Helminths, Emerging/Reemerging, Biowarfare agents Flashcards
Lymphatic Filariasis
Filarial nematode
Wuchereria bancrofti and Brugia malayi
inflammatory parasitic infection of lymphatic vessels causing lymphangitis and sometimes obstruction
EPIDEMIOLOGY: elephantiasis is most severe form, malayi only coastal southern asia and western pacific islands
ETIOLOGIC: larvae migrate to lymphatics/LN -> mature -> mate -> females release microfilariae ->lymphangitis (filaria fevers) -> scarring/obstruction
PATHOLOGY: white thread like worm convoluted in LN, stain with giemsa, dilated lymphatic vessels, thickened endothelial lining, eosinophils, after multiple infections -> lymphatics become densely fibrotic and contain calcified worms
CLINICAL FEATURES: usually resolves asymptomatically or have recurrent filarial fevers with malaise, small subset get lymphatic obstruction and skin becomes thickened and warty, Rx diethylcarbamazine, ivermectin
TROPICAL PULMONARY EOSINOPHILIA - caused by occult filariasis (antibodies), southern India, pacific islands, cough wheezing, diffuse pulmonary infiltrates, peripheral eosinophilia, can be fatal
Onchocerciasis
Filarial nematode - onchocerca volvulus
“river blindness” - chronic inflamm of skin, eyes, lymphatics
EPIDEMIOLOGY: simulium damnosum blackflies transmits larvae to humans, endemic in rivers and streams
PATHOPHYSIOLOGY: worms do not cause tissue damage or inflamm response, females release many microfilariae which migrate and cause onchocercal lesions, when they dies, inflamm response causes damage
PATHOLOGY: thin long nematode, inchocercal nodules (fibrous encapsulation of many adult worms), ocular involvement
CLINICAL FEATURES: come from microfilariae death, generalized pruruitis that sometimes interferes with sleeping, loss of vision, lymphadenopathy which can lead to elephantiasis, Rx systemic antihelminthic therapy (ivermectin)
Loiasis
Filarial nematode - loa loa - african eyeworm
EPIDEMIOLOGY/PATHOPHYSIOLOGY: central and west africa, transmitted by mango flies, microfilariae circulate during day, reside in capillaries at night, travels in subconjunctival tissues
PATHOLOGY: migrating worms no inflammation, static ones are surrounded by eosinophils, inflamm cells + giant cells, generalzed loiasis with obstructive fibrin thrombi, brain involvement can lead to sudden diffuse cerebral ischemia
CLINICAL FEATURES: most asymptomatic, persist for years, pruritic red subcut CALABAR swellings, ocular swelling, itching, pain, paralysis from dead worms in nerves, Rx microfilariacides
Ascariasis
Intestinal nematode-ascaris lumbricoides
most common helminthic infection, warm climates, poor sanitation
PATHOPHYSIOLOGY: live in small intestine, gravid females lay eggs that come out with feces -> ingested eggs hatch -> penetrate bowel wall -> venous circulation -> lungs -> alveoli -> trachea/glottis -> swallowed to small bowel
PATHOLOGY/CLINICAL FEATURES: adult worms - no pathologic changes, heavy infections complicated by vomiting, malnutrition, obstruction, egg deposition leads to necrosis, granulomatous inflammation, fibrosis, fatal pneumonia, Dx eggs in stools, worms coming out, Rx ascaricidal drugs
Trichuriasis
Intestinal nematode
Trichuris trichiura=Whipworm
EPIDEMIOLOGY: Humans ingest eggs in contaminated soil, food or drink; worldwide; children mostly susceptible
ETIOLOGY:
PATHOPHYSIOLOGY: The anterior “whip” end of Trichuris trichiura is threaded into the superficial mucosa of the colon–> causes small erosions, focal active inflammation and continuous loss of small quantities of blood
PATHOLOGY: in small intestines (cecum & colon)
CLINICAL FEATURES: Most asymptomatic; cramping abdominal pain, bloody diarrhea,
weight loss and anemia; rectal prolapse (rare); characteristic eggs in the stool; Rx mebendazole
Hookworms
Intestinal nematode
Necator americanus (American) & Ancylostoma duodenale (old world)= hookworm
EPIDEMIOLOGY: cause serious public health problems worldwide
ETIOLOGY: Filariform larvae directly penetrate the human epidermis on contact and enter the venous circulation–> travel to
lungs –> lodge in alveolar capillaries–>rupture into alveoli–> migrate to trachea –> to glottis–>swallowed;
PATHOPHYSIOLOGY: lacerate bowel mucosa–>intestinal blood loss–>anemia
PATHOLOGY; grossly visible; attach to mucosal wall with tooth-like buckle plates–> clamp off part of villus –> ingest it
CLINICAL FEATURES: Most asymptomatic; Allergic reactions to cutaneous inoculation and lung migration; intestinal blood loss; asthma-like symptoms; the most important cause of chronic anemia worldwide; pruritic eruption (“ground itch”) where skin penetration occurs; Rx
Strongyloidiasis
Intestinal nematode
Strongyloides stercoralis=threadworm
EPIDEMIOLOGY: smallest of the intestinal nematodes; Appalachian region of U.S. has endemic pockets
ETIOLOGY; rhabditiform larvae= noninfectious
PATHOLOGY
PATHOPHYSIOLOGY: in small bowel (buried in the crypts of the duodenum or jejunum mucosa); can undergo autoinfection with noninfective rhabditiform larvae; filariform is infective stage that penetrates human skin; has lymphocytes/plasma cells/eosinophils infiltrate
CLINICAL FEATURES: Most asymptomatic; Abdominal pain and diarrhea; dissemination to extraintestinal sites in immunocompromised cause fatal disseminated strongyloidiasis or hyperinfection syndrome; moderate eosinophilia; Rx thiabendazole or ivermectin
Pinworm infection (enterobiasis)
Intestinal nematode
Enterobius vermicularis = Pinworm
EPIDEMIOLOGY: people can be infected at any age; most common among young children; ingest eggs; person to person via fingers, bed linens, towels and clothing
ETIOLOGY
PATHOPHYSIOLOGY: adult female worm resides in the cecum and appendix but migrates to the perianal and perineal skin to deposit eggs
PATHOLOGY: migrating worms deposit eggs at night–>cause itching
CLINICAL FEATURES: Perianal and perineal itching; Rx mebendazole
Trichinosis
Tissue nematode
Trichinella spiralis= roundworm
EPIDEMIOLOGY: zoonotic, infect other animals, domestic and wild; under-reported in U.S.
ETIOLOGY: humans ingest inadequately cooked pork with encysted T. spiralis larvae-> develop into adult in intestines–>enter blood–>lodge and encyst in skeletal striated muscle ; larvae can invade nearly any tissue but can survive only in striated skeletal muscle, where they encyst and remain viable for years; cause myositis especially prominent in the diaphragm, extrinsic ocular muscles, tongue, intercostal muscles, gastrocnemius and deltoids
PATHOPHYSIOLOGY:
PATHOLOGY: infected myocytes undergo basophilc degeneration and swelling–>cause eosinophil and macrophage inflammatory infiltrate–>larvae grow and become encapsulated–> decreased inflammation–>Several years later, larvae die and the cysts calcify; small bowel is grossly unremarkable
CLINICAL FEATURES: mostly involve small numbers of cysts; mostly asymptomatic=self-limited, patients recover in a few months; severe disease = abdominal pain, diarrhea, fever, weakness, severe pain and tenderness of affected muscles, extreme eosinophilia, periorbital edema, meningoencephalitis, myocarditis; Rx Severe= corticosteroids;
Antihelminthic drugs required to remove adult worms from the intestine
visceral larva migrans (toxocariasis)
Tissue nematode
Toxocara canis & Toxocara cati = round worms = most common cause
EPIDEMIOLOGY: Transmitted by Cats and Dogs; sporadic disease of young children
ETIOLOGY: zoonotic; live in the intestines of dogs and cats,; humans ingest embryonated ova–>larva infest intestinal wall and enter blood–>In tissues, larvae die and elicit small granulomas–>heal by scarring
PATHOPHYSIOLOGY
PATHOLOGY; infection of deep organs by helminthic larvae migrating in aberrant hosts
CLINICAL FEATURES: mostly asymptomatic; child with hypereosinophilia, pneumonitis and hypergammaglobulinemia and commonly ocular manifestations; CC= loss of vision in 1 eye = toxocaral endophthalmitis
self limited infection, disappear within 1 year
Rx=diethylcarbamazine and thiabendazole
cutaneous larva migrans
Tissue nematode
Mostly caused by Strongyloides stercoralis, Ancylostoma braziliensis and Necator americanus
EPIDEMIOLOGY: Outbreaks in subtropical and tropical beaches; common in plumbers who crawl under houses and animal caretakers
ETIOLOGY: cats and dogs infected are major source
PATHOPHYSIOLOGY
PATHOLOGY: larval nematodes migrate through skin –> cause severe inflammation–> Pruritic “creeping” Eruption on skin
CLINICAL FEATURES; Dx= “serpiginous urticarial trails” raised lesion = ; Rx=Thiabendazole
dracunculiasis
Tissue nematode
Dracunculus medinensis= guinea worm
infection of connective and subcutaneous tissues= Long Adult Worms beneath the Skin
EPIDEMIOLOGY: zoonotic, intermediate host= microscopic aquatic crustacean Cyclops; transmitted in contaminated drinking water; common in rural sub-Saharan Africa, the Middle East, India and Pakistan
ETIOLOGY & PATHOLOGY: adult female nematode in subcutaneous tissues releases numerous larvae through ulcerated blister –> blister immersed in water–>Cyclops crustaceans ingest larvae–>humans ingest cyclops–>1 yr later–>systemic allergic symptoms appear (pruritic urticarial rash; reddish vesiculate papule around ankles); Second-ary infection of the blister occur with spreading cellulitis; Dead worms cause intense inflammatory response–> debilitating
CLINICAL FEATURES: Rx=extracted by local practitioners by progressively twisting it onto a small stick; anthelminthics
schistosomiasis (bilharziasis)
trematodes (flukes)
Schistosoma mansoni (tropical Africa, parts of southwest Asia, South America and the Caribbean islands), Schistosoma haematobium (tropical Africa and parts of the Middle East) and Schistosoma japonicum (parts of China, the Phil- ippines, Southeast Asia and India)
Intense inflammatory and immune responses damage the liver, intestine or urinary bladder
EPIDEMIOLOGY: causes greater morbidity and mortality than all other worm infections; disabling
ETIOLOGY: asexual generations in invertebrate host (snail) and sexual generations in the vertebrate host; motile miracidium penetrates snail in water; final larval stage cercaria penetrate human skin–>become schistosomula–>form male and female worms in intestinal venules of the portal; Female S. mansoni and S. japonicum deposit eggs in intestinal venules; S. haematobium lays eggs in urinary bladder venules
PATHOPHYSIOLOGY:
PATHOLOGY: cause circumscribed granuloma (a cellular infiltrate of eosinophils and neutrophils around an egg)–>obstruct microvascular blood flow –>cause ischemic damage–>progressive scarring and dysfunction;
S. mansoni –> invade IMV–> damage distal colon and liver–>periportal ‘pipestem’ fibrosis–>obstruct portal blood flow –>cause portal hypertension + inflammatory polyps and foci of mucosal and submucosal fibrosis in intestines
urogenital schistosomiasis: S. haematobium –> infect rectum, bladder and pelvic veins–>can cause squamous cell carcinoma of the bladder
S. japonicum–>SMV–>damage small bowel, ascending colon and liver.
CLINICAL FEATURES: skin penetration cause self-limited, intensely pruritic rash; chronic liver granulomatous tissue damage, portal hypertension, splenomegaly, ascites and bleeding esophageal varices, abdominal pain and bloody stools, hematuria, recurrent urinary tract infections, progressive urinary obstruction, chronic cystitis, bladder cancer, renal failure; Dx=schistosome eggs in the urine or feces; Rx= systemic antihelminthics; scarring irreversible
clonorchiasis
trematodes (flukes)
EPIDEMIOLOGY ETIOLOGY PATHOPHYSIOLOGY PATHOLOGY CLINICAL FEATURES
paragonimiasis
trematodes (fluke)
Clonorchis sinensis = Chinese liver fluke
EPIDEMIOLOGY: ingesting inadequately cooked fresh- water fish containing larvae: endemic in east Asia, from Vietnam to Korea; Adult worms are flat and transparent ; Adult worms are flat and transparent, live in human bile ducts and pass eggs to the intestine and feces; specific snail injest egg–> egg hatches into a miracidium–>Cercariae escape from snail –> find and penetrate fish–> encyst in fish-> humans eat the fish–> cercariae emerge in duodenum–> enter common bile duct through the ampulla of Vater –> mature in distal bile ducts–>pass eggs to feces
ETIOLOGY:
PATHOPHYSIOLOGY
PATHOLOGY
CLINICAL FEATURES: cause mild symptoms; most infected persons are asymptomatic; death associated withbiliary obstruction by bile duct stones, bacteria cholangitis, cholangiocarcinoma, pancreatitis; bile ducts are thickened and dilated due to adult flukes; transient fever and chills
Dx= eggs in stools or duodenal aspirates; Rx = systemic antihelminthic
