Arthropods Attacks II

IHAB YOUNIS, M.D.

Leishmaniasis

After Sir William Leishman (1865–1926), British medical officer

The typical lesions of cutaneous leishmaniasis were described as early as 900 BC and have been referred to as the "Balkan sore" in the Balkans, the "Delhi boil" in India, the "Baghdad boil" in Iraq, and "saldana" in Afghanistan

Etiology approximately 1.5 million new cases of

cutaneous leishmaniasis and 500,000 cases of visceral leishmaniasis occur worldwide each year

Incidence is highest in tropical and subtropical regions where conditions are favorable for sandflies

Causative agent

Within the female sandfly gut, the protozoa multiply and migrate toward the pharynx

As the leishmaniae replicate, they create a blockage in the fly's esophagus. The sandfly then clears out its esophagus by expelling leishmaniae into the skin of the host, from where they pass into the blood and tissues of the human host

They are phagocytosed into macrophages of the reticuloendothelial system, where they multiply by binary fission

When the infected cells rupture, the infection spreads to other macrophages and is carried throughout the body

Temperature is an important factor that helps determine the localization of leishmanial lesions. Species causing visceral leishmaniasis are able to grow at core temperatures, while those responsible for cutaneous leishmaniasis grow best at lower temperatures

Types

Cutaneous leishmaniasis

Mucocutaneous leishmaniasis

Visceral leishmaniasis

Cutaneous leishmaniasis

Causative agents

Old world :- Leishmania tropica- Leishmania major- Leishmania infantum- Leishmania aethiopica

Clinically Initial lesions can appear immediately after a

bite, or the incubation period may last for several months

Systemic signs usually are absent Ulcers usually are found on exposed areas of

skin, especially the extremities and face

Lesions can be single or multiple

Initially, the lesion is a small, red papule up to 2 cm in diameter. Over several weeks, the papule becomes darker and will crust in the center, eventually ulcerating

The ulcer shows raised edges and surrounding dusky red skin The ulcers can be moist or open with seropurulent exudate or dry with a crusted scab

After about 3-6 months, the ulcers heal, leaving a raised border Regional adenopathy, satellite lesions, and subcutaneous nodules can be present Untreated sores can leave depigmented retracted scars

Mucocutaneous leishmaniasis

Mucosal lesions can progress to involve the entire nasal mucosa and the hard and soft palates

Without treatment, nasal mucosa and palates become deformed with ulceration and erosion

Bones are spared but there is severe disfigurement

Visceral leishmaniasis

Bouts of fever Hepatosplenomegaly Darkening of the skin is characteristic (thus, the name kala azar or black fever in Assamese ) Patients may die of hemorrhage, severe anemia or secondary

bacterial infections

Histopathology

Lab studies Direct evidence of infection

1-Peripheral blood smear: amastigotes are

seen inside monocytes and neutrophils

2-Culture on NNN medium : takes about a

month

3-Animal inoculation: a sensitive method but

can take several weeks

Indirect evidence of infection 1-Detection of hypergammaglobinemia for Kala

azar 2-Detection of IgM antibody 3-Leishmanin skin test (Montenegro test) is a

delayed hypersensitivity reaction. - Intradermally, 0.1 mL of killed promastigote

antigen are injected. The test is read after 72 hours - The leishmanin skin is negative during active

visceral leishmaniasis and usually becomes positive only after successful therapy

- It also is positive in dermal leishmaniasis. This test is useful only for epidemiological purposes, indicating prior exposure to infection

Treatment

Sodium stibogluconate (Pentostam 100 mg/ml)

For all forms of the disease, treatment should be started with a 200-mg test dose and then followed by daily injections of 20 mg/kg IV (preferably) or IM

Intralesional Pentostam(0.2-0.8 ml) is effective but injection is painfull

Cutaneous disease should be treated for 20 d

Mucocutaneous and visceral disease should be treated for 28 d

May cause myalgias and arthralgias (50%), fever, phlebitis, rash, and GI symptoms

Meglumine antimoniate(Glucantime 300 mg/ml)

Dosed exactly the same and is equivalent in efficacy and toxicity to sodium stibogluconate

Amphotericin B (AmBisome) A second-line drug to be used after failure of

antimonials to treat mucocutaneous and visceral leishmaniasis

Given as a slow infusion (4-6 h) of 1 mg/kg qd for 20 d

Oral drugs such as ketoconazole, itraconazole, and allopurinol also are effective but only in combination with the first-line drugs

Other approaches include surgical excision and cryotherapy

Jellyfish Stings

Etiology

With more than 10,000 species in the sea, jellyfish are responsible for the most common human envenomations

More than 100 species are toxic to humans

The tentacles are covered with specialized stinging cells termed nematocytes

Each nematocyte contains a stinging apparatus known as the nematocyst

The stinging process of the nematocyte resembles a jack-in-the-box mechanism: stimulation of the sensory hairs surrounding the pressurized nematocyte results in a calcium-mediated bioelectric signal that causes an opening of its lid, allowing the ejection of the nematocyst into the prey to express the venom

The nematocyst is capable of penetrating up to a depth of 0.9 mm. This depth deposits the toxin into the microvasculature of the dermal tissue to be absorbed into the systemic circulation of the prey

The nematocysts' size and arrangement on

jellyfish tentacles differ from species to species which is reflected in the skin pattern left via the sting

Composition of venom

catecholamines, vasoactive amines (eg, histamine, serotonin), kinins, collagenases, hyaluronidases, proteases, phospholipases, fibrinolysins, dermatoneurotoxins, cardiotoxins, neurotoxins, nephrotoxins, myotoxins, and antigenic proteins

Clinically Toxicity and variations of symptoms depend

on several factors. Patient age and health Patient body weight relative to the toxin amount Patient surface area involved in the sting (any

sting >50% of limb area is associated with severe envenomation)

Thickness of the skin at contact points Site of envenomation (proximity to head=quicker

venom absorption into central circulation) Species and maturity of the jellyfish

Hot water sensation with skin tingling or stinging may be reported at the body site where the jellyfish originally made contact

Tenderness, burning, and pruritus, which may spread centrally and differ in intensity depending on the species involved

Erythematous papules and blisters in a whiplike pattern with desquamation within 1-8 weeks

Local neuropraxia occurring adjacent to sting site from immunologic reaction to toxin or to toxin-induced alteration of the nerve's ionic permeability

Tender regional lymphadenopathy Distant skin site reactions secondary to a

hypersensitive response to the antigenic component of the venom

Long-term skin effects

Keloids Pigmented striae Lichenification from persistent rubbing Granuloma Ulceration and necrosis Gangrene Fat atrophy Scarring and contractures

Systemic effects Cardiovascular: Peripheral and coronary

vasospasm&heart failure or arrhythmia Respiratory:Laryngeal edema,bronchospasm,

respiratory failure Neurologic:Autonomic dysfunction,spastic

paralysis Cerebral edema, seizures, headache, agitation, coma

Gastrointestinal:Nausea and vomiting,abdominal muscle rigidity and pain,hepatic inflammatory necrosis from direct toxin injury to hepatocytes

Lab Studies

CBC count to evaluate toxin-induced hemolysis Electrolyte levels, BUN/creatine ratio, and

glucose levels to determine if an abnormality is present that can worsen the toxin-induced muscular paresis

Liver function tests, which are elevated because of toxin-induced liver inflammation

Others according to case e.g. EEG

Treatment

Local skin treatment

Rinse the wound with sterile normal saline to prevent nematocyte activation(seawater carries marine pathogens). Avoid using fresh water and rubbing the skin, since these activities trigger unfired nematocytes

Soak the wound in 5% acetic acid for 15-30 minutes to further inhibit nematocyte discharge

After the inactivation, carefully remove any visible tentacles with forceps

Administer systemic antibiotics if signs of secondary infection exist

Apply topical anesthetics once the nematocytes/nematocysts are removed. Cold pack compresses at the sting site for 5-10 minutes relieve all but the most severe site pain. Avoid direct application of ice to the area, since the hypotonic water from the melting ice may stimulate unremovable, unfired nematocytes. Also, avoid hot compresses, since they increase systemic uptake of venom

Administer antihistamines and topical and systemic corticosteroids for severe local reactions as well as to decrease the probability of serum sickness

Administer muscle relaxants(eg,benzodiazepine, methocarbamol) for severe local spasms

Narcotic analgesias are appropriate for severe local pain not responding to topical anesthetics.

Administer a tetanus shot as a prophylactic measure

Other systems e.g.

Apply a lymphatic-venous compression bandage proximally to the sting site

Provide supportive care (eg, central venous monitoring, fluids)

Ophthalmic care

Surgical Care

Once the nematocytes are inactivated, they can be removed by dusting the area with a paste of shaving cream, baking soda, and talc for 1 hour to coalesce the nematocyte, followed by scraping the area with a dull object (eg, spoon). Strong adhesive tape applied to the area and then removed also can be used