Parasites and Stings (Andrew's Chapter 20)

Cutaneous Leishmaniasis - subtypes - how does it appear clinically - typical course of disease

Cutaneous leishmaniasis is divided into two subsets based on the geographic region where the infection is acquired: Old World and New World. These two groups differ with regard to the causative organisms, vectors, reservoirs, clinical presentation, and prognosis. Both Old World and New World cutaneous leishmaniasis usually begin as a small, well-circumscribed papule at the inoculation site. This lesion may slowly enlarge over several weeks into a nodule or plaque and then become ulcerated or verrucous (Figs 83.4 & 83.5). Exposed sites such as the face, neck, arms, and legs are most commonly involved. The majority of acute cutaneous infections resolve spontaneously within several months with scarring14 (cicatricial stage; Fig. 83.7), but a minority become chronic or disseminated.

Chigger Bites

A Type of mite Chigger bites are intensely pruritic, especially in highly sensitized individuals. Grouped papules, vesicles, or bullae are typically found on the lower extremities, or where elastic meets the skin. Seasonal penile swelling associated with pruritus and dysuria in children, referred to as "summer penile syndrome", appears to represent a hypersensitivity response to chigger bites. The topical antipruritics and anesthetics discussed above may be helpful. Most patients presenting to a dermatologist require potent topical or intralesional corticosteroid therapy. Vigorous washing with soap and water immediately after the exposure is helpful. Treatment of clothing with permethrin is a useful strategy for prevention.

Larva Migrans - aka - cause? How is the condition acquired? - Clinical presentation, rate of migration

AKA creeping eruption caused by penetration by the larvae of a cat and dog hookworm, Ancylostoma braziliense People who go barefoot on the beach, children playing in sandboxes, carpenters and plumbers working under homes, and gardeners are often victims. The most common areas involved are the feet, buttocks, genitals, and hands. Intermittent stinging pain occurs, and thin, red, tortuous lines are formed in the skin. The larval migrations begin 4 days after inoculation and progress at the rate of about 2 cm/day. However, they may remain quiescent for several days or even months before beginning to migrate. The linear lesions are often interrupted by papules that mark the sites of resting larvae

Platyhlminthes- AKA? Shistosome cercarial Dermatitis - clinical presentation - animal hosts, how is the disease acquired? - Two types? Course of disease?

AKA flatworms which consist of two clases the trematodes and cestodes. Cercarial dermatitis is a severely pruritic, widespread, papular dermatitis caused by cercariae of schistosomes. animal hosts are waterfowl, rodents, muskrats and then snails. Exposure to cercariae occurs when a person swims or, more often, wades in water containing them. They attack by burrowing into the skin, where they die. The species that causes this eruption cannot enter the bloodstream or deeper tissues. After coming out of the water, the bather begins to itch, and a transient erythematous eruption appears, but after a few hours, the eruption subsides, together with the itching. After a quiescent period of 10-15 hours, the symptoms then recur, and erythematous macules and papules develop throughout the exposed parts that were in the water (Fig. 20.14). After several days, the dermatitis heals spontaneously. There are two types: the freshwater swimmer's itch and the saltwater marine dermatitis, or clam digger's itch. Cercarial dermatitis is not communicable.

Mucocutaneous/Mucosal Leishmaniasis -when does it usually develop - most common causative species? - clinical spectrum of disease

After a variable time period ranging from a few months to more than 20 years, mucocutaneous/mucosal disease develops in some patients infected with Leishmania spp. in the Viannia subgenus (known as the L. braziliensis complex), most commonly L. braziliensis and occasionally L. panamensis, L. guyanensis, or hybrid genotypes16. Mucosal lesions range from edema of the lips and nose to perforation of the nasal septum or (less often) the laryngeal cartilage or palate. Infiltration and/or ulceration of the mucosal surfaces of the nose, lips, and oropharynx are typical features (Figs 83.9 & 83.10); ocular or genital involvement is rare. In some patients, there is extensive loss of tissue in both the mouth and nose, causing a characteristic "tapir face" known as espundia. Hoarseness may result from vocal cord involvement

Seaweed Dermatitis - Cause? - occurs when? Found where? clinical presentation?

Although caused by a marine alga and not by an animal, seaweed dermatitis deserves mention with other problems associated with swimming or wading. The dermatitis occurs 3-8 hours after the individual emerges from the ocean. The distribution is in parts covered by a bathing suit: scrotum, penis, perineum, and perianal area. The dermatitis is caused by a marine plant, Lyngbya majuscula Gomont. It has been observed only in bathers swimming off the windward shore of Oahu, Hawaii. Seabather's eruption, clam digger's itch, and swimmer's itch must be differentiated from seaweed dermatitis caused by marine algae. Prophylaxis is achieved by refraining from swimming in waters that are turbid with such algae. Swimmers should shower within 5 minutes of swimming. Active treatment in severe cases is the same as for acute burns.

Bed Bugs - Name of bug - characteristic biting pattern? - Treatment

Bedbugs have flat, oval bodies and retroverted mouthparts used for taking blood meals (Fig. 20.30). Cimex lectularius is the most common species in temperate climates, and Cimex hemipterus is most common in tropical climates. Both are reddish brown and about the size of a tick. C. hemipterus is somewhat longer than C. lectularius. Bedbugs hide in cracks and crevices, then descend to feed while the victim sleeps. It is common for bedbugs to inflict a series of bites in a grouping or row ("breakfast, lunch, and dinner") (Fig. 20.31). Bites may mimic urticaria, and patients with papular urticaria commonly have antibodies to bedbug antigens. Unilateral eyelid swelling has been described as a common sign of bedbug bites in children. Bullous and urticarial reactions also occur. Bedbugs have been suggested as vectors for Chagas disease, Bartonella quintana, and hepatitis B, although data are sparse. Bedbug bites can be treated via topical steroids as above. Ivermectin treatment is emerging as a potential ancillary measure. Bedbugs that fed once on humans 3 hours after they received 200 µg/kg of oral ivermectin had a 63% mortality rate, and survivors were unable to complete their life cycle.

Blister Beetles - produce what agent?

Blister beetles (order Coleoptera) belong to the family Meloidae. These insects produce the blistering agent cantharidin, which serves to protect them from predators. Members of the family Oedemeridae are classified as "false" blister beetles but also produce cantharidin, whereas rove beetles of the family Staphylinidae make another vesicant, pederin (see below). Clinical features Contact with blister beetles typically results in the development of vesicles and bullae within 12-24 hours. Topical application of cantharidin has been used for the treatment of molluscum contagiosum and warts since the 1950s (see Chs 79 & 81). Pathology Histologic sections of the blisters demonstrate acantholysis in suprabasal keratinocytes. Disruption of cell outlines and cellular necrosis may be noted. The profile of adhesion molecule loss in cantharidin blisters is similar to that seen in Darier disease. Treatment Avoidance is the best measure, but immediate washing with soap and water may be of some benefit.

Bug Bite Treatment

Camphor and menthol lotion and gel formulations may be useful in the control of pruritus. Topical anesthetic preparations can also be helpful, and those containing pramoxine are readily available and present a low risk of contact dermatitis. For more persistent bite reactions, topical corticosteroids are often required. In young children, mid-strength corticosteroid preparations may suffice, while in older children and adults, class 1 or 2 corticosteroids are preferable. These agents can be applied under occlusion to enhance efficacy, but for a predetermined time period to avoid potential side effects of cutaneous atrophy and striae. When topical agents fail, intralesional corticosteroid injection (e.g. triamcinolone 5-10 mg/ml) or excision of the pruritic nodule may be necessary. Occasionally, pseudolymphomatous nodules may require higher triamcinolone concentrations (e.g. 20-40 mg/ml).

Chagas disease - caused by what organism, what vector - typically found in what countries? - clinical features? what is romana sign - what are the features of chronic chagas disease? occurs in what % of patients

Caused by T. Cruzi with the vector Reduviid bugs. Typically found in central and south America Clinical Features: Acute Phase: The site of entry develops erythema, swelling, and lymphadenopathy. When the portal of entry is the conjunctiva swelling of the periocular tissues is called Romana sign. Other acute findings are fever, fatigue, malaise. Indeterminate phase: This stage is characterized by asymptomatic parasitemia and positive serology Chronic Chagas disease: Occurs in 30% of patients. The heart is the most commonly affected organ with CHF and or heart block. The GI tract is also affected with megacolon and or megaesophagus

Centipede Bites

Centipede bites are manifested by paired hemorrhagic marks that form a chevron shape caused by the large, paired mouthparts. The bite is surrounded by an erythematous swelling (Fig. 20.25) that may progress into a brawny edema or lymphangitis. Locally, there may be intense itching and pain, often associated with toxic constitutional symptoms. Most centipede bites run a benign, self-limited course, and treatment is only supportive. Treatment is largely symptomatic. Rest, ice, and elevation may be sufficient, but topical or intralesional anesthetics may be required in some cases. Tetanus immunization should be considered if the patient has not been immunized within the past 10 years. Centipede bites can result in Wells syndrome, requiring topical or intralesional corticosteroids. Rarely, bites may produce more serious toxic responses, including rhabdomyolysis, myocardial ischemia, proteinuria, and acute renal failure. These have been reported after the bite of Scolopendra heros, the giant desert centipede. Although centipedes have sometimes been found in association with corpses, injuries from the centipede tend to be postmortem and are rarely the cause of death. Ingestion of centipedes by children is usually associated with transient, self-limited toxic manifestations.

Other Jelly Fish Stings - what is considered the most dangerous jelly fish? - How can you confirm envenomation?

Chironex fleckeri, the Pacific box jellyfish or sea wasp, is generally considered the most dangerous of the jellies, and stings often result in shock. Confirmation of envenomation can be obtained by tape stripping of nematocysts from skin. Physalia physalis, the Portuguese man of war, is found in southern waters of the Atlantic. Physalia utriculus, the blue bottle jellyfish, is seen in the Pacific. Cyanea and Chrysaora sea nettles are common causes of jellyfish dermatitis. Storms frequently drive jellies into shallow water in great numbers.

Mites

Cutaneous reactions to mites are common and include papular, papulovesicular, bullous, urticarial, and morbilliform eruptions (Fig. 85.14). Chigger bites most often affect the lower legs, skin at the edges of underwear, and the genital region. Larvae of trombiculid mites in Asia are vectors for scrub typhus, while house mouse mites transmit rickettsialpox (see Ch. 76). Eschars at the site of the bite are a clue to rickettsial disease, and serologic testing can be helpful. As with tickborne rickettsial diseases, biopsy of the eschar can be sent for immunohistochemical staining or PCR to distinguish typhus group organisms from the spotted fever group Skin lesions in humans may be treated with topical antipruritics such as camphor and menthol, or with topical anesthetics such as pramoxine. Potent topical corticosteroid preparations can be helpful, especially when occluded. Intralesional corticosteroid injections and excision of pruritic nodules may be necessary. Bullous and excoriated lesions can develop secondary infections, and appropriate wound care is important. Popular home remedies typically center around efforts to remove or kill attached mites, and counterirritants (e.g. propylene glycol-containing deodorant sticks) are often applied in an effort to reduce itching. Patients may present with irritant and allergic contact dermatitis to antiseptics, nail polish, or even battery acid.

Histo of Bug Bites

Histologic features suggestive of a bite or sting include the presence of a wedge-shaped perivascular lymphocytic infiltrate with eosinophils, endothelial prominence, and overlying spongiosis or focal epidermal necrosis. Marked spongiosis can result in blister formation, and Langerhans cell hyperplasia may be evident

Leishmaniasis Clinical Pathology - Key finding? - Where can amastigotes be found in disseminated disease?

Histologically, cutaneous lesions typically show ulceration, pseudoepitheliomatous hyperplasia, and a mixed inflammatory infiltrate composed of histiocytes, lymphocytes, plasma cells, and neutrophils. Amastigotes present within dermal macrophages, especially those in the papillary dermis (Fig. 83.12), are evident in ∼50% of skin biopsies. Over time, lesions develop an increasing number of giant cells and fewer parasites; in longstanding cutaneous leishmaniasis, tuberculoid granulomas with caseation necrosis may be observed. In the cicatricial stage, the epidermis becomes flattened and hyperpigmented in areas with dermal fibrosis. Identical changes are seen in mucosal lesions. In diffuse cutaneous leishmaniasis, numerous amastigotes are present within foamy histiocytes; in contrast, the disseminated form features a primarily lymphoplasmacytic infiltrate with few amastigotes. The parasite can be detected in the lymph nodes, bone marrow, and spleen in patients with visceral leishmaniasis.

Cnidarians? - include what animals? Portuguese Man of War Dermatitis - clinical presentation - possible systemic manifestations? - what is found in the nematocysts?

Include: jellyfish, hydroids, Portuguese men-of-war, corals, and sea anemones. These are all radial marine animals, living mostly in ocean water Clinical Presentation: - characterized by linear lesions that are erythematous, urticarial, and even hemorrhagic. The forearms, sides of the trunk, thighs, and feet are common sites of involvement. The usual local manifestation is sharp, stinging, and intense pain. Internally, there may be severe dyspnea, prostration, nausea, abdominal cramps, lacrimation, and muscular pains. Death may occur if the areas stung are large in relation to the patient's size. The fluid of the nematocysts contains toxin that is carried into the victim through barbs along the tentacle. The venom is a neurotoxic poison that can produce marked cardiac changes. Each Portuguese man-of-war is a colony of symbiotic organisms consisting of a blue to red float or pneumatophore with a gas gland, several gastrozooids measuring 1-20 mm, reproductive polyps, and the fishing tentacles bearing the nematocysts from which the barbs are ejected.

Loiasis - initial clinical appearance - Predilection of infected area? - Vector for disease, areas of infection - Treatment

Infection with Loa loa is often asymptomatic. In infected persons, the parasite develops slowly, and even 3 years can elapse between infection and appearance of symptoms, although the usual interval is 1 year. The first sign is often painful, localized, subcutaneous, nonpitting edema called Calabar or fugitive swelling (Fig. 20.20A). One or more, slightly inflamed, edematous, transient swellings occur, usually about the size of a hen's egg. They typically last a few days and then subside, although recurrent swellings at the same site may eventually lead to a permanent, cystlike protuberance. These swellings may result from hypersensitivity to the adult worm or to materials elaborated by it. Eosinophilia may be as high as 90% and often is 60%-80%. The filariae may be noticed subcutaneously in the fingers, breasts, eyelids, or submucosally under the conjunctivae. The worm may be in the anterior chamber of the eye, the myocardium, or other sites. It has a predilection for loose tissues such as the eye region, the frenum of the tongue, and the genitalia. The wanderings of the adult parasite may be noticed because of a tingling and creeping sensation. The death of the filaria in the skin may lead to the formation of fluctuant cystic lesions. Loiasis is widely distributed in West and Central Africa, where it is transmitted by the mango fly, Chrysops dimidia or Chrysops silacea. This fly bites only in the daytime. Humans are the only important reservoir for the parasite. The observation of the worm under the conjunctiva, Calabar swellings, eosinophilia, and microfilariae in peripheral blood establish the diagnosis. Demonstration of the characteristic microfilariae in the blood during the day is possible in only about 20% of patients. Specific serologic tests are available, and luciferase immunoprecipitation systems can provide rapid diagnostic results, with improved sensitivity and specificity compared with enzyme-linked immunosorbent assay (ELISA). Removal of the adult parasite whenever it comes to the surface of the skin is mandatory (Fig. 20.20B). This must be done quickly by seizing the worm with forceps and placing a suture under it before cutting down to it. Worms that are not securely and rapidly grasped may escape into the deeper tissues. Diethylcarbamazine kills both adults and microfilariae and is given in increasing doses for 21 days. In regions where onchocerciasis and loiasis both are endemic, and where ivermectin is used in a community-based elimination strategy for onchocerciasis, simultaneously infected patients with a high L. loa load have a greater risk of serious side effects. If ivermectin treatment of these patients is undertaken, proper monitoring and appropriate supportive treatment should be available in anticipation of this risk. Diethylcarbamazine is an effective chemopreventive therapy, using 300 mg/week in temporary residents of regions of Africa where L. loa is endemic.

Ixodes tick - descibe what it looks like - name the species - vectors for what disease

Ixodes scapularis (formerly also known as I. dammini), the eastern black-legged tick, is the best known of the Ixodes ticks. Adult females are typically found attached to the host in late fall and spring. Ixodes ticks are vectors for Lyme disease, babesiosis, and human granulocytic anaplasmosis. Babesiosis is a malaria-like illness, whereas anaplasmosis is an acute febrile illness characterized by leukopenia, thrombocytopenia, and increased serum hepatic transaminases. In the western US, I. pacificus (the western black-legged tick) is the major vector for Lyme disease (see Fig. 76.12). In the Great Lakes region and eastern US, I. scapularis is the major vector. I. ricinus and I. persulcatus are important vectors for Lyme disease in Europe and Eurasia, respectively. Because the larval and nymph stages of the tick often attach to birds in the spring and summer, avian migration (particularly of robins) may be responsible for the broad geographic distribution of the tick and of Lyme disease.

Leeches - what happens after leeches attach - how can lesions be removed? - what are the possible complications of leech attachment?

Leeches, of the class Hirudinea, are of marine, freshwater, or terrestrial types. After attaching to the skin or mucosa, they secrete an anticoagulant, hirudin, and then engorge themselves with blood. Local symptoms at the site of the bite may include bullae, hemorrhage, pruritus, whealing, necrosis, or ulceration. Allergic reactions, including anaphylaxis, may result. Leeches may be removed by applying salt, alcohol, or vinegar or by use of a match flame. Bleeding may then be stopped by direct pressure or by applying a styptic pencil to the site. Leeches may be used medicinally to salvage tissue flaps that are threatened by venous congestion. However, bleeding, Aeromonas infection, anetoderma, and pseudolymphoma may be complications of their attachment.

Leishmaniasis - Transmitted via? name the two species - what are the four major clinical patterns?

Leishmaniasis encompasses a spectrum of chronic infections in humans and several animal species. It is caused by over 20 species of Leishmania, flagellated protozoans belonging to the order Kinetoplastidae. Transmission is via the bite of infected female sandflies from the genera Phlebotomus (Old World) and Lutzomyia (New World). It has a world wide distribution There are four major clinical patterns: (1) cutaneous, which is restricted to the skin and is seen more often in the Old World; (2) mucocutaneous, which affects both the skin and mucosal surfaces and occurs almost exclusively in the New World; (3) diffuse cutaneous, which occurs mainly in the New World (4) visceral, which affects the organs of the mononuclear phagocyte system, e.g. liver, spleen2

Loxosceles Spiders

Loxosceles spiders are found throughout the world and classically have a dark brown, violin-shaped marking on the dorsal cephalothorax (Fig. 85.16). In the US, bites from L. reclusa (the brown recluse spider), L. laeta, L. rufescens, L. deserta, and L. arizonica can cause skin necrosis, although reactions to the latter three species are generally mild. Many other spiders are capable of producing dermonecrotic or systemic reactions, and bites of these spiders are often erroneously attributed to the brown recluse spider. Brown recluse spiders are most common in the south central US, from Tennessee and Missouri to Oklahoma and Texas (Fig. 85.17). They are often found in woodpiles, in attics, and under radiators. Most bites occur when the spider has been disturbed. Loxosceles spiders are non-aggressive, and there are reports of families living in houses infested by thousands of brown recluse spiders without a single bite. This suggests that brown recluse bites are overdiagnosed, especially in regions where the spider is rare. The diagnosis can be confirmed by an enzyme immunoassay to detect Loxosceles venom in a skin biopsy specimen or plucked hairs (obtained up to 4 days after the bite) or by a passive hemagglutination inhibition test (up to 3 days after the bite); in addition, reduced glycophorin A on the erythrocyte surface may represent a marker of venom exposure. Sphingomyelinase D is the major toxin in brown recluse venom, and it interacts with serum amyloid protein.

Leishmaniasis subtype causes - old world - new world - diffuse cutaneous - visceral

Old World cutaneous leishmaniasis is usually due to L. major or L. tropica, and less often L. infantum (Europe) or L. aethiopica (Ethiopia and Kenya) (see Table 83.1). In the New World, cutaneous leishmaniasis is caused primarily by subspecies of L. mexicana and the L. braziliensis complex, whereas mucocutaneous/mucosal disease is associated with the latter organisms. Diffuse cutaneous leishmaniasis is most commonly associated with L. amazonensis3. Infections with L. donovani(e.g. India, Bangladesh, the Sudan) and L. infantum (e.g. Europe,especially in the setting of HIV infection) as well as the subspecies L. infantum chagasi are the major causes of visceral leishmaniasis

More Amebiasis Cutis - how can amebiasis be diagnosed? - what tests can be used to test for recurrent or active disease? - if you were suspecting it as a cause of chronic urticaria what would you do? - Differential diagnosis? - Treatment?

The histologic findings are those of a necrotic ulceration with many lymphocytes, neutrophils, plasma cells, and eosinophils. E. histolytica is found in the tissue, within blood and lymph vessels. The organism measures 50-60 µm in diameter and has basophilic cytoplasm and a single, eccentric nucleus with a central karyosome. The organism is frequently demonstrable in fresh material from the base of the ulcer by direct smear. Culture of the protozoa confirms the diagnosis. Indirect hemagglutination test results remain elevated for years after the initial onset of invasive disease, whereas the results of gel diffusion precipitation tests and counterimmunoelectrophoresis become negative at 6 months. This property can be used to test for recurrent or active disease in persons coming from endemic areas. DDx: - When the perianal or perineal areas are involved, granuloma inguinale, lymphogranuloma venereum, deep mycosis, and syphilis must be considered. In chronic urticaria, fresh stool examinations by a trained technician are necessary. Treatment: The treatment of choice is metronidazole (Flagyl), 750 mg orally three times daily for 10 days. Abscesses may require surgical drainage.

Major groups responsible in humans for bites, stings, and parasitic infections

The major groups of animals responsible for bites, stings, and parasitic infections in humans belong to the phyla Arthropoda, Chordata, Cnidaria (formerly Coelenterata), Nemathelminthes, Platyhelminthes, Annelida, and Protozoa.

Brown Recluse

The majority of bites by Loxosceles spiders, including the brown recluse, do not cause serious reactions. Local pain is frequently delayed until several hours after the bite, which most often occurs on an extremity (Fig. 85.18). Cutaneous reactions typically begin with erythema and then develop central vesiculation or duskiness with a blanched halo, which may evolve into hemorrhagic bullae and necrosis37. Dermonecrotic reactions can eventuate in dry, necrotic eschars or ulceration. Upper airway obstruction caused by envenomation of the neck by brown recluse spiders has been reported. Systemic reactions include thrombocytopenia and Coombs-positive hemolytic anemia38,39. L. arizonica, a spider found in the southwestern US, causes less severe necrosis but has been implicated as a cause of shock. Histologic findings have been best described in laboratory models of brown recluse spider envenomation in rabbits40. The findings are time-dependent, with early biopsy specimens demonstrating a neutrophilic infiltrate. Later changes include "mummified" coagulative necrosis of the epidermis, adnexal epithelium, and superficial dermis. A neutrophilic band-like infiltrate may still mark the border between viable skin and eschar. Small vessel vasculitis and thrombosis are often evident adjacent to the neutrophilic band, and larger vessel vasculitis resembling polyarteritis nodosa may account for the extent of tissue necrosis seen after some bites. Arterial thrombosis leading to gangrene of the foot has been reported41. Treatment Optimal treatment to prevent dermonecrotic reactions remains elusive. Most bites can be treated with rest, ice, and elevation. Intradermal injection of polyclonal anti-Loxosceles Fab fragments can attenuate necrosis in an animal model up to 4 hours after envenomation, and antivenin may reduce the ultimate size of the necrotic area even when administered up to 48 hours after envenomation42. Hyperbaric oxygen therapy may decrease the final size of ulceration, although results have varied. Studies with more widely available agents such as dapsone, colchicine, and prednisone have been inconsistent and often disappointing43. Dapsone therapy is complicated by the risk for hemolysis, especially in individuals who have a glucose-6-phosphatase dehydrogenase (G6PD) deficiency. Current recommendations for systemic therapy are limited to antivenin (if available) and prednisone (for systemic reactions). Anecdotal reports and some animal data also suggest that intralesional triamcinolone may have some efficacy for dermonecrotic reactions43. The complement inhibitor eculizumab was recently shown to prevent brown recluse venom-induced hemolysis in vitro, and clinical studies are needed to determine the drug's therapeutic potential for brown recluse bite reactions.

Pediculosis - name the three types of pediculosis

Three varieties of the flattened, wingless Anoplura insects infest humans: Pediculus humanus var. capitis (head louse), P. humanus var. corporis (body louse), and Phthirus pubis (pubic or crab louse) (Fig. 20.33). Rarely, zoonotic lice or louselike psocids will cause infestation. Pediculosis Capitis Patients present with intense pruritus of the scalp and often have posterior cervical lymphadenopathy. Excoriations and small specks of louse dung are noted on the scalp, and secondary impetigo is common. Lice may be identified, especially when combing the hair. Nits may be present throughout the scalp but are most common in the retroauricular region. Generally, only those ova close to the scalp are viable, and nits noted along the distal hair shaft are empty egg cases. In extremely humid climates, however, viable ova may be present along the entire length of the hair shaft. Peripilar keratin (hair) casts are remnants of the inner root sheath that encircle hair shafts and may be mistaken for nits. Whereas nits are firmly cemented to the hair, casts move freely along the hair shaft. Head lice readily survive immersion in water but remain fixed to scalp hairs.

Prevention of chiggers and Tick bites - name some tick born diseases? - name an agent that can be used for prevention? - possible adverse outcome?

Tick-borne diseases include rickettsial fevers, ehrlichiosis, Lyme disease, babesiosis, relapsing fever, and tularemia. Most require a sustained tick attachment of more than 24 hours for effective transmission Permethrin-treated clothing, used in conjunction with a repellent, provides exceptional protection against bites in most areas of the world. Permethrin has a good record of safety, although there is a report of congenital leukemia with 11q23/MLL rearrangement in a preterm female infant whose mother had abused permethrin because of a pathologic fear of spiders. Permethrin can induce cleavage of the MLL gene in cell culture, providing a plausible link between the agent and the leukemia.

Visceral Leishmaniasis - aka, primary cause - clinical presentation

Visceral leishmaniasis, or kala-azar, occurs when the parasite spreads to the bone marrow, spleen, and liver3. It is primarily caused by L. donovani in adults and L. infantum or L. chagasi in children. The incubation period ranges from 1 to 36 months. Fever, wasting, cough, lymphadenopathy, and hepatosplenomegaly are the most common systemic findings (Table 83.4). There may be an abrupt onset or slow progression, and fever may be continuous or intermittent. Additional complications include enteritis, oronasal or gastrointestinal hemorrhage, pneumonia, and nephritis, which may lead to death14. Cutaneous manifestations may be disease-specific papules, nodules, or ulcers at infected sites as well as nonspecific findings such as purpura, hyperpigmentation, xerosis, and kwashiorkor-like hair discoloration. Post-kala-azar dermal leishmaniasis develops as a sequela of untreated or treated visceral leishmaniasis3 (Fig. 83.11). This form of cutaneous leishmaniasis is most commonly seen in Sudan and India, where it occurs in 50% and 10% of patients cured of visceral leishmaniasis, respectively17. Onset may be up to 20 years after treatment17. Skin findings include hypopigmented macules, malar erythema, skin-colored nodules, and verrucous papules18.

Widow Spiders

Widow spiders (Latrodectus spp.) are found worldwide, with five species including black, brown, and red variants in North America alone. Latrodectus mactans is the most common black widow spider in North America, with a range that extends to the Caribbean islands. L. tredecimguttatus, L. curacaviensis, and L. indistinctus are black widow spiders found in Europe, South America, and Africa (referred to as a button spider), respectively. Female black widow spiders from North American species have a red hourglass-shaped mark on the ventral abdomen, while species from other areas of the world have different red patterns. Brown (L. geometricus) widow spiders characterized by an orange ventral hourglass shape have a widespread distribution that includes the US, South America, and Africa. Australia has the red-back spider (L. hasselti) and New Zealand the red katipo spider (L. katipo). Widow spiders are typically found in woodpiles, in shoes, and under outhouse seats. Human envenomation usually occurs when the spider's environment is disturbed, and the spider is inadvertently trapped or pressed against the skin. Widow spiders are more aggressive when protecting an egg sack.

Phylum Protozoa - how many cell organisms? - divided based on what? - name the classes

are one-celled organisms, divided into classes according to the nature of their locomotion. Class Sarcodina organisms move by temporary projections of cytoplasm (pseudopods); class Mastigophora by means of one or more flagella; and class Ciliata by short, hairlike projections of cytoplasm (cilia). Class Sporozoa have no special organs of locomotion.

Hookworm Disease - causative organisms - clinical presentation - Talk about the hookworm life cycle in the human body

ground itch, uncinariasis, ancylostomiasis, necatoriasis The earliest skin lesions (ground itch) are erythematous macules and papules, which in a few hours become vesicles. These itchy lesions usually occur on the soles, toe webs, and ankles; they may be scattered or in groups. The content of the vesicles rapidly becomes purulent. These lesions are produced by invasion of the skin by the Ancylostoma or Necator larvae, and they precede the generalized symptoms of hookworm disease by 2 or 3 months. The cutaneous lesions last less than 2 weeks before the larvae continue their human life cycle. There may be as high as 40% eosinophilia about the fifth day of infection. The onset of the constitutional disease is insidious and is accompanied by progressive iron deficiency anemia and debility. During the course of hookworm disease, urticaria often occurs. The skin ultimately becomes dry and pale or yellowish. Hookworm is a specific communicable disease caused by Ancylostoma duodenale or Necator americanus. In the soil, under propitious circumstances, hookworms attain the stage of infective larvae in 5-7 days. When they come into accidental contact with bare feet, these tiny larvae (which can scarcely be seen with a small pocket lens) penetrate the skin and reach the capillaries. They are carried in the circulation to the lungs, where they pass through the capillary walls into the bronchi. They move up the trachea to the pharynx and, after being swallowed, eventually reach their habitat in the small intestine. Here they bury their heads in the mucosa and begin their sexual life.

Filariasis - Causative organisms? - Characterized by what clinically? - vector of disease? - When does elephantiasis usually occur? - Onset of elephantiasis is characterized by what?

Filariasis is a widespread tropical disorder caused by infestation with filarial worms of Wuchereria bancrofti, Brugia malayi, or Brugia timori species. It is characterized by lymphedema, with resulting hypertrophy of the skin and subcutaneous tissues, and by enlargement and deformity of the affected parts, usually the legs, scrotum, or labia majora. The disease occurs more frequently in young men than women. Filaria are transmitted person to person by the bites of a variety of mosquitoes of the Culex, Aedes, and Anopheles species. The adult worms are threadlike, cylindrical, and creamy white. The females are 4-10 cm long. Microfilarial embryos may be seen as coiled, each in its own membrane near the posterior tip. Fully grown, sheathed microfilariae are 130-320 µm long. The adult worms live in the lymphatic system, where they produce microfilariae. These either remain in the lymphatic vessels or enter the peripheral bloodstream. An intermediate host is necessary for the further development of the parasite. It is important to realize that infestation by the filaria is often asymptomatic, and elephantiasis usually occurs only if hundreds of thousands of mosquito bites occur over a period of years, The onset of elephantiasis is characterized by recurrent attacks of acute lymphangitis in the affected part, associated with chills and fever (elephantoid fever) that last for several days to several weeks. These episodes recur over several months to years. After each attack, the swelling subsides only partially, and as recrudescences supervene, thickening and hypertrophy become increasingly pronounced. The overlying epidermis becomes stretched, thin, and shiny, and over years, leathery, insensitive, and verrucous or papillomatous from secondary pyogenic infection. The patient may have a dozen or more attacks in a year.

Amblyomma Ticks - describe the tick, and where it is found - what two conditions does it serve as the vector for? - associated with an allergy to what food via what mechanism?

Amblyomma ticks are particularly common in the southern US. This, plus the characteristic white dorsal spot of the female A. americanum (Fig. 85.10; see Fig. 76.1), has given rise to the common name "lone star tick". Once the tick has been removed, delayed-type hypersensitivity to tick antigens can lead to a reaction at the attachment site. Papular, nodular, and bullous lesions are common. A. americanum is the major vector of Ehrlichia chaffeensis, the agent of human monocytic ehrlichiosis31. This disease has been documented in more than 30 states, with systemic symptoms similar to those of RMSF (e.g. fever and headache) and variable cutaneous manifestations (see Ch. 76). A. americanum is also the primary vector for Ehrlichia ewingii infection. Southern tick-associated rash illness (STARI; "Missouri Lyme disease") was originally described in Missouri but can also occur in other southern and southeastern states. It presents with an expanding erythematous annular plaque 3-14 days after A. americanum attachment, often in association with fever, headache, myalgias, and arthralgias. Borrelia lonestari has been implicated as a potential cause. Amblyomma tick bites have been associated with allergy to beef, pork, and lamb via development of IgE antibodies specific to galactose- α-1,3-galactose, a blood group substance of non-primate mammals. Urticaria, angioedema, or anaphylaxis typically develops 3-5 hours after eating red meat

Other Amebas - name two other amebas that can cause skin lesions? - most common manifestation of infection with these amebas? - Acanthamoeba: typically seen in whom? presentation - Balamuthia mandrillaris: typically involves what area?

Amebas of the genera Acanthamoeba and Balamuthia may also cause skin lesions in infected hosts. These organisms are ubiquitous in the environment and are found in soil, water, and air. Granulomatous amebic encephalitis is the most common manifestation of infection with these amebas. Acanthamoeba is almost always seen in immunocompromised ppl with disseminated pink or violaceous nodules that enlarge, suppurate, and form ulcers. CNS involvement is common and leads to death quickly. Organisms are visible on biopsy and culture is definitive. Treatment is 5-fluorocystosine and sulfadiazine In Balamuthia mandrillaris involvment of the central face is typical.

Class Sarcondina Amebiasis Cutis - causative organism, mostly found where? Typical presentation - Typical lesions - what can be the sole manifestation of early amebiasis

Amebiasis Cutis and other amebias Entamoeba histolytica-induced cutaneous ulcers usually result from extension of an underlying amebic abscess; the most common sites are the trunk, abdomen, buttocks, genitalia, and perineum. Those on the abdomen may result from hepatic abscesses. Mostly found in the tropics. Infection can be asymptomatic or associated with hepatic abscess and bloody diarrhea. In the United States the disease occurs chiefly in institutionalized patients, world travelers, recent immigrants, migrant workers, and men who have sex with men. Penile ulcers are associated with insertive anal intercourse. Most lesions begin as deep abscesses that rupture and form ulcerations with distinct, raised, cordlike edges, and an erythematous halo approximately 2 cm wide. The base is covered with necrotic tissue and hemopurulent pus containing amebas. These lesions are from a few centimeters to 20 cm wide. Without treatment, slow progression of the ulcer occurs in an increasingly debilitated patient until death ensues. Patients may also present with fistulas, fissures, polypoid warty lesions, or nodules. The sole manifestation of early amebiasis may be chronic urticaria!!

Clinical Presentation of African Trypansomiasis -Diagnosis -Differential diagnosis -Treatment

An indurated, painful reaction develops at the portal of entry of the organisms, referred to as a "trypanosomal chancre" 1-2 weeks after fly bite. I-3 weeks after infection the patient develops fevers, malaise, symmetrical lymphadenopathy. A transient eruption of annular and targetoid erythematous patches or urticarial plaques may occur in concert with fever spikes. The final stage of disease is characterized by neurologic manifestations Diagnosis: - PCR is the most sensitive test - identification of parasites in the skin, blood, or CSF DDx includes annular erythemas, primary syphillis or HIV First-line treatments for the early/hemolymphatic stage of East and West African trypanosomiasis are suramin and pentamidine, respectively. For the meningoencephalitic stage, melarsoprol is utilized for East African disease, while eflornithine ± nifurtimox has become the first-line treatment for the West African form.

Insect repellents - what % of DEET should be used in children? - what type of toxicitiy has been reported with the use of DEET? - Most affective candles?

DEET (N,N-diethyl-3-methylbenzamide, previously called N,N-diethyl-m-toluamide). DEET has been tested against a wide range of arthropods, including mosquitoes, sandflies, ticks, and chiggers. The American Academy of Pediatrics recommends concentrations of 30% or less in products intended for use in children. Some evidence suggests that children do not have a higher incidence of adverse reactions than adults, but even in adults, neurotoxicity has been occasionally reported. High concentrations of DEET can produce erythema and irritation or bullous eruptions. Extended-release products reduce the need for repeated application and appear to minimize the risk of complications. Overall, DEET has a good safety record in widespread use. Picaridin is a piperidine-derived repellent ingredient that is also effective against a range of arthropods. Some studies have shown that picaridin is less irritating than DEET while providing comparable efficacy. The best studies for the evaluation of repellents are field trials that involve a range of arthropods. "Arm box" studies are still performed but must be interpreted with caution. Citronella candles have little documented efficacy, but neem oil is an effective mosquito repellent used in many areas of the world that are endemic for malaria. Geraniol candles show some efficacy, but only in the area immediately surrounding the candles. Repellency decreases significantly at a distance of even 2 m. Candles with geraniol are twice as effective as those with linalool and five times as effective as those with citronella. IR3535 (ethyl-butyl-acetyl aminopropionate) in a variety of formulations has also demonstrated good efficacy against mosquitoes, with complete protection in field trials of 7.1-10.3 hours.

Dermacentor ticks - name the two species and where they are found - primary vector for what disease?

Dermacentor ticks are commonly found in open areas with low bushy vegetation, but they are scarce in heavily wooded areas. Peak abundance of the tick is in April and May, declining by July. D. variabilis is found throughout the US, except for the Rocky Mountain states. In parts of Canada, its range overlaps with that of D. andersoni, which is generally confined to the Rocky Mountains. In Georgia and South Carolina, D. variabilis is the second most common tick found on humans (A. americanum being the most common). Dermacentor ticks preferentially attach to the head and neck region; in contrast, Amblyomma americanum prefers the lower legs, buttocks and groin, and Ixodes scapularis shows less site preference but most often attaches to the trunk. D. variabilis is the major vector for RMSF in the US33. The highest incidence of RMSF is in the eastern states, especially in North Carolina (see Fig. 76.2). RMSF typically presents with fever and headache. An acral eruption of erythematous macules and/or petechiae may be evident but is commonly absent early in the disease process. As many as 40% of patients with RMSF are not aware of a recent tick bite. As the mortality rate in RMSF is heavily dependent on the interval between onset of symptoms and initiation of antibiotic therapy, the disease should be considered in every patient with fever and a headache in endemic areas. D. andersoni is the major vector for RMSF in the Rocky Mountain states, and it is also the vector for the viral illness Colorado tick fever. Because the symptoms of Colorado tick fever overlap with those of RMSF, specific diagnostic tests such as paired serologic studies (acute and convalescent) and immunohistochemical staining, direct immunofluorescence, or PCR-based analysis of lesional skin biopsy specimens can help to confirm the diagnosis of RMSF (although empiric treatment should not be delayed until the results are available). Additional diseases that can be transmitted by Dermacentor ticks include tularemia, rickettsial infections in Europe and Asia, 364D rickettsiosis in California (Dermacentor occidentalis), and occasionally, human monocytic ehrlichiosis and Q fever (Coxiella burnetii).

Chagas Disease - best method for diagnosis of acute disease? chronic? - Treatment, treatment for chronic?

Diagnosis: acute Chagas disease is typically based upon the microscopic identification of either trypomastigotes in the blood (or CSF) or amastigotes within tissue. Because the concentration of parasites is low even in the acute stage, hemoconcentration techniques are used to enhance the yield. PCR currently represents the most sensitive diagnostic method for acute disease, with positive results days to weeks earlier than microscopy; PCR is especially useful for the diagnosis of infections acquired vertically, via organ transplantation, or after laboratory exposure54. Cultures of blood, CSF, or tissue are less sensitive for detection of acute T. cruzi infection. Serologic tests such as ELISAs and immunofluorescent antibody assays (IFAs) are used to establish the diagnosis of chronic Chagas disease Treatment: Treatment is most effective early in the course of Chagas disease55. Benznidazole and nifurtimox (both available through the CDC) can reduce the severity and duration of symptoms associated with the acute phase, with a parasitologic cure in 60-90% of patients51a,56. Because benznidazole is better tolerated, it is favored by most experts. There is no treatment shown to slow or improve chronic chagas disease

Pediculosis Capitis Treatment - name some therapeutic options?

Effective therapeutic agents must kill or remove both lice and ova. Ulesfia (containing benzyl alcohol) is the first nonneurotoxic U.S. Food and Drug Administration (FDA)-approved treatment for lice and represents a significant advancement. Topical spinosad, 4% dimeticone liquid gel, malathion gel, and topical ivermectin are other innovations in the treatment of head lice, but permethrin remains the most widely used pediculicide in the United States, despite widespread resistance. It is available as an over-the-counter (OTC) 1% cream rinse (Nix) and a 5% prescription cream (Elimite) that is marketed for the treatment of scabies. The 1% cream rinse must be applied after shampooing and drying the hair completely. Applying to dry hair lessens dilution of the medication. Product labeling states the medication should be applied for 10 minutes, then rinsed off, but longer applications may be required. Shampooing should not take place for 24 hours afterward. Permethrin has a favorable safety profile, although congenital leukemia has been reported, as noted earlier, and the use of insecticidal shampoos is statistically associated with leukemia. Other reported side effects include acute onset of stuttering in a toddler. Pyrethrins, combined with piperonyl butoxide (RID, A-200, R+C shampoo), are other OTC products. Lindane is rarely used because of low efficacy and potential neurotoxicity. Carbaryl is used in many parts of the world, but not in the United States. Because of the potential toxicity associated with chemical pediculicides, future therapies will be asphyxiating agents, such as those containing benzyl alcohol or dimeticone. Cure rates with dimethicone are significantly higher than with permethrin in some studies, but some dimethicone products are flammable. Other agents that asphyxiate or desiccate contain isopropyl myristate 50% or Neem oil. Nit combing is an important adjunct to treatment but is impractical as a primary method of therapy. Metal combs are more effective than plastic combs. Acidic cream rinses make the hair easier to comb but do not dissolve nit cement, which is similar in composition to amyloid. Various "natural" remedies are marketed that contain coconut oil, anise oil, and ylang ylang oil, but these agents are potential contact allergens, and data are sparse regarding their safety and efficacy. Some data support the efficacy of tea tree oil, which is more potent than lavender or lemon oil. Other studies also support combination lotions containing 5% lavender, peppermint, and eucalyptus oils, or 10% eucalyptus and peppermint oils in various combinations of water and alcohol. The addition of 10% 1-dodecanol improves efficacy.

Exaggerated insect bite reactions can be seen in what context? - what should be done as a result? What adverse hematologic and cardiac issues have been seen following bee stings?

Exaggerated insect bite reactions (e.g. papulovesicular, nodular) can represent a manifestation of chronic lymphocytic leukemia and less often other hematologic malignancies (see Ch. 33). In addition, hypersensitivity to mosquito bites with bullous and necrotic skin lesions may occur in individuals (typically Asian or Hispanic children and adolescents) with chronic EBV infection and proliferation of EBV carrying natural killer (NK) cells (see Ch. 80)1. Screening for hematologic malignancies and latent EBV infection, including in situ hybridization to detect EBV RNA in biopsy specimens of lesional skin if positive serology, should be considered in patients with unusual arthropod bite reactions. Bee and wasp stings typically produce immediate burning pain, which is followed by the development of local erythema and swelling that usually subsides within a few hours to days but can be more severe and persistent in sensitized individuals. Atrial arrhythmias have been reported after bee stings in the absence of anaphylaxis. Killer bee and wasp attacks may be associated with myoglobinuria or hemoglobinuria and acute tubular necrosis. Although bee stings have been utilized as an alternative therapy for inflammatory arthritis, beekeepers may develop a chronic arthropathy related to stings.

African Trypansomiasis - what are the two forms? causative agent for both? - vector for disease?

Fatal if left untreated There are two forms: - West african form: due to Trypanosoma brucei gambiense, is a chronic, anthroponotic disease with primarily neurologic features. - The East African form, caused by Trypanosoma brucei rhodesiense, is an acute, zoonotic disease (with antelopes as a reservoir) that is often fatal. Fortunately, T. b. rhodesiense only occasionally infects humans, mainly farmers, hunters, and tourists Both types of T Brucei are transmitted by tsetse flies genus glossina

Fleas - most common flea on a dog? - Fleas serve as vectors for what diseases?

Fleas (order Siphonaptera) are ubiquitous pests and show little host specificity. The most common flea on dogs is Ctenocephalides felis, the cat flea. Pulex irritans, the human flea (Fig. 85.8), is a common dog flea in some locations. It is also found on wild animals with no human contact. Flea bites present as intensely pruritic papulovesicles, usually located on the lower legs. Other parts of the body may also be affected, especially when an infested pet has been groomed or held. Flea allergy is common, and allergic patients tend to react to a wide range of fleas. Flea pupae can lie dormant for many months then hatch rapidly in response to vibration. Individuals who enter a vacant house can find that fleas rapidly besiege them. Fleas serve as vectors for endemic (murine) typhus, flea-borne spotted fever, plague, and (primarily among cats) Bartonella henselae infection (see Chs 74 & 76). Endemic typhus is common in southern Texas and California, where the cat flea and Xenopsylla cheopis (the oriental rat flea) are the primary vectors, respectively. Lufenuron, available in oral and injectable formulations, prevents fleas from reproducing and is an effective treatment for infested animals. Topical fipronil can then be used to prevent flea infestation in animals. Boric acid, growth regulators such as pyriproxyfen, and insecticides may be helpful adjunctive treatments for the infested environment. The best source of information is a knowledgeable veterinarian. Tungiasis is usually treated surgically. A double-blinded randomized controlled trial of oral ivermectin (300 mcg/kg on two consecutive days) showed it to be ineffective in treating patients with multiple lesions.

Dracunculiasis - Limited to what area of the world? - causative organism and method of infection - Clinical Presentation - Treatment?

Guinea worm disease is now limited to remote villages in several sub-Saharan African countries. It is caused by Dracunculus medinensis and is contracted through drinking water that has been contaminated with infected water fleas in which Dracunculus is parasitic. In the stomach, the larvae penetrate into the mesentery, where they mature sexually in 10 weeks. The female worm then burrows to the cutaneous surface to deposit her larvae and thus causes the specific skin manifestations. As the worm approaches the surface, it may be felt as a cordlike thickening and forms an indurated cutaneous papule. The papule may vesiculate, and a painful ulcer develops, usually on the leg. The worm is often visible. When the parasite comes in contact with water, the worm rapidly discharges its larvae, which are ingested by water fleas (Cyclops), contaminating the water. The cutaneous lesion is usually on the lower leg, but it may occur on the genitalia, buttocks, or arms (Fig. 20.18). In addition to the ulcers on the skin, there may be urticaria, GI upset, eosinophilia, and fever. Surgical removal is the treatment of choice. Metronidazole, 500 mg/day, resolves the local inflammation and permits easier removal of the worm. Immersion in warm water promotes emergence of the worm. Global eradication is within reach, and Guinea worm disease may become a historical footnote.

More Hookworm - Most Common Locations for hookworms - How is the diagnosis established? - Treatment?

Hookworm is prevalent in most tropical and subtropical countries and is often endemic in swampy and sandy localities in temperate zones. In these latter regions, the larvae are killed off each winter, but the soil is again contaminated from human sources the following summer. N. americanus prevails in the Western Hemisphere, Central and South Africa, South Asia, Australia, and the Pacific islands. The defecation habits of infected individuals in endemic areas are largely responsible for its widespread distribution, as is the use of human feces for fertilization in many parts of the world. In addition, the climate is usually such that people go barefoot because of the heat or because they cannot afford shoes. Infection is thereby facilitated, especially through the toes. Finding the eggs in the feces of a suspected individual establishes the diagnosis. The ova appear in the feces about 5 weeks after the onset of infection. The eggs may be found in direct fecal films if the infection is heavy, but in light infections, it may be necessary to resort to zinc sulfate centrifugal flotation or other concentration methods. Mixed infections frequently occur. Albendazole, 400 mg once, or mebendazole, 100 mg twice daily for 3 days or 500 mg once, or pyrantel pamoate, 11 mg/kg (maximum 1 g) each day for 3 days, is effective. Prophylaxis is largely a community problem and depends on preventing fecal contamination of the soil. This is best attained by proper sanitary disposal of feces, protecting individuals from exposure by educating them about sanitary procedures, and mass treatment through public health methods.

Treatment of Jelly Fish Stings - generally treat with what? - box jellyfish stings should always be treated with what? which should not? - what should be done with large visible tentacles? - What to do after decontamination? - specific antivenon is available for what? how should it be adminstered?

Hot water immersion may be an effective remedy for many stings, but scald injuries must be avoided. In the case of box jellies, ice has been shown to be equally effective, but ice can worsen stings of some other jellies. Undischarged nematocytes should be removed. Fresh water, and even sea water, may cause them to discharge. Pacific Chironex (box jellyfish) nematocytes should always be inactivated with 5% acetic acid (vinegar) when it is available, but Pacific Physalia (bluebottle) nematocytes may discharge on contact with vinegar. Large, visible tentacles may be removed with forceps in a double-gloved hand. Remaining nematocysts may be removed by applying a layer of shaving cream and shaving the area gently. Meat tenderizer may cause tissue damage and has been shown to be no better than placebo in some studies. Pressure dressings and abrasion will worsen the envenomation. Topical anesthetics or steroids may be applied after decontamination. Systemic reactions may occur through either large amounts of venom or a previously sensitizing exposure from which anaphylaxis may result, and systemic treatment with epinephrine, antihistamines, or corticosteroids may be needed. Specific antivenin is available for the box jellyfish, Chironex fleckeri. This should be administered intravenously to limit myonecrosis. Magnesium sulfate (MgSO4) may also be of value in the setting of box jellyfish envenomation. Recurrent jellyfish reactions have shown partial responses to tacrolimus ointment 0.1%.

Acquired Toxoplasmosis - important in what patients? - infection typically occurs how? - treatment?

Important in adults who are pregnant, immunocomproimised patients Toxoplasma gondii is a crescent-shaped, oval, or round protozoan that can infect any mammalian or avian cell. Toxoplasmosis is often acquired through contact with animals, particularly cats. Reservoirs of infection have been reported in dogs, cats, cattle, sheep, pigs, rabbits, rats, pigeons, and chickens. The two major routes of transmission of T. gondii in humans are oral and congenital. Meats consumed by humans may contain tissue cysts, thus serving as a source of infection when eaten raw or undercooked. There is no evidence of direct human-to-human transmission, other than from mother to fetus. The diagnosis cannot be made on clinical grounds alone. It may be established by isolation of T. gondii; demonstration of the protozoa in tissue sections, smears, or body fluids by Wright or Giemsa stain; characteristic lymph node histology; and serologic methods. In the patient with bone marrow transplantation, the organism has caused interface dermatitis, creating the potential for misdiagnosis as graft-versus-host disease. A combination of pyrimethamine (Daraprim) and sulfadiazine acts synergistically and forms an effective treatment, but toxicity is substantial. Dosages and total treatment time vary according to the age and immunologic competence of the infected patient.

Trichinosis - causative organism? how is the disease acquired? - treatment

Ingestion of Trichinella spiralis larva-containing cysts in inadequately cooked pork, bear, or walrus meat may cause trichinosis. It usually causes a puffy edema of the eyelids, redness of the conjunctivae, and sometimes urticaria or angioedema associated with hyperpyrexia, headache, erythema, GI symptoms, muscle pains, and neurologic signs and symptoms. Ten percent of patients develop a bilateral, asymptomatic hand swelling that is especially prominent over the digits, as well as erythema along the perimeters of the palms and volar surfaces of the digits, which progresses to desquamation. In 20% of cases, a nonspecific macular or petechial eruption occurs, and splinter hemorrhages are occasionally present. Eosinophilia is not constant but may be as high as 80%. In the average patient, eosinophilia begins about 1 week after infection and attains its height by the fourth week. The immunofluorescence antibody test has the greatest value in establishing early diagnosis. The bentonite flocculation test, ELISA, and other serologic tests are limited by their inability to detect infection until the third or fourth week. Diagnosis is confirmed by a muscle biopsy that demonstrates larvae of T. spiralis in striated muscle. Unfortunately, trichinae cannot usually be demonstrated unless eosinophilic vasculitis and granulomas have been described on biopsy. A 2-mm-thick slice of the muscle biopsy may be compressed between two glass slides to demonstrate the cysts. Trichinosis is treated with albendazole, 400 mg twice daily for 14 days. Corticosteroid agents are effective in controlling the often severe symptoms and should be given at doses of 40-60 mg/day.

Larva Currens - causative organism? - How does the infection occur? - Migration time - Treatment

Intestinal infections with Strongyloides stercoralis may be associated with a perianal larva migrans syndrome called larva currens because of the rapidity of larval migration (currens means "running" or "racing"). Larva currens is an autoinfection caused by penetration of the perianal skin by infectious larvae as they are excreted in the feces. An urticarial band is the prominent primary lesion of cutaneous strongyloidiasis. Strongyloidiasis, as with the creeping eruption secondary to it, is often a chronic disease; infections may persist for more than 40 years. Approximately one third of patients infected are asymptomatic. Signs and symptoms of systemic strongyloidiasis include abdominal pain, diarrhea, constipation, nausea, vomiting, pneumonitis, urticaria, eosinophilic folliculitis, and a peripheral eosinophilia. The skin lesions originate within 30 cm of the anus and characteristically extend as much as 10 cm/day. Administration of ivermectin, 200 µg/kg/day for 2 days, or thiabendazole, 50 mg/kg/day in two doses (maximum 3 g/day) for 2 days, is the treatment of choice. Immunosuppressed hosts may be treated with thiabendazole, 25 mg/kg twice daily for 7-10 days

Dog and Cat Bites

Introduction Cat bites are commonly provoked, whereas dog bites are often unprovoked. Dog bites are particularly common in children, and the dog is usually a family pet or a neighbor's dog. Rabies still occurs almost everywhere in the world, with exceptions including New Zealand, parts of Europe, parts of South America, and isolated Pacific islands. Rabies associated with dog bites remains a problem in low-income countries. Fortunately, because of vaccination programs, rabies related to dog bites is rare in high-income countries, where most human rabies is associated with bat exposure. In the US, rabies is carried primarily by bats, raccoons, and skunks. Although unvaccinated dogs occasionally acquire rabies from wild animals, the canine rabies virus variant that is responsible for dog-to-dog transmission has not been detected in the US since 2004. Oral rabies vaccination programs using bait to target gray foxes and coyotes in Texas and raccoons in the eastern US have helped to decrease the spread of rabies. Local health authorities should be contacted to report a dog or cat bite and (if necessary) to arrange for quarantine. Latex agglutination testing of dog saliva for rabies antigen is 95% sensitive compared to fluorescent antibody testing on brain smears. Clinical features Common pathogens associated with bite wounds include streptococci, staphylococci, Pasteurella spp., Capnocytophaga canimorsus, and anaerobes. Breast implant infection and lung abscesses due to Pasteurella multocida have been linked to cat exposure, and staphylococcal endocarditis has been reported after a cat bite (without a preceding local infection); brain abscess formation has been observed following a dog bite. In immunocompromised patients, there is a significant risk of Pasteurella or Capnocytophaga sepsis. Capnocytophaga canimorsus sepsis has a high mortality rate and has been associated with purpura fulminans. Human bites have a higher likelihood of infections with Staphylococcus aureus and Eikenella corrodens. The most common pathogens associated with bite wound infections are listed in

Scorpions

Introduction Many toxic scorpions exist worldwide. Scorpions are typically found under tabletops, in woodpiles, and in shoes. They sting when disturbed and accidentally trapped by a hand or foot. Several clinically relevant species are listed in Table 85.8. Clinical features Local and systemic symptoms (e.g. pain, paresthesia) are typically out of proportion to cutaneous signs such as erythema and edema, which are not usually prominent at the site of the sting. Most fatalities are related to cardiorespiratory manifestations, including cardiogenic shock and pulmonary edema, in children younger than 10 years of age. Pancreatitis is also an important cause of morbidity after scorpion envenomation. Treatment Antivenin is available in endemic areas and, along with supportive care, has been shown to reduce morbidity and mortality from severe scorpion envenomation46,47. However, application of ice is sufficient for most minor scorpion envenomations. Prazosin reverses the autonomic storm characteristic of Indian red scorpion (Mesobuthus tamulus) envenomation, resulting in accelerated recovery and preserved myocardial function. Tacrolimus was also found to have protective effects against systemic toxicity from scorpion envenomation in an animal model

Snake Bites

Introduction Snake bites occur primarily in individuals who engage in outdoor activities, especially camping and hiking. Occupational bite injuries may also affect those who raise snakes and are particularly common in those who extract venom. Death from a snake bite is rare in the US but more common in Africa and Asia50. Clinical features Snake bites are typically associated with marked edema within an hour of the envenomation. Hemorrhage and necrosis are common. The presence of paired bite marks is often noted. Treatment Antivenin therapy is an important part of management and may be of benefit even when administration is delayed. Adverse reactions to antivenin include serum sickness and anaphylaxis. Preparations to treat anaphylaxis should be made before initiating antivenin therapy. Hypersensitivity to antivenin is a particular problem for those who have been previously treated. The evaluation of antivenin reactions is complicated because serum sickness and snake bites share some signs and symptoms, and repeated snake bites can be independently associated with IgE-mediated anaphylaxis. Even in individuals who have never received previous treatment, snake antivenin can result in anaphylactoid reactions. Thrombocytopenia induced by rattlesnake venom is only partially reversed by antivenin (Crotalidae) administration, and disseminated intravascular coagulation caused by North American crotalid snakebites can occur even after antivenin treatment. The risk of severe bleeding is higher in patients who take antiplatelet drugs51. Tourniquets to limit systemic toxicity from the venom may lead to tissue ischemia if improperly applied. Studies have not been performed for all snakes, but tourniquet application appears to be of little benefit.

Tarantulas

Introduction Tarantulas are large hairy spiders common in the southwestern US, and related species are found throughout the world. They are often sold in pet stores. Most tarantula bites do not produce severe systemic toxicity. Many species of tarantulas possess urticating hairs in a characteristic patch on the dorsal abdomen. These hairs are used in a defensive fashion to drive predators from the spider's burrow. Vibrations of the hind legs are used to flick hairs at the perceived attacker. Urticating hairs are absent on most African and Asian species. Clinical features Itching at the site of urticating hair penetration may persist for several weeks after exposure. Hairs that penetrate the cornea can result in ophthalmia nodosa, a chronic granulomatous reaction that can lead to loss of vision. Pathology Urticating tarantula hairs penetrate the stratum corneum and epidermis and may extend as deep as the reticular dermis.

Caterpillar Dermatitis - clinical presentation - cause of eruption - name some important caterpillars in the US

Irritation is produced by contact of caterpillar hairs with the skin. Toxins in the hairs can produce severe pain, local pruritic erythematous macules, and wheals, depending on the species. If the hairs embed in the clothing, widespread persistent dermatitis may result. Characteristic railroad track pattern. Not only the caterpillars, but also their egg covers and cocoons usually contain stinging hairs. In the United States the most common caterpillars of medical importance are the brown-tail moth caterpillar (Nygmia phoeorrhoea), puss caterpillar (Megalopyge opercularis) (Figs. 20.27 and 20.28), saddleback caterpillar (Sibine stimulate; Fig. 20.29), io moth caterpillar (Automeris io), crinkled flannel moth caterpillar (Megalopyge crispata), Oklahoma puss caterpillar (Lagoa crispata), Douglas fir tussock moth caterpillar (Orgyia pseudotsugata), buck moth caterpillar (Hemileuca maia), and flannel moth caterpillar (Norape cretata).

Gnathostomaiasis - clinical presentation - Name of the clinical manifestation - Causative organism, most cases occur where? how is the condition acquired - Treatment?

Migratory, intermittent, erythematous, urticarial plaques characterize human gnathostomiasis. Each episode of painless swelling lasts from 7-10 days and recurs every 2-6 weeks. Movement of the underlying parasite may be as much as 1 cm/hr. The total duration of the illness may be 10 years. Histopathologic examination of the skin swelling will demonstrate eosinophilic panniculitis. The clinical manifestation has been called larva migrans profundus. The nematode Gnathostoma dolorosi or G. spinigerum is the cause, and most cases occur in Asia or South America. Eating raw flesh from the second intermediate host, most often freshwater fish, especially eel, in such preparations as sashimi and ceviche, allows humans to become the definitive host. Eating raw squid or snake is a less common exposure. As the larval cyst in the flesh is digested, it becomes motile and penetrates the gastric mucosa, usually within 24-48 hours of ingestion. Symptoms then occur as migration of the parasite continues. Surgical removal is the treatment of choice, if the parasite can be located. This may be combined with albendazole, 400 mg/day or twice daily for 21 days, or ivermectin, 200 µg/kg/day for 2 days. Creeping eruption caused by a recently recognized causative parasite of the nematode superfamily Spiruroidea has been reported in Japan. Eating raw squid was associated with the onset of long, narrow lesions that were pruritic, linear, and migratory. Surgical removal is the treatment of choice currently, as data on ivermectin are mixed.

Moth Dermatitis

Moth dermatitis may be initiated by the hairs of the brown-tail moth (Euproctis chrysorrhoea), goat moth (Cossus cossus), puss moth (Dicranura vinula), gypsy moth (Lymantria dispar), and Douglas fir tussock moth (Hemenocampa pseudotsugata). In Latin America, the moths of the genus Hylesia are most frequently the cause of moth dermatitis. Severe conjunctivitis and pruritus are the first signs and may persist for weeks aboard ships that have docked in ports where the moth is common. Caripito itch is named after Caripito, Venezuela, a port city where the moth is found. Korean yellow moth dermatitis is caused by Euproctis flava Bremer. Saturnid caterpillars (Lonomia sp.) are associated with a severe and often fatal hemorrhagic diathesis. In India, inhalation of tiger moth fluids, scales and hairs has been implicated as a causes of severe fever and death during the monsoon season. Topical applications of various analgesics, antibiotics, and oral antihistamines are of little help. Topical or oral corticosteroids are sometimes helpful, as is scrubbing and tape stripping of skin. Contaminated clothing may need to be discarded if dermatitis persists after the clothing is washed.

New World Cutaneous Leishmaniasis - possible subtypes Disseminated cutaneous leishmaniasis - most often result from what? - results in what clinical setting

New World cutaneous leishmaniasis has a wide clinical spectrum, including plaque-like, sporotrichoid, pustular, impetigo-like, eczematoid, sarcoid-like, lupoid, erysipeloid, papulotuberous, verrucous14, disseminated, and diffuse presentations. Disseminated cutaneous leishmaniasis, which most often results from L. braziliensis or L. amazonensis infection, is characterized by multiple (10 to >300) secondary lesions, either in proximity to or distant from the primary site. The lesions resemble those of classic cutaneous leishmaniasis, including papules and small nodules that may have an acneiform appearance, and ulceration is common Diffuse cutaneous leishmaniasis is a rare presentation that develops in the setting of reduced cell-mediated immunity, analogous to lepromatous leprosy. L. aethiopica (in Africa) and L. amazonensis (in the Americas) are the most common pathogens (see Table 83.1). Multiple nodular and keloid-like lesions on the face and limbs are usually observed3 (Fig. 83.8A); ulceration is uncommon but occasionally occurs secondary to trauma. Nasal infiltration and mucosal ulceration may develop due to spread from nearby skin lesions, but destruction of the nasal septum is rare. There may also be laryngeal and pharyngeal involvement

Onchocerciasis - cause of disease? - vector of disease? - found in what areas of disease? - presentation? - Hanging groin?

Onchocerciasis is caused by Onchocerca volvulus, which is transmitted to humans by the bite of the black fly of the genus Simulium. Onchocerciasis occurs in Africa on the west coast, in the Sahara, Sudan, and the Victoria Nile division, where it is known as river blindness. In Central and South America, this disease can be found in Guatemala, Brazil, Venezuela, and southern Mexico. Clinical Presentation: - The skin lesions of onchocerciasis are characterized by pruritus, dermatitis, and onchocercomas. Early in the course of the infection, an itchy papular dermatitis may occur. In Central America, another manifestation of the acute phase of onchocerciasis is acute swelling of the face with erythema and itching, known as erisipela de la costa. In Zaire and Central America, an acute urticarial eruption is seen. The inflammation, which is accompanied by hyperpigmentation, is known as mal morado. As time passes, the dermatitis becomes chronic and remains papular; however, thickening, lichenification, and depigmentation occur. After a time, firm subcutaneous nodules, pea-sized or larger, develop on various sites of the body. These nodules are onchocercomas (Fig. 20.22) containing myriad microfilariae. Firm, nontender lymphadenopathy is a common finding in patients with chronically infected onchocerciasis. "Hanging groin" describes the loose, atrophic skin sack that contains these large inguinal nodes

More Widow Spiders

Pathogenesis Black widow venom contains latrotoxins that act by depolarizing neurons, increasing intracellular calcium, and stimulating uncontrolled exocytosis of neurotransmitters. Divalent cation-dependent tetramers related to α-latrotoxin can insert into lipid bilayers, forming membrane pores. Calcium-independent receptors for latrotoxin have also been identified. Clinical features The degree of morbidity caused by widow spider bites varies depending upon the species, age and sex of the spider (with only adult females capable of envenomation), amount of venom injected, and site of the bite. Local skin reactions are usually limited to transient erythema, edema, sweating, and piloerection. Extracutaneous manifestations are often prominent and can include painful muscle spasms (initially around the bite site, then more widespread), symptoms suggestive of an acute surgical abdomen, headache, and nausea; generalized diaphoresis may also occur. The symptoms of brown widow bites tend to be milder and restricted to the tissues near the bite. Treatment Benzodiazepines and intravenous calcium gluconate can be helpful for associated tetany. In one study, calcium gluconate was shown to be superior to methocarbamol (Robaxin®). Antivenin can produce rapid relief of tetany and complications such as priapism that are unresponsive to other agents. Purified equine Fab fragment-based antivenin is associated with a lower risk of hypersensitivity reactions than classic antivenin.

Enterobiasis Pinworm infection: - chiefly occurs in whom? symptoms? what can be exacerbated? Oxyuriasis: - Is caused by what? infests what body parts? how do the worms migrate? - how is diagnosis best made? - treatment

Pinworm infection, seatworm infection, oxyuriasis Pinworm infection: Occurs most chiefly in children with the major symptoms of pruritus ani. Restlessness, insomnia, enuresis, and irritability are a few of the many symptoms ascribed to this exceedingly common infestation. Mastocytosis can be exacerbated Oxyuriasis: Oxyuriasis is caused by the roundworm Enterobius vermicularis, which may infest the small intestines, cecum, and large intestine of humans. The worms, especially gravid ones, migrate toward the rectum and at night emerge to the perianal and perineal regions to deposit thousands of ova; then the worm dries and dies outside the intestine. These ova are then carried back to the mouth of the host on the hands. The larvae hatch in the duodenum and migrate into the jejunum and ileum, where they reach maturity. Fertilization occurs in the cecum, thus completing the life cycle. Rarely is it feasible to identify a dead pinworm in the stool. Diagnosis is best made by demonstration of ova in smears taken from the anal region early in the morning before the patient bathes or defecates. Such smears may be obtained with a small, eye curette and placed on a glass slide with a drop of saline solution. It is also possible to use cellophane tape, looping the tape sticky-side out over a tongue depressor and then pressing it several times against the perianal region. The tape is then smoothed out on a glass slide. A drop of a solution containing iodine in xylol may be placed on the slide before the tape is applied to facilitate detection of any ova. These tests should be repeated on 3 consecutive days to rule out infection. Ova may be detected under the fingernails of the infected person. Albendazole, 400 mg, or mebendazole, 100 mg, or pyrantel pamoate, 11 mg/kg (maximum 1 g), given once and repeated in 2 weeks, is effective. Personal hygiene and cleanliness at home are important. Fingernails should be cut short and scrubbed frequently; nails should be thoroughly cleaned on arising, before each meal, and after using the toilet. Sheets, underwear, towels, pajamas, and other clothing of the affected person should be laundered thoroughly and separately.

Sea Urchin Injuries - What is contained within sea urchin spines? what can develop as a result? - How can spines be removed?

Puncture wounds inflicted by the brittle, fragile spines of sea urchins, mainly of genus Diadema or Echinothrix, are stained blue-black by the black spines and may contain fragments of the spines. The spines consist of calcium carbonate crystals, which most frequently induce an irritant reaction with pain and inflammation of several days' duration. Foreign body or sarcoid-like granulomas may develop (Fig. 20.13), as may a vesicular hypersensitivity reaction, 10 days after exposure. Injuries by spines of the genus Tripneustes have been reported to cause fatal envenomation, but this genus is not found on U.S. coasts. Starfish also have thorny spines that can sting and burn if they are stepped on or handled. Several different types of stinging fish also produce puncture wounds. Stingrays, scorpionfish, stonefish, catfish, and weaverfish may cause such envenomations. These wounds should be immersed in nonscalding water (45°C [113°F]) for 30-90 minutes or until the pain subsides. Calcified fragments may be visible on x-ray evaluation, with fluoroscopy guiding extraction of spines, especially on the hands and feet. Sea urchin spines have been effectively removed using the erbium:yttrium-aluminum-garnet (YAG) laser. Debridement and possibly antibiotic therapy for deep puncture wounds of the hands and feet are recommended. There is a specific antivenin for stonefish stings.

Seabathers eruption - Cause - clinical presentation, how long does the eruption last?

Seabather's eruption is an acute dermatitis that begins a few hours after bathing in the waters along the Atlantic coast. It affects covered areas of the body as cnidarian larvae become entrapped under the bathing suit and the nematocyst releases its toxin because of external pressure. Thus the buttocks and waist are affected primarily, with the breast also involved in women (Fig. 20.11). Erythematous macules and papules appear and may develop into pustules or vesicles. Urticarial plaques are also present in a smaller number of patients. Crops of new lesions may occur for up to 72 hours, and the eruption persists for 10-14 days on average. It is quite pruritic. Outbreaks in Florida are usually caused by larvae of the thimble jellyfish, Linuche unguiculata, which patients report as "black dots" in the water or their bathing suits. The larvae of the sea anemone Edwardstella lineata caused one epidemic of seabather's eruption in Long Island, New York. This organism also has nematocysts; thus the mechanism of the eruption is the same as with the jellyfish-induced eruption. It is likely that different cnidarian envenomations in different waters produce a similar clinical picture. Other reports focus on spring plants, dinoflagellates, protozoans, or crustaceans as potential causes. Because the eruption results from trapping of cnidarian larvae with their nematocysts or other toxic or irritant substances under the bathing suit, it may be limited by seabathers who remove their suit and shower soon after leaving the water

Old World Cutaneous Leshmaniasis - describe the following forms: zoonotic antroponotic recidivans

Several clinical forms of Old World cutaneous leishmaniasis have been described, including zoonotic, anthroponotic, recidivans, and lupoid leishmaniasis. Zoonotic cutaneous leishmaniasis (rural, moist, or early ulcerative form) usually has a mild, rapid course and is caused by L. major. Anthroponotic cutaneous leishmaniasis (urban, dry, or late ulcerative form), has a more chronic course and is caused by L. tropica3. Leishmaniasis recidivans is a chronic, destructive form that is characterized by recurrence at the site of an original ulcer, generally within 2 years and often at the edge of the scar.

Millipede burns

Some millipedes secrete a toxic liquid that causes a brownish pigmentation or burn when it comes into contact with skin. Burns may progress to intense erythema and vesiculation. Millipedes may be found in laundry hung out to dry, and millipede burns in children have been misinterpreted as signs of child abuse. Recognition of the characteristic curved shape of the burn can be helpful in preventing misdiagnosis. Some millipedes can squirt their venom, and ocular burns are reported. Washing off the toxin as soon as possible will limit the toxic effects. Other treatment is largely symptomatic. Diplopods have evolved a complex array of chemicals for self-defense (Fig. 20.26). Some primates take advantage of these chemicals. Two millipede compounds, 2-methyl-1,4-benzoquinone and 2-methoxy-3-methyl-1,4-benzoquinone, demonstrate a repellent effect against Aedes aegypti mosquitoes. Tufted and white-faced capuchin monkeys anoint themselves with the secretions to ward off mosquitoes. Effective commercial repellents are available for human use; millipede juice is not recommended.

Visceral Schistosomiasis - name the types that can cause systemic disease? - what are bilharziomas? - treatment

The cutaneous manifestation of schistosomiasis may begin with mild itching and a papular dermatitis of the feet and other parts after swimming in polluted streams containing cercariae. The types of schistosome causing this disease can penetrate into the bloodstream and eventually inhabit the venous system, draining the urinary bladder (Schistosoma haematobium) or the intestines (Schistosoma mansoni or Schistosoma japonicum). After an asymptomatic incubation period, the person may develop a sudden illness with fever and chills, pneumonitis, and eosinophilia. Petechial hemorrhages may occur. Cutaneous schistosomal granulomas most frequently involve the genitalia, perineum, and buttocks. The eggs of S. haematobium or S. mansoni usually cause these bilharziomas (Fig. 20.15). Vegetating, soft, cauliflower-shaped masses, fistulous tracts, and extensive hard masses occur; these are riddled by sinuses that exude a seropurulent discharge with a characteristic odor. Katayama fever is frequently present along with S. japonicum infection; it occurs with the beginning of oviposition, 4-8 weeks after infection. This condition is seen mainly in China, Japan, and the Philippines. In addition to the urticaria, fever, malaise, abdominal cramps, arthritis, and liver/spleen involvement are seen. This is thought to be a serum sickness-like reaction. For both S. haematobium and S. mansoni, praziquantel (Biltricide), 40 mg/kg orally for each of two treatments in 1 day, is the therapy of choice. S. japonicum treatment requires 60 mg/kg in three doses in 1 day.

More Larva Migrans - how is the diagnosis made? - Treatment options? - What condition can complicate this condition

The diagnosis is typically made clinically, although biopsy may sometimes demonstrate the organism, and even dermoscopy has been used. Ivermectin, 200 µg/kg, generally given as a single 12-mg dose and repeated the next day, or albendazole, 400 mg/day for 3 days, is an effective treatment. Criteria for successful therapy are relief of symptoms and cessation of tract extension, which usually occurs within 1 week. Both ivermectin and metronidazole have been used topically, as has thiabendazole, compounded as a 10% suspension or a 15% cream. Another condition, not to be confused with this helminthic disease, which also is called creeping eruption (or sandworm, as it is known in South Africa, particularly in Natal and Zululand), is caused by a small mite about 300 µm long that tunnels into the superficial layers of the epidermis. Loeffler syndrome, consisting of a patchy infiltrate of the lungs and eosinophilia as high as 50% in the blood and 90% in the sputum, may complicate creeping eruption.

Diagnosis of Leishmaniasis - how is it diagnosed, where should it be taken from? - what stains can be helpful - what skin test can be done, when is it positive - culture media

The diagnosis of cutaneous leishmaniasis can be confirmed by demonstrating the presence of amastigotes in dermal macrophages within skin biopsy specimens, tissue impression smears (touch preparations), and smears obtained by dermal scraping or needle aspiration of skin lesions2,14,20. Although routine hematoxylin and eosin staining allows the visualization of the amastigotes, Giemsa, Wright, or Feulgen stains can help to identify the organisms in smears and tissue: the cytoplasm appears blue, the nucleus pink and the kinetoplast a deep red14; CD1a immunostaining can also highlight the amastigotes (see Fig. 83.12). The edge of a relatively new ulcer is the location of choice for obtaining dermal scrapings, a biopsy specimen, or a needle aspirate; the latter two types of samples may be used for culture and polymerase chain reaction (PCR)-based assays Montenegro Skin test: uses leishmanial antigens to induce a cell-mediated response, has traditionally been an important diagnostic tool. A phenolated suspension of killed promastigotes is injected intradermally, usually on the volar aspect of the forearm. The test is considered positive if a papule >5 mm in diameter forms at the site of inoculation after 48-72 hours Nicolle-Novy-MacNeal (NNM) media or chick embryo media

Differential Diagnosis and Treatment - treatment for cutaneous and visceral disease

The differential diagnosis of cutaneous leishmaniasis includes persistent arthropod bite reaction, basal cell carcinoma, tuberculosis, non-tuberculous mycobacterial infections, and subcutaneous mycoses; other infectious causes of lesions in a lymphocutaneous pattern are listed in Table 77.17. Mucocutaneous leishmaniasis can resemble paracoccidioidomycosis and tertiary syphilis. In addition, granulomatosis with polyangiitis (formerly Wegener granulomatosis) and angiocentric NK/T-cell lymphoma should be considered when ulcerative mucocutaneous lesions affect the central part of the face. Cocaine-induced nasal Without treatment, Old World cutaneous leishmaniasis typically resolves within 2-4 months (L. major) or 6-15 months (L. tropica). Indications for systemic treatment of Old World cutaneous leishmaniasis include (1) an immunocompromised host; (2) >4 lesions of substantial size (e.g. >1 cm) or individual lesion(s) measuring ≥5 cm; (3) markedly enlarged regional lymph nodes; and (4) involvement of the mucosa, face, ears, genitalia, fingers, toes, or skin overlying a joint22-24. Local therapy or, if the lesions are healing spontaneously within 6 months, observation are options for patients who do not meet these criteria. New World cutaneous leishmaniasis caused by L. mexicana resolves within 3 months in >75% of cases. In contrast, cutaneous disease caused by L. braziliensis and L. panamensis spontaneously heals in less than 10% and 35% of cases, respectively. Therefore, systemic treatment is indicated when L. braziliensis complex infection is suspected in order to accelerate healing, decrease scarring (especially in cosmetically sensitive sites), and prevent dissemination, relapse, or the development of mucosal disease Parenteral pentavalent antimonials and miltefosine are first-line systemic treatments for cutaneous and mucocutaneous/mucosal leishmaniasis, whereas liposomal amphotericin B is the treatment of choice for visceral leishmaniasis

Trypansomiasis - what two conditions - causative organisms

Three species of trypanosome are pathogenic to humans: Trypanosoma gambiense and T. rhodesiense in Africa and T. cruzi in America. - Chagas Disease - African Trypansomiasis

More Filariasis - treatment of disease?

The microfilariae should be sought on fresh coverslip films of blood (collected at night), urine, or other body fluid and examined with a low-power objective lens. Calcified adult worms may be demonstrated on x-ray examination, and ultrasound can detect adult worms. At times, adult filariae are found in abscesses or in material taken for pathologic examination. Specific serologic tests and a simple card test for filarial antigen are available. The prognosis in regard to survival is good, but living becomes burdensome unless the condition is alleviated. Diethylcarbamazine, in increasing doses over a 14-day period, is the treatment of choice. This regimen clears microfilariae but not adult worms. A single dose of ivermectin may also be effective. Doxycycline and rifampicin kill the intracellular symbiotic bacteria, Wolbachia. This leads to long-term sterility of adult female worms and both are being studied to determine their place in the treatment of both bancroftian filariasis and onchocerciasis. A worldwide effort to eliminate these diseases is underway. Surgical procedures have been devised to remove the edematous subcutaneous tissue from the scrotum and breast. Prophylactic measures consist of appropriate mosquito control. Diethylcarbamazine has been effective in mass prophylaxis. If a trip of over 1 month to areas with endemic Wuchereria bancrofti is planned and extensive exposure to mosquitoes is likely, taking diethylcarbamazine, 500 mg/day for 2 days each month, is recommended.

Cysticercosis Cutis - how does infection take place? life cycle - how do cutaneous lesions appear? - how is the diagnosis made? - treatment? How do you treat calcified nodules?

The natural intermediate host of the pork tapeworm, Taenia solium, is the pig, but under some circumstances, humans act in this role. The larval stage of T. solium is Cysticercus cellulosae. Infection takes place by the ingestion of food contaminated with the eggs or by reverse peristalsis of eggs or proglottides from the intestine to the stomach. Here the eggs hatch, freeing the oncospheres. These enter the general circulation and form cysts in various parts of the body, such as striated muscles, brain, eye, heart, and lung. In the subcutaneous tissues, the lesions are usually painless nodules that contain cysticerci. They are more or less stationary, usually numerous, and often calcified and are therefore demonstrable radiographically. Pain and ulceration may accompany the lesions. The disease is most prevalent in countries where pigs feed on human feces. It may be confused with gumma, lipoma, and epithelioma. A positive diagnosis is established solely by incision and examination of the interior of the calcified tumor, where the parasite will be found. Fine-needle aspiration has also been used to establish the diagnosis. Albendazole or praziquantel is effective; however, the status of the CNS, spinal, and ocular involvement needs to be thoroughly assessed before treatment. The length of therapy and use of concomitant corticosteroids depend on the location of the cysts. However, none of the regimens clears the calcified parasites, which need to be surgically removed.

More Onchocerciasis - treatment of choice?

The presence of eosinophilia, skin lesions, and onchocercomas with ocular lesions is highly suggestive in endemic areas. Specific serologic and PCR-based diagnostic tests from blood and skin biopsies are available Onchocercomas may be surgically excised whenever feasible. Ivermectin as a single oral dose of 150 µg/kg is the drug of choice.

Fire Ant Bites - how does fire ant venom work? - fire ant bites are milder when? - clinical presentation? - treatment?

The range of Solenopsis invicta, the red imported fire ant (originally from South America), has spread to encompass much of the southern and southwestern US, and its territory continues to expand Fire ant venom is complex and acts by increasing membrane permeability and allowing release of histamine from mast cells. Allergic responses are directed at proteins within the venom. The venom is less concentrated in winter months, so winter sting reactions may be milder. Fire ant stings begin as extremely painful wheals and evolve into intensely pruritic vesicles and sterile pustules. Life-threatening anaphylactic reactions to fire ant stings have become a significant problem in the southern US. Local reactions may be treated with potent topical or intralesional corticosteroids.

General Ticks - How should ticks be removed? - what about antibiotic prophylaxis for tick bites?

Ticks should be removed as completely as possible, and care should be taken not to squeeze the abdomen. Gentle traction is generally preferred, but a twisting motion can also be used; the latter technique may leave a small mouthpart. Several plastic tick removal devices are marketed. The "Tick NipperTM" is an inexpensive plastic device that grasps the tick just behind the mouthparts without severing them. A tick removal device can also be made by cutting a V-shaped notch in a plastic spoon or credit card with a sharp pair of scissors or hot blade. Petroleum jelly, fingernail polish, isopropyl alcohol, and hot matches are generally ineffective. Hands should be washed if they were in contact with the tick. Antibiotic prophylaxis after tick bites remains controversial, and most authorities do not recommend its routine use, including for prevention of Lyme disease (see Ch. 19). However, in patients from endemic areas (>20% of ticks infected) in whom the tick, identified as a nymphal or adult I. scapularis, has been attached for >36 hours and prophylaxis can be started within 72 hours of tick removal, a single 200 mg dose of doxycycline may decrease the risk of developing Lyme disease (from 3.2% in the placebo group to 0.4% in the treatment group in one study)26,27. A meta-analysis of antibiotic prophylaxis concluded that in order to prevent one case of Lyme disease, 50 people bitten by an Ixodes tick would need to be treated - the risk in the placebo group was 2.2% compared with 0.2% in the antibiotic-treated group28. Routine serologic testing for Lyme disease in individuals bitten by Ixodes ticks is not useful, and there is no evidence that molecular testing for Borrelia burgdorferi in a tick is helpful in predicting the risk of Lyme disease in a human bitten by that tick29. Treatment regimens for erythema migrans are outlined in Table 19.4. The utility of antibiotic prophylaxis in preventing other tick-borne illnesses has not been established. For example, in a guinea pig model of RMSF, a single dose of oxytetracycline was found to prevent disease if given shortly before the expected onset of illness. However, administration any earlier merely delayed the development of clinical symptoms, making correct timing of administration of a single dose difficult. Single-dose doxycycline for Lyme disease prophylaxis should be avoided in RMSF-endemic areas, since changing the course of RMSF could potentially delay definitive treatment.

Toxoplasmosis - cause? - triad for congenital disease, clinical presentation - List the TORCH infections

Toxoplasmosis is a zoonosis caused by a parasitic protozoan, Toxoplasma gondii. Infection may be either congenital or acquired. However, a full-term child delivered to an infected mother may have a triad of hydrocephalus, chorioretinitis, and cerebral calcification. In addition, there may be hepatosplenomegaly and jaundice. Skin changes in toxoplasmosis are rare and clinically nonspecific. In congenital toxoplasmosis, macular and hemorrhagic eruptions predominate. Blueberry muffin lesions, reflecting dermatoerythropoiesis, may be seen. Occasionally, abnormal hair growth and exfoliative dermatitis have also been observed. The differential diagnosis of congenital toxoplasmosis is the TORCH syndrome (toxoplasmosis, other agents, rubella, cytomegalovirus, and herpes simplex). In acquired toxoplasmosis, early skin manifestations consist of cutaneous and subcutaneous nodules and macular, papular, and hemorrhagic eruptions

More dog and cat bites

Treatment A combination of a β-lactam antibiotic and a β-lactamase inhibitor (e.g. amoxicillin/clavulanic acid) provides good coverage for most organisms associated with dog and cat bites52-54. Alternatives include: (1) second-generation cephalosporins with anaerobic activity (e.g. cefoxitin, cefotetan); (2) penicillin plus a first-generation cephalosporin; or (3) clindamycin plus a fluoroquinolone. The need for hospitalization of patients with Pasteurella-infected animal bite wounds is strongly associated with initial use of suboptimal antibiotic therapy. With appropriate antibiotic therapy, primary repair is appropriate for dog bites to the face

Reduviid bugs

Triatome reduviid bugs (kissing bugs, assassin bugs, conenose bugs) descend on their victims while they sleep and feed on an exposed area of skin. The bite is typically painless, although the bugs are capable of producing a more painful defensive bite. Swelling and itching occur within hours of the bite (Fig. 20.32). Central and South America and the southern US clinical features: Triatomine bug bites are typically painless, and the first sign is delayed erythema, swelling, and pruritus at the site. Exaggerated responses in the form of large urticarial plaques or vesiculobullous lesions occasionally develop. These insects are known as "kissing bugs" because of their tendency to bite the face, especially around the lips. Unilateral eyelid and periorbital swelling 1-2 weeks after conjunctival exposure to infected triatomine feces is referred to as Romaña sign and represents a chagoma. Trypanosomes subsequently infect the autonomic nervous system, resulting in chronic complications that include cardiomegaly and megacolon (see Ch. 83). Triatomine bugs and cockroaches share antigens that are strongly immunogenic in atopic patients. Romana sign is unilateral eye swelling after a nighttime encounter with a triatome bug. It resembles the "eyelid sign" associated with bedbugs. Trypanosoma cruzi is transmitted by the feces and rubbed into the bite. American trypanosomiasis can produce heart failure and megacolon. Triatome bugs infest thatch, cracks, and crevices, and infestation is associated with poor housing conditions. In nonendemic areas, bites are sporadic and often followed by a red swelling suggestive of cellulitis. Anaphylaxis has also occurred. A related arthropod, the wheel bug Arilus cristatus, is widely distributed and has an extremely painful defensive bite, but it is not known to carry disease.

Class Mastigophora - what three diseases?

Trichomoniasis Leishmaniasis Human trypansosomiasis

Trichomoniasis - caused by what organism? common cause of what condition - diagnosis - can cause what on the penis? - Treatment? what should patients be warned about with this medication? Treatment of pregnant women?

Trichomoniasis is caused by Trichomonas vaginalis, a colorless piriform flagellate 5-15 µm long. T. vaginalis is demonstrated in smears from affected areas. Testing by direct immunofluorescence is sensitive and specific, and polymerase chain reaction (PCR) analysis is now available. Trichomonas vulvovaginitis is a common cause of vaginal pruritus, with burning and a frothy leukorrhea. The vaginal mucosa appears bright red from inflammation and may be mottled with pseudomembranous patches. The male urethra may also harbor the organism; in the male it causes urethritis and prostatitis. Occasionally, men may develop balanoposthitis. Erosive lesions on the glans and penis or abscesses of the median raphe may occur. Metronidazole, 2 g in a single oral dose, is the treatment of choice. Alternatively, 500 mg twice daily for 7 days may be given, and intravaginal metronidazole/miconazole is also effective. Patients should be warned not to drink alcohol for 24 hours after or dosing because of the disulfiram-type effects of this medication. Male sex partners should also be treated. The use of metronidazole is contraindicated in pregnant women, and clotrimazole, applied intravaginally at 100 mg a night for 2 weeks, may be used instead. Disulfiram and nithiamide show in vitro evidence of activity and could prove useful for resistant organisms.