONTAGIOUS
- 1 day prior to symptom onset and up to 1-2 weeks after symptom onset
- meaning that someone can pass the flu onto someone else before they even have symptoms
DIAGNOSIS
⦁ ** Rapid influenza diagnostic test - nasal swab
- results within minutes
- varies in reliability
- often detects certain types of influenza…not strain
- more accurate / reliable tests, but not worth time/$
⦁ viral culture
⦁ PCR (polymerase chain reaction)
TREATMENT
- usually used for high-risk patients or if severe
o NEURAMINIDASE INHIBITORS
- inhibit neuraminidase and prevent the Influenza A and B virus from breaking out of host cells and infecting other cells
⦁ Oseltamivir (Tamiflu) - SE = N/V
⦁ Zanamivir (Relenza) - inhaled
- ** Tamiflu + Relenza = only effective if given with 48 hours of symptom onset
- but still only shown to reduce length of flu symptoms by 1-2 days… does not reduce contagiousness
- can also be given prophylactically to people exposed to the virus
o M2 PROTON CHANNEL INHIBITORS
- prevents viral replication inside host cell
- however, the virus’ M2 gene mutates often, allowing it to become resistant to M2 inhibitors
⦁ Amantadine
⦁ Rimantadine - less SE than amantadine
o SYMPTOMATIC TREATMENT
⦁ fluids
⦁ fever / muscle aches - Tylenol
⦁ rest
o PREVENTION
⦁ influenza vaccine
- Trivalant = Inactivated influenza vaccine (killed virus)injected into muscle
- Live attenuated influenza vaccine = weakened virus - intranasal (only given if age 2-49, not immune compromised / pregnant / DM / lung or heart dz)
Both are Trivalant = meaning they contain a mixture of the 3 strains predicted to dominate in the coming season - based on previous seasons as well as current strains across the globe
The KILLED viral vaccine for influenza is SAFE FOR PREGNANT WOMEN, regardless of what stage in pregnancy. If a woman was to get the flu during pregnancy, there is a higher risk of premature labor and delivery.
RISKS ASSOCIATED WITH FLU VACCINE
⦁ most flu viruses are produced by growing in a chicken embryo, so vaccine contains small amounts of egg protein
- problem for those with an egg allergy
⦁ Guillain - Barre Syndrome
- autoimmune disorder of peripheral nervous system - associated with flu vaccine - don’t get it if hx of GBS
⦁ children < 6 months = too young to get flu vaccine - but at highest risk for serious influenza complications
- so vaccinate their caregivers / surrounding people
LIVE ATTENUATED VACCINES ⦁ MMR ⦁ Intranasal Influenza ⦁ Rotavirus ⦁ Varicella ⦁ Zostavax (Not Shingrex = inactivated) ⦁ Yellow Fever
PINWORMS
The pinworm (ENTEROBIUS VERMICULARIS) is a parasitic nematode (type of roundworm) and a common intestinal PARASITE
- transmitted by the fecal-oral route
- Spread: fecal-oral route (contaminated hands, food and sometimes water)
The disease is spread among people by pinworm eggs. As a patient itches the anal area where the eggs are located, the eggs cling to the fingers and can easily be transmitted to other people either directly or through food or surfaces. The eggs can thrive for 2-3 weeks on an inanimate object.
- Seen in children ages 5-10
- uncommon in children < 2 year old
- 4-6 week incubation period after ingestion of eggs before symptoms occur
- patient then develops INTESTINAL INFECTION (enterobiasis) = which is asymptomatic in 1/3 of individuals
The pinworm is a white, threadlike organism that resides in the cecum, colon, and crawl out of the anus at night
LIFECYCLE
⦁ After ingestion, eggs hatch + release larvae in the small intestine
⦁ Adult worms establish in the cecum, appendix and ascending colon
⦁ Gravid females migrate to the rectum onto perianal skin to deposit eggs (usually occurs at night)
SYMPTOMS
⦁ Itchy butt!
⦁ squirming when sitting
⦁ restlessness at night
- tickling / tingling / may even be painful
DIAGNOSIS
⦁ Stool test for Ova + Parasites
⦁ “scotch tape test” = wrap clear scotch tape around glass slide with sticky side out. touch slide to 4 quadrants of perianal skin. examine under microscope for pinworm eggs
- the best tape sample is collected first thing in the morning before bathing, or several hours after going to bed (female pinworm lays eggs at night)
under microscope, pinworm eggs look like almonds and are bean-shaped
⦁ Nocturnal examination of the perianal area
TREATMENT
⦁ ALBENDAZOLE (Albenza) = 1st line tx of choice; 400mg PO single dose - may repeat in 2 weeks
⦁ MEBENDAZOLE (vermox) 100mg PO single dose - may repeat in 2-3 weeks
BENDazoles for worms because they are BENDy
- MOA = inhibit glycogen metabolism in worms, starving them to death; this only kills adult worms, so drug must be readministered after eggs hatch
⦁ PYRANTEL PAMOATE - OTC + Cheap (2nd line)
Pyrantel Pamoate MOA = causes neuromuscular blockade in pinworms
*** do NOT use either treatments above in children < 2
- treat entire family (so contagious)
Patient will present as → a 4-year-old is brought to the office by his mother because the daycare teachers noticed he is unusually restless at school. The mother also noticed that he has not been sleeping well lately and has started wetting the bed at night. The child is alert and cooperative but scratches his buttocks while you are interviewing. Cellophane tape applied to the perianal area reveals football-shaped ova under the microscope.
MEASLES = RUBEOLA
Measles / Rubeola = one of the most contagious infectious diseases
Remains a leading cause of death, especially among children, and particularly in areas with low rates of vaccination
Caused by ** MEASLES VIRUS **
= PARAMYXOVIRUS family (also causes Mumps)
Transmission = AIRBORNE PARTICLES = what makes it so contagious - tiny particles released into the air when someone coughs or sneezes –> can remain in that air space / nearby surfaces for up to 2 hours
- if someone breathes in that air, or touches space and then touches eyes / nose / mouth
Measles is so contagious that if one person is contagious, 90% of non-immune people around will also get infected
Measles quickly invades the epithelial cells of trachea or bronchi
Measles uses Hemagluttinin (H protein) to bind to cells
Measles virus = single stranded RNA virus with helical capsid symmetry with envelope = negative sense (has to be transcribed by RNA polymerase into a positive sense mRNA strand) –> then ready to be translated into viral proteins and be sent out to other cells –> carried from local tissue in the lungs to lymph nodes –> blood –> various organ systems (lungs / intestines / brain)
Incubation period of Measles = 10-14 days
1) 3 day prodromal period (fever + 3 Cs) =>
2) Then Koplik spots (lasts 2-3 days) =>
3) then 1-2 days after koplik spots pop up ==> rash
rash lasts about 7 days (fades from top to bottom)
Prodromal period of Measles = typically about 3 days
⦁ High Fever (unlike Rubella = mild fever) + 3 Cs
⦁ Cough
⦁ Conjunctivitis (of sclera)
⦁ Coryza (swelling of nasal mucosa = stuffy nose)
PRODROMAL PERIOD X 3 days = Fever + 3C’s
- Then rash on mucous membranes
- looks like “ SALT GRAINS” on a wet background =
- ** KOPLIK SPOTS ** - commonly seen on inside of cheeks = ** small red spots in buccal mucosa with pale blue / white center ***
Exanthem period of Measles = about 7 days
⦁ Morbiliform (maculopapular) BRICK-RED rash - STARTS AT HAIRLINE / FACE –> spreads to extremities (Cephalocaudal)
(opposite of Roseola = starts on trunk, spreads to face)
⦁ Rash DARKENS + COALESCES (unlike rubella)
Rash fades from top to bottom
Some patients also get Photophobia - Vitamin A supplement can help with this
Recovery period of Measles = 10-14 days - usually left with a persistent cough
Once someone has Measles and recovers from it = have lifelong immunity!
Because Measles can spread to various organ system like Lungs, Intestines, Brain = can lead to serious complications such as Pneumonia, Diarrhea and Encephalitis –> can all lead to Death
⦁ Giant Cell Pneumonia = rare respiratory disease that is seen after Measles that occurs in immunocompromised
Measles also suppresses the immune system x 6 weeks = can lead to bacterial superinfectious such as Otitis Media and Bacterial Pneumonia
- these complications = worst among Infants (highest mortality rate with Measles)
** COMPLICATION IN CHILDREN < 2 **
⦁ SUBACUTE SCLEROSING PANENCEPHALITIS 7-10 years later after Measles infection = chronic inflammation of the entire brain
⦁ symptoms are subtle at first = mood changes, but can eventually become severe (seizures, coma, death)
DIAGNOSIS
⦁ Serology - look for Measles antibodies in blood serum
PREVENTION
⦁ Measles vaccine = Live attenuated vaccine (weakened) = given at 12-15 months old, then again at 4-6 y/o
⦁ 95% efficacy rate
⦁ can be given to HIV patients without signs of immunodeficiency
⦁ cannot be given in pregnancy (live)
MEASLES VACCINE
⦁ is a live vaccine - can therefore cause mild measles symptoms
⦁ A morbilliform rash is a common side effect - spread across patient’s CHEST, is not itchy or painful
⦁ will present 7-14 days after vaccine is given
Another source of protection for young infants = Mother’s Anti-Measles Antibody (Immunoglobulin) = transferred via placenta - lasts until about 9 months old
TREATMENT
⦁ no specific anti-viral treatment
⦁ medications aimed at treating superinfections, maintaining hydration, fever + pain relief
⦁ Vitamin A = boosts antibody response and decreases risk of complications + helps with photophobia that may be SE
ROCKY MOUNTAIN SPOTTED FEVER
= RICKETTSIA RICKETTSII
Rocky Mountain Spotted Fever (RMSF)
In North + South America
Caused by: ** RICKETTSIA RICKETTSII **
- a species of bacterium that is spread to humans by the American dog tick
Rickettsia rickettsii is a gram-negative, intracellular, coccobacillus bacterium
The most common hosts for the R. rickettsii bacteria are Ixodes ticks (specifically DERMACENTOR TICK) = American dog tick
Usually patient will have just gone camping or was outdoors for extended period of time
SYMPTOMS - 2-14 days after tick bite = develop: ⦁ fever** ⦁ headache** ⦁ chills ⦁ myalgias ⦁ *** red maculopapular rash FIRST ON WRISTS + ANKLES and PALMS + SOLES **** (unlike epidemic typhus - rickettsia prowazekii) then spreads centrally over next 2-3 days ⦁ rash typically spares the face
Rash = occurs 2-5 days after onset of fever
⦁ may have seizures
⦁ * hyponatremia *
⦁ * elevated liver enzymes *
⦁ * thrombocytopenia *
remember that rashes on the palms and soles are characteristic of only a few conditions: RMSF, secondary syphilis, coxsackievirus (hand-foot-mouth), and adverse drug reactions
RMSF rash typically presents on ** WRISTS + ANKLES **
then spreads to PALMS / SOLES, then centrally
DIAGNOSIS
⦁ primarily clinical - based on fever / rash / hx of tick exposure
- don’t wait for serologies in order to treat!
⦁ Indirect fluorescent antibody (IFA) test = standard method of diagnosis of RMSF
⦁ Biopsy of rash
TREATMENT
⦁ ** Doxycycline 200mg x 1, then 100mg BID x
- until patient improves
- until patient has been afebrile x 24-48 hrs
- until it has been at least 7 days of treatment
ideally start Doxy within 5 days of symptom onset to reduce mortality
- still give Doxy to children < 8 if concerned about RMSF
⦁ 2nd line = Chloramphenicol
- treatment of choice in pregnancy!
- 3rd trimester usage = associated with gray baby syndrome
TX = Discharge on oral doxycycline, close follow-up
Given the rapid and potentially fatal course of RMSF, empiric treatment with doxycycline should be initiated immediately in any patient with suspected RMSF.
- ex: if patient has rash on palms/soles, no travel hx, but is sexually active with multiple partners, while want to test RPR for syphilis, 1st step is to treat with doxy for RMSF, as can then confirm if RMSF via PCR or check for syphilis with RPR
Patient will present as → a 21-year-old male who three days after returning from a camping trip has developed fever, chills, myalgias, and headache. He then developed a rash on the wrists, ankles, palms, soles, and forearms that rapidly extended to the neck, axillae, buttocks, and trunk.
EPIDEMIC TYPHUS
= CAUSED BY ** RICKETTSIA PROWAZEKII **
ePidemic = Prowazekii
Based on genomic sequencing, R. Prowazekii has been found to be the closest free-living relative of MITOCHONDRIA***
VECTORS
⦁ human lice
⦁ flying squirrel
⦁ flying squirrel flea + lice
SYMPTOMS
⦁ headache
⦁ fever
⦁ rash - starts on trunk (unlike RMSF), spreads to extremities, spares palms + soles
ENDEMIC (MURINE) TYPHUS
= CAUSED BY ** RICKETTSIA TYPHI **
VECTORS
⦁ rat flea
⦁ mouse flea
⦁ cat flea
