ID pt 2 electric boogaloo

what are group A strep

G+, beta hemolytic, cause infections from pharyngitis to skin infxn to endocarditis to esteomyelitis

what are strep pyrogenic exotoxins

aka erythrogenic toxins, can cause scarlet fever in susceptible pts

acute rheumatic fever may follow

pharyngitis, beginning 1-4 wks after onset of sx

what is the Jones criteria for

dx acute rheumatic fever, must meet at least 2 major or 1 major and 2 minor criteria PLUS evidence of recent GAS inxn by bac cx data, rapid strep test, or elevated anti strep antibody titers

major Jones criteria

pancarditis

polyarthritis

SQ nodules

erythema marginatum

chorea

minor Jones criteria

presence of heart block

arthralgia

elevated ESR/CRP

fever

leukocytosis

hx of prior rheumatic fever

tx rheumatic fever

antimicrobial tx of pharyngitis to reduce risk of complications, GAS universally susceptible to penicillin

prevent recurrent rheumatic fever

tx w/ continuous course of antimicrobial ppx for at least 5 yrs

PCN V, erythromycin if PCN allergic

what is TB

usually caused by Mycobacterium tuberculosis, primarily affects lungs but can invade other organs as well

stages in TB pathogenesis

primary infxn (TB infxn)

secondary infxn/reinfxn (TB dz)

primary TB infxn

microorganisms enter lungs, engulfed by macrophages, cause local inflammatory rxn, usually on periphery of upper lobe

some bacilli migrate to lymph nodes, activate type IV or cell mediated hypersensitivity response

what are Ghon complexes

healthy person resists primary TB invasion, lesions remain small and become walled off by fibrous tissue, eventually calcifying (Ghon complex)

if pts resistance and immune response stay high during primary TB infxn, what happens

bacilli remain walled off w/i tubercle, no active dz and asx, immune response by 6-8 wks

what happens if you give tuberculoprotein to someone several weeks after TB exposure

they are hypersensitive and will produce a positive skin rxn, large area of induration

CXR and sputum culture to determine if active infxn is present

what will happen in pt w/ low resistance when they get primary TB infxn

it may not be controlled and progress to active infxn, spreading throughout lungs and other organs

what is miliary/extrapulmonary TB

rapidly progressive form in which multiple granulomas affect large areas of the lungs and rapidly disseminate into the circulation and to other tissues like bone or kidney

what is secondary/reinfxn TB

stage of active infxn, often arises years after primary infxn when bacilli hidden in tubercles are reactivated, usually b/c of decreased host resistance

what happens to the lungs in secondary TB

cavitation: formation of large open area in lung and erosion into bronchi and blood vessels, bacilli pass into sputum

hemoptysis as blood vessels are eroded

how is M tuberculosis transmitted

oral droplets released from a person c active infxn that are inhaled into the lungs, you need sustained contact to get it though

what can cause TB in unpasteurized milk

Mycobacterium bovis

who gets TB

crowded conditions, immunocomp, malnutrition, alcoholism, war, chronic dz, genetic susceptibility, children get it more easily than adults

anorexia, malaise, fatigue, weight loss, afternoon low grade fever/night sweats, increasingly severe and productive prolonged cough, purulent sputum often containing blood

TB

dx primary TB

positive tuberculin test, but that sucks so actually gold quantiferon

confirm active TB

CXR, acid fast staining of sputum, sputum cx, CT more sensitive that XR, nucleic acid amplification

tx TB

isoniazid, rifapentine, rifampin, ethambutol, pyrazinamide, streptomycin

directly observed therapy

check LFTs before starting tx

when is sputum cx negative in TB

after 1-2 mo of tx, risk of transmission is much less

what is recommended for contacts of TB pts

ppx isoniazid for 1 yr and tuberculin testing

baby TB testing

on or before 1st birthday unless sx and hx suggest earlier testing

Entamoeba complex morphologically identical species

Entamoeba dispar, Entamoeba moshkovskii, Entamoeba histolytica

cause amebiasis

what happens in amoebiasis

penetration of E histolytica into intestinal wall, causes diarrhea

if severe, dysentery or extraintestinal dz, m/c liver abscess

who gets amoebiasis

humans are only host, m/c in subtropical and tropical areas under conditions of crowding, poor sanitation, poor nutrition

how do you get amoebiasis

ingestion of cysts from fecally contaminated food or water, person to person spread, flies and other arthropods as mechanical vector, human excrement as fertilizer

typical intestinal amoebiasis

organism lives as a commensal, carrier is asx

sx intestinal ameobiasis

diarrhea after 2-4 wks, may begin w/i a week of infxn, gradual onset of abdominal pain and diarrhea

fever uncommon

periods of remission and recurrence may last days-weeks or longer

microscopic hematochezia

intestinal amoebiasis abdominal exam

distention, tenderness, hyperperistalsis, hepatomegaly

more severe intestinal amoebiasis presentation

colitis and dysentery w/ worse diarrhea (10-20 BM qd), blood stools

high fevers, prostration, vomiting, abdominal pain/tenderness, hepatic enlargement, HoTN

intestinal amoebiasis dysentery

who is more likely to get severe presentations of intestinal amoebiasis

young children, pregnant women, malnourished, CCS use

fulminant amoebic colitis can progress to

necrotizing colitis, intestinal perforation, mucosal sloughing, severe hemorrhage

long term complications of intestinal amoebiasis

chronic diarrhea w/ weight loss, bowel ulcerations, amoebic appendicitis

what are amoebomas

localized granulomatous lesions, can present after either dysentery or chronic intestinal infxn

amoeboma clinical findings

pain, obstructive sx, hemorrhage, may also suggest intestinal carcinoma

m/c extraintestinal manifestation of amoebiasis

amoebic liver abscess

acute/gradual onset of abdominal pain, fever, enlarged and tender liver, anorexia, weight loss, diarrhea in a few pts, intercostal tenderness on PE

extraintestinal amoebiasis

where are amoebic liver abscesses usually located

single in right lobe, m/c in men

what happens if you don’t tx amoebic liver abscess

rupture into pleural, peritoneal, pericardial space, often fatally

leukocytosis, hematochezia, ±fecal leukocytes

amoebiasis

+LFTs if extraintestinal

dx amoebiasis

finding E hystolytica or its antigen, serologic tests

intestinal m/c dx by identifying organisms in stool, identification of amoebic trophozoites/cysts

eval at least 3 stool samples

QUIK CHEK assay for rapid point of care dx

amoebiasis colonoscopy of uncleansed bowel

typically no specific findings in mild intestinal dz, in severe dz may be ulcers w/ intact intervening friable mucosa resembling IBD

dx hepatic amoebic abscess

serologic tests for anti amoebic antibodies are almost always positive except v early in infxn, so retest negative result in a week

amoebic liver abscess imaging

US, CT, MRI, round/oval low density nonhomogeneous lesions w/ abrupt transition from nl liver to lesion, hypoechoic centers

tx amoebiasis

metro or tinidazole to eradicate tissue trophozoites and luminal amoebicide to eradicate intestinal cysts

tx asx infxn w/ E histolytica

luminal agent

diloxanide furoate, iodoquinol, paromomycin

tx intestinal amoebiasis

metro or tinidazole plus luminal agent

tinidazole has simpler dosing, faster response, and fewer SE

avoid metro/tinidazole in pregnancy

successful tx of severe amoebic colitis may be followed by

postdysenteric colitis w/ continued diarrhea w/o persistent infxn, syndrome resolves in weeks-months

tx amoebic hepatic abscess

metro or tinidazole plus luminal agent

metro IV if needed

needle aspiration if large, dx is uncertain, imminent rupture

helminthic infxns

trematodes/flukes

cestodes/tapeworms

nematodes/roundworms

fever, HA, myalgias, cough, urticaria, diarrhea, eosinophilia

acute schistosomiasis

abdominal pain, diarrhea, hepatomegaly, anorexia, weight loss, portal HTN

intestinal schistosomiasis

hematuria, dysuria, hydronephrosis, urinary infxn

urinary schistosomiasis

dx schistosomiasis

characteristic eggs w/ a spike on them in feces/urine, biopsy of rectal/bladder mucosa, positive serology

tx schistosomiasis

praziquantel

prevent schistosomiasis

avoid freshwater exposure in endemic areas, vigorous toweling after exposure, improve sanitation/water supplies, eliminate snail habitats, preventative tx

what is fasciolasis

infxn from Fasciola hepatica, sheep liver fluke, from ingestion of encysted metacercariae on watercress or other aquatic veg, prevalent in sheep raising areas

how does fasciolasis happen

metacercariae excyst, penetrate peritoneum, migrate through liver, mature in bile ducts where they cause local necrosis and abscess formation

two fasciolasis syndromes

acute migration of worms and chronic infxn of biliary tract

abdominal pain, fever, weight loss, urticaria, eosinophilia, leukocytosis 6-12 wks after ingesting watercress

fasciolasis migration of larvae

tx fasciolasis migration of larvae

triclabendazole

how do you contract paragonimiasis

consumption of raw/undercooked/pickled freshwater shellfish

metacercariae excyst, penetrate peritoneum, pass into lungs, mature into adult worms over ~2 mo

most pts c paragonimiasis have

moderate worm burdens, asx

dx paragonimiasis

characteristic eggs in sputum or stool, identify worms in biopsied tissue

multiple exams/concentration techniques may be needed

tx paragonimiasis

praziquantel

tapeworms that cause noninvasive infxns

beef: Taenia saginata

pork: Taenia solium

fish: Diphyllobothrium latum

dwarf: Hymenolepis nana

how do you get T saginatat

gravid segments passed in human feces to soil, cows eat it

eggs hatch and release embryos that encyst in cattle muscle as cysticerci

humans eat raw/uncooked infected beef

asx, abdominal pain, GI sx, eosinophilia after eating sus beef

T saginata

how do you get T solium

pigs eat human feces

humans as definitive host: eat undercooked pork leading to tapeworm infxn

humans as intermediate host: consume food contaminated w/ human feces containing T soilium eggs leading to cysticercosis

asx, GI sx, passage of proglottids after eating sus pork

T solium

how do you get D latum

ingestion of undercooked freshwater fish

eggs from human feces are taken up in crustaceans, fish eat those guys, and then people eat the fish

asx, nonspecific GI sx, diarrhea, passage of proglottids from sus fish

D latum

only tapeworm that can be transmitted between humans

H nana

how do you get H nana

eat food contaminated w/ human feces

eggs hatch in intestines, oncospheres penetrate mucosa, encyst as cysticeroid larvae, rupture after ~4 days to release adult worms

auto infxn can lead to amplification of infxn

can also be from eating infected insects

dx H nana

characteristic eggs or proglottids in stool

multiple specimen exams/concentration techniques may be needed

tx noninvasive tapeworm infxn

praziquantel

tx H nana

praziquantel is not effective against maturing cysts

praziquantel SE

HA, malaise, dizziness, abdominal pain, nausea

what is cysticercosis

tissue infxn w/ cysts of T solium that develop after humans ingest food contaminated w/ eggs from human feces, act as intermediate host for parasite

intracerebral/subarachnoid/spinal cord lesions, intraventricular cysts

neurocysticercosis, lesions may persist for years before sx which are generally due to local inflammation or ventricular obstruction

dx neurocysticercosis

CSF show lymphocytic/eosinophilic pleocytosis, decreased glucose, elevated protein

antibody and antigen detection assays

neurocysticercosis imaging

do both CT and MRI, multiple parenchymal cysts, parenchymal calcifications

why is neurocysticercosis tx controversial

benefits of cyst clearance must be weighed against potential harm of inflammatory response to dying worms

neurocysticercosis tx options

antihelminthic therapy hastens radiologic improvement in parenchymal cysticercosis, some randomized trials show that CCS alone are as effective as specific therapy and also control seizures

m/c intestinal helminth

Ascaris lumbricoides

how do you get Ascaris lumbricoides

ingestion of eggs in contaminated food

larvae hatch in small intestine, penetrate into bloodstream, migrate to lungs, travel via airways back to GI tract where they grow into adult worms and live 1-2 yrs

fever, nonproductive cough, chest pain, dyspnea, eosinophilia, occasionally eosinophilic PNA

Ascaris worms are migrating through lungs

adults may be coughed up, vomited, emerge through nose/anus

very heavy Ascaris infxn can cause

intestinal obstruction, volvulus, inussusception, dath

tx Ascaris

albendazole, mebendazole, pyrantel pamoate

may cause mild GI toxicity

Enterobius vermicularis aka

pinworm

how do you get Enterobiasis

person to person via ingestion of eggs after contact w/ the hands or perianal region of infected individual/food/fomites

eggs hatch in duodenum and larvae migrate to cecum, females mature in ~1 mo and are viable for another month, they migrate through anus to deposit large numbers of eggs on perianal skin

perianal pruritis, insomnia, restlessness, enuresis, excoriation and impetigo, mild GI sx

pinworm

dx pinworm

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