Tropical and HIV Dermatology

Tropical and HIV Dermatology
Dr. Thor Swanson AAFP Global Health Conf. September 2012

Author’s Information Dr. Thor Swanson is Board-Certified in Family Medicine and Addiction Medicine and lives in Sioux City, Iowa. He holds additional credentials in HIV Medicine (AAHIVM), Tropical Medicine (ASTM&H), Travel Medicine (ISTM), and Chronic Pain (AAPM) and has practiced cross-cultural medicine in Nepal (1996), Tanzania (2001), Kenya (2006-7) as well as daily in Sioux City, IA ( and 2007-Present). He holds visiting faculty appointments at the University of Iowa and the University of South Dakota and is a community faculty member at Siouxland Medical Educational Foundation (family medicine residency) in Sioux City, IA.

Author’s Information (9/12)
Thanks to Dr. Anosh Mazhari for helping start this presenation. Dr. Anosh Mazhari was born in Ethiopia and spent his formative years in Pakistan where he graduated from medical school. From 2009 until 2012 he was a resident at Siouxland Medical Educational Foundation in Sioux City. He currently practices Family Medicine in Minnesota.

Description This seminar will provide a brief introduction to tropical and HIV dermatology in both the North American and overseas’ settings. The program will review many tropical and HIV-related diseases with dermatological manifestations including fungal, mycobacterial, bacterial and viral diseases and more. The lecture will include pictures and clinical anecdotes from the presenters’ experiences working in the US, South Asia, Africa, and Latin America.

Objectives 1. Discuss the importance of knowing tropical and HIV dermatology in general. 2. Review common dermatological manifestations of tropical fungal diseases. 3. Review common dermatological manifestations of HIV-related diseases. 4. Recount atypical dermatological signs of mycobacterial and bacterial diseases. 5. Speak about the dermatological appearances of viral diseases. 6. Use pictures and clinical cases from around the world, including the US, South Asia, Africa, and Central America to do the above.

Introductory Why do a lecture on tropical and HIV dermatology seminar at AAFP Global Health? Increasing physicians doing short-term and long-term mission stints and seeing cases there Increasing Americans doing short-term and long-term mission stints and possibly contracting cases Continuing tropical immigrants coming to USA and Canada (and developed countries)

Overview: Some HIV Basics Noninfectious Dermatoses
Fungal Disease and Mycoses Mycobacterial Diseases Bacterial Diseases and Pyodermas Treponematoses and Genital Ulcers Parasitic Dermatoses Viral Diseases Neoplastic Diseases

HIV Basics.

What is HIV? HIV stands for: Human: this virus infects people
Immunodeficiency: the virus weakens the immune system Virus: HIV is a virus like polio, measles, and influenza HIV stands for: Human Immunodeficieny Virus

How does the HIV virus cause disease?
HIV disables the body's immune system and destroy its ability to fight certain diseases. HIV infects several kinds of cells in the body, the most important of which is a type of white blood cell called the CD4 T lymphocyte (CD4 T cell). The CD4 T cell is a major component of the human immune system that helps keep people free from many infections and some cancers.

Global summary of the AIDS epidemic, 2008
Number of people living with HIV in 2008 Total 33.4 million [31.1 – million] Adults 31.3 million [29.2 – million] Women (aged 15 and above) 15.7 million [14.2 – million] Children under 15 years 2.1 million [1.2 – 2.9 million] Total 2.7 million [2.4 – 3.0 million] Adults 2.3 million [2.0 – 2.5 million] Children under 15 years [ – ] Total 2.0 million [1.7 – 2.4 million] Adults 1.7 million [1.4 – 2.1 million] Children under 15 years [ – ] People newly infected with HIV in 2008 AIDS-related deaths in 2008 December 2009

Rashes of Acute Antiretroviral Syndrome

Acute Antiretroviral Syndrome
The initial event in HIV infection is the acute retroviral syndrome which is accompanied by a precipitous decline in CD4 cell counts and high concentration of HIV RNA in plasma. Credits: p. 1 in John Bartlett and Joel Gallant, 2007 Medical Management of HIV Infection, Baltimore: Johns Hopkins Medicine Health Publishing Business Group.

Dermatological Diseases and CD4 Counts in Longer-term HIV/AIDS

Noninfectious Dermatoses: Scaling Diseases
Seen with Increased incidence in HIV+ patients

Noninfectious Dermatoses: Scaling Diseases
Seborrheic Dermatitis Xerosis and Eczema Psoriasis

Noninfectious Dermatoses: Scaling Diseases: Seborrheic Dermatitis

Noninfectious Dermatoses: Scaling Diseases: Seborrheic Dermatitis (SD)
Common dermatitis affecting up to 2% of population (in West) Particularly affects areas where sebaceous glands are most numerous (scalp, forehead, eyebrows, eyelids, ears, cheeks, presternal and intrascapular areas). Fig left- Seborrheic dermatitis, note the marked scaling. Fig 6.3-right- Seborrheic dermatitis, diffuse erythema and scaling of forehead. Credits: Ferri, Atlas, p. 26.

Often the lesions are sharply marginated, dull red, or yellowish and covered with a greasy scale. They are often easily confused with psoriasis. Dandruff and cradle cap are also sometimes included in the spectrum of SD. SD is one of the most common dermatoses seen in AIDS. It has also been associated with stress, HIV, and neurologic disorders, including Parkinson’s disease. Credits: Ferri, Atlas, p. 26.

Treatment: Topical ketoconazole, hydrocortisone. Second-line therapies include miconazole nitrate, lithium succinate, and selenium sulfide. Credits: Ferri, Atlas, p. 26.

Noninfectious Dermatoses: Scaling Diseases Seborrheic Dermatitis- HIV-Frequency
In the pre-HAART era, SD occurred in 1% to 3% of the general population and in 40% and 80% of patients with AIDS-related complex and AIDS, respectively. In advanced HIV disease, SD may cover the trunk and limbs extensively and may simulate other forms of dermatitis such as atopic dermatitis. It is logical to assume that with depressed cellular immunity, growth of Pityrosporum might be more florid with HIV infection and produce the dermatitis; however, it is also possible that the dermatitis is a reaction of the presence of the yeast and that the more extensive eruption in HIV patients is also due to the altered immune status which has made the patient more “allergic” to it. Credits: AAHIVM Fundamentals, 2007 ed., Seborrheic Dermatitis, p. 431.

Treatment for SD is the same regardless of HIV serostatus.
Noninfectious Dermatoses: Scaling Diseases Seborrheic Dermatitis- HIV-Treatment Treatment for SD is the same regardless of HIV serostatus. Topical Steroid: Mid-potency such as triamcinalone 0.1% or weaker (desonide 0.05%), hydrocortisone 2.5% for the face +/- ketoconazole 2% cream applied twice per day for the duration of the flare only Shampoos: Tar-based (Z-tar, Pentrax, DHS tar, T-gel, lonil T plus), selenium sulfide (Selsun, Exelderm), or zinc pyrithione (Head and Shoulders, Zincon, DHS zinc) applied daily, or ketoconazole shampoo applied twice weekly Credits: AAHIVM Fundamentals, p. 431; Bartlett, 2007 Medical Management of HIV, p. 409.

Seborrheic Dermatitis in HIV Patient
F Credits: From FIGURE in Mandell et. al, Infectious Diseases, (Courtesy of Stephen Raffanti, MD, MPH.)

HIV-Seborrheic Dermatitis
Description: Axillary dermatitis that cleared with oral ketoconazole plus topical steroids. Credits: Toby A. Maurer, MD and Timothy G. Berger MD; UCSF; Nat’l Library of Medicine

Noninfectious Dermatoses: Scaling Diseases- Xerosis and Eczema

Noninfectious Dermatoses: Scaling Diseases- Xerosis and Eczema- Basic Info
Fig 6.1 (Right) Eczema, This is a plaque of discoid eczyma. Small vesicles are present at the edge of the lesions. The term eczema refers to a group of disorders that share similar clinical and histologic features but may have different causes. The earliest lesions are erythema and aggregates of tiny pruritic vesicles, which rupture readily, exuding clear liquid, and later became encrusted. More chronic lesions became scaly and thickened (lichenification), especially if the skin is continually scratched or rubbed. Therefore, the clinical features of dermatitis depend on the duration of the lesions, site(s) involved, and presence of scratching. Credits: Ferri, Atlas, p.25.

Noninfectious Dermatoses: Scaling Diseases- Xerosis and Eczema- Atopic Dermatitis
Fig. 6-2 (Right)- Atopic Dermatitis. These crusted, exudative, and infected lesions with lichenification are characteristic. Atopic dermatitis is a genetically determined eczematous erpution that is pruritic, symmetrical, and associated with a personal family history of allergic manifestations (atopy). The highest incidence is in children (5% to 10%). More than 50% of children with generalized atopic dermatitis develop asthma and allergic rhinitis by the age of 13 years. Credits: Ferri, Atlas, p.25.

In AD, there can be a wide spectrum of presentations.
Noninfectious Dermatoses: Scaling Diseases- Xerosis and Eczema- Atopic Dermatitis In AD, there can be a wide spectrum of presentations. The primary lesions are a result of itching caused by severe and chronic pruritis. The repeated scratching modifies the skin surface, producing lichenification, dry and scaly skin, and redness. The lesions are typically on the neck, face, upper trunk, an bends of elbows and knees (symmetrical on flexural surfaces of extremities). There is dryness, thickening of the involved areas, discoloration, blistering, and oozing. Credits: Ferri, Atlas, p.25.

Noninfectious Dermatoses: Scaling Diseases- Xerosis and Eczema-HIV
Presentation Xerosis is usually generalized but is frequently most noticeable on the shins, where it may have the typical cracked appearance of so-called “eczema craquele.” Xerosis is frequently accompanied by generalized pruritis. Treatment HAART should be instituted in patients for whom it is otherwise appropriate because it is generally associated with improvement in HIV-related skin diseases. Mid-potency steroids (preferably lubricant-containing ointments rather than creams) can be helpful. Emollient creams and bath oils can also help provide relief. Using only lukewarm water and gentle cleansers for bathing is important. Applying lotions and creams immediately after bathing can be helpful. The use of antihistamines and cold compresses can help relieve itching. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., p

Noninfectious Dermatoses: Scaling Diseases- Psoriasis

Definition- Psoriasis is a chronic skin disorder characterized by excessive proliferation of keratinocytes, resulting in the formation of thickened scaly plaques, itching, and inflammatory changes of the epidermis and dermis. The various forms of psoriasis include guttate, pustular, and arthritis variants. Ferri, Atlas, 2009, p. 33.

Cause- Unknown Familial clustering (genetic transmission with a dominant mode with variable penetrants) 1/3 of persons affected have a positive family history. Within the past decade, several putative loci for genetic susceptibility to psoriasis have been reported. One locus (psoriasis susceptibility 1 [PSORS1] locus) I the MHC region on chromosome 6 is considered the most important susceptibility locus. Ferri, Atlas, 2009, p. 33.

Noninfectious Dermatoses: Scaling Diseases- Psoriasis- PE and Clinical Findings
Fig. 7-1 Plaque psoriasis- close up view showing the thick scale. The primary psoriatic lesion is an erythematous papule topped by a loosely adherent scale (see 7-1). Scraping the scale results in several bleeding points (Auspitz sign). Ferri, Atlas, 2009, p. 33.

Fig. 7-2 Psoriasis. Typical plaque distribution shows a bilateral and fairly symmetrical distribution. In this example, the silvery scale is well demonstrated. Chronic plaque psoriasis generally manifests with symmetrical, sharply demarcated, erythematous, silver-scaled patches affecting primary the intergluteal folds, elbows, scalp, fingernails, toenails and knees (7-2). This form accounts for 80% of psoriasis cases. Ferri, Atlas, 2009, p. 33.

Prosiasis can also develop at the site of any physical trauma (sunburn, scratching). This is known as Koebner’s phenomenon. Nail involvement is common (pitting of the nail plate), resulting in hyperkeratosis, and onychodystrophy, with onycholysis. Ferri, Atlas, 2009, p. 33.

Fig 7-3 Guttate psoriasis. This infant shows a characteristic distribution over the trunk. Pruritis is variable. Joint involvement can result in sacroilitis and spondylitis. Guttate psoriasis is generally preceded by streptococcal pharyngitis and manifests with multiple droplike lesions on the extremities and trunk (Fig. 7-3). Ferri, Atlas, 2009, p. 33.

Noninfectious Dermatoses: Scaling Diseases- Psoriasis- Treatment
Sunbathing generally leads to improvement. Eliminate triggering factors (e.g. stress, certain medications [lithium, beta blockers, antimalarials]). Patients with psoriasis benefit from a daily bath in warm water followed by the application of a cream or ointment moisturizer. Regular use of an emollient moisturizer limits evaporation of water from the skin and allows the stratum corneum to rehydrate itself. Ferri, Atlas, 2009, p. 34.

Noninfectious Dermatoses: Scaling Diseases- Psoriasis- Treatment
Therapeutic options vary according to the extent of disease. Approximately 70% to 80% of all pts. Can be treated adequately with tropical therapy. Patients with limited disease (less than 20% of the body) can be treated with topical steroids, calcipotriene, tar products, anthralin, and retionoids. Therapeutic options for persons with generalized disease (affecting more than 20% of the body) include UVB light exposure three times weekly and oral PUVA. Systemic tx. Includes methotrexate and cyclosporine for severe psoriasis. Chronic plaque psoriasis may be treated with alefacept, a recombinant protein that selectively targets T lymphocytes or etanercept, a tumor necrosis factor (TNF) antagonist. Ferri, Atlas, 2009, p. 34.

Psoriasis A(TL). Typical erythematous plaques are topped by a silver scale. B(TR). Thick tenacious scale on a red base extends from the forehead to the scalp of this 10-year-old girl. C(ML). Large plaques are located over the shins and right knee. D(MR). In this child lesions are prominent over the pressure point of the knee and the distal fingers. E(B). The skin of the palms is markedly thickened, with silvery fissuring of the palmar creases. Credits: Fig 8.3, Zitelli et al., Atlas of Pediatric Physical, 6th ed., 2012.

Noninfectious Dermatoses: Scaling Diseases- Psoriasis- HIV-Frequency
Psoriasis may present for the first time during HIV infection, or preexisting psoriasis may be exacerbated in HIV-infected patients. Credits: AAHIV Fundamentals of HIV Medicine, 2007 ed., p. 432

Noninfectious Dermatoses: Scaling Diseases of HIV- Psoriasis- Treatment
- In the 1980’s, zidovudine was observed to improve psoriasis, and it has since been recognized that psoriasis clears with improvement in immune function due to administration of HAART. Even in those with low CD4 counts, psoriasis responds extremely well to antiretroviral-induced immune reconstitution, sometimes combined with retinoid acitretin (Soriatane). With immune reconstitution, it is usually possible to discontinue the acitretin. In persons who have not yet started HAART or are intolerant to it, acitretin has been shown to be efficacious at low doses. Transaminases and triglycerides should be monitored with acitretin use, particularly in those on antiretrovirals. Acitretin has been reported to aid in the arthritic component of Reiter’s-like arthritis. Credits: AAHIV Fundamentals of HIV Medicine, 2007 ed., p. 432

Noninfectious Dermatoses: Scaling Diseases- Psoriasis- HIV-Treatment
Topical Psoriasis treatments include topical steroids and Vitamin D analogs (calcipitriene). Ultraviolet light can be used for treatment of HIV-infected patients with psoriasis, win no evidence of adverse effects on CD4 counts. Immunosuppressive agents such as methotrexate had been contraindicated early in the epidemic because there was a higher rate of mortality associated with this drug in HIV infected patients; however, such agents can now be used with caution (to avoid exacerbating immune compromise). Newer biologic treatments for psoriasis such as etanercept (Enbrel) and infliximab (Remicade) are highly efficacious but the safety profile in HIV-infected patients is not yet known and they are not used by most dermatologists to treat these patients. Credits: AAHIV Fundamentals of HIV Medicine, 2007 ed., p. 432

Psoriasis in HIV patients
In a cohort of 50 HIV-infected individuals with psoriasis, the clinical patterns of psoriasis were reported to be plaque type (78%), inverse (37%), guttate (29%), palmoplantar (8%), erythrodermic (14%), and pustular (8%). Palmoplantar and inverse pattern psoriasis were more common in those patients who developed their psorriasis after HIV infection. From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1125, picture from p

Noninfectious Dermatoses: Pruritic and Papular Diseases

Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV
Eosinophilic Folliculitis Prurigo Nodularis and Pruritis Drug Eruptions Acne

Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV- Eosinophilic Folliculitis

Noninfectious Dermatoses: Pruritic and Papular Diseases- Eosinophilic Folliculitis- HIV-Cause
The cause of this eruption is not clearly understood, although it has been postulated by some that it may be a hypersensitivity reaction to Demodex folliculorum mite, which is a normal commensal inhabitant of human skin. Histopathologic examination of lesions reveals no organisms, but hair follicles are infiltrated with inflammatory cells, mostly eosinophils, hence the name. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., pp

HIV-related Eosinophilic Folliculitis
Description: Eosinophilic folliculitis that, on biopsy, showed acute follicular inflammation with a significant component of eosinophils Credits: Toby A. Maurer, MD, UCSF and Timothy G. Berger, MD, UCSF; National Library of Medicine Image Lib.

EF is very prevalent in patients with advanced HIV disease.
Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV- Eosinophilic Folliculitis- HIV-Frequency EF is very prevalent in patients with advanced HIV disease. EF is associated with low CD4 counts (below 250 cells/mm3) and low nadir counts (below 200 cells/mm3). In addition, EF is now often seen in those experiencing immune reconstitution in the first three to six months of HAART use. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., pp

EF is usually quite pruritic.
Noninfectious Dermatoses: Pruritic and Papular Diseases- Eosinophilic Folliculitis-HIV-Presentation EF is usually quite pruritic. EF lesions consist of small follicular papules and pustules approximately 2-3 mm in diameter, often with minimal or no surrounding erythema. Primary lesions themselves may be quite insignificant, because the main changes may be simply excoriations secondary to intense pruritis. Sites frequently involved include the face, especially the forehead, the neck, the area below and behind the ears, the chest, the back and the lateral surfaces of the upper arms. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., pp

EF tends to be resistant to treatment.
Noninfectious Dermatoses: Pruritic and Papular Diseases- Eosinophilic Folliculitis- HIV-Diagnosis and Treatment EF tends to be resistant to treatment. Topical medications, even potent steroids, seldom provide relief, but high-dose oral itraconazole (Sporonox) can sometimes be effective and is usually given in doses of mg daily. It must be taken chronically because the condition recurs when it is discontinued. It appears to work via the antieosinophilic action of this agent, rather than through any antifungal effect; other antifungals (ketoconazole and fluconazole) are not beneficial. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., pp

Administration of systemic corticosteroids may also be effective.
Noninfectious Dermatoses: Pruritic and Papular Diseases- Eosinophilic Folliculitis- HIV Diagnosis and Treatment Other treatments that have been found to provide some relief are oral metronidazole, topical permethrin (Elimite), and isotretinoin (Accutane). Administration of systemic corticosteroids may also be effective. In patients experiencing the immune reconstitution folliculitis, oral ivermection has been shown to work in those who have failed topical remedies. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., pp

Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV- Eosinophilic Folliculitis- Other
It is important to note that the eruption can first appear or be exacerbated when a patient initiates antiretroviral therapy, and can be mistaken as an allergic drug eruption. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., pp

Eosiniophilic Folliculitis: IRIS
In patients with low CD4 cts., in most cases of pruritis, primary or secondary dematoses rather than metabolic disorders are the cause. The differential diagnosis of primary pruritic skin disorders includes eosinophilic folliculitis, papular pruritic eruption of HIV, adverse cutaneous drug reactions, atopic dermatitis, scabies and insect bites. Much less commonly, systemic and metabolic disorders such as lymphoma, renal failure, viral hepatitis (hepatitis B or C), or obstructive liver disease are associated with pruritis in the absence of cutaneous findings. From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p , picture from p

Eosiniophilic Dermatitis in HIV Patient
Credit: Figure from Mandell et. al., Infectious Diseases, (Courtesy of Stephen Raffanti, MD, MPH.)

Noninfectious Dermatoses: Pruritic and Papular Diseases- Prurigo Nodularis

Noninfectious Dermatoses: Pruritic and Papular Diseases- Prurigo Nodularis- General
Fig 6-16 Nodular prurigo showing typical globular nodules; the intervening skin appears normal. Dermatosis characterized by the development of chronic, intensely pruritic, lichenified, and excoriated nodules. Individual lesions are often described as globular with a warty and excoriated surface and may measure up to 2 cm in diameter (Fig. 6-16). Credits: Ferri, Atlas, p. 30.

The palms and soles are typically uninvolved.
Noninfectious Dermatoses: Pruritic and Papular Diseases- Prurigo Nodularis- General There are often grouped and symmetrical, occurring predominantly predominantly on extensor aspects of the distal limbs. The palms and soles are typically uninvolved. Credits: Ferri, Atlas, p. 30.

Noninfectious Dermatoses: Pruritic and Papular Diseases- Prurigo Nodularis- General
General- Psychosocial disorders have been reported in a high proportion of patients. Increased prevalence is noted wiith gluten enteropathy. Lab testing- HIV, ALT, AST, serum creatinine, serum IgE, histology with immunoflourescence. Treatment: corticosteroids (PO, intralesional), occlusion, cryotherapy, UVB phototherapy, PUVA. Credits: Ferri, Atlas, p. 30.

Frequency: Common usually with CD4<200 cells/mm
Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV- Prurigo Nodularis-HIV Frequency: Common usually with CD4<200 cells/mm Cause: A report from Uganda based on skin biopsies concluded that most were due to “anthropod-induced prurigo of HIV.” Presentation: Hyperpigmented, hyperkeratotic, often excoriated papules and nodules up to 1 cm; 90% are above nipple line. Major symptom is severe pruritus. Usually associated with other signs of chronic pruritis or excoriations including lichen simplex, simplex chronicus, patches of hyperpigmentation, linear erosions, ulcerations, and scars. Credits: Bartlett, John G and Gallant, Joel E Medical Management of HIV Infection, pp

Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV- Prurigo Nodularis-HIV
Differential: warts, traumatized folliculitis, deep fungal infections, perforating diseases. Diagnosis: Clinical features; biopsy may be necessary. This typically shows dense perivascular and interstitial infiltrates with eosinophils. Treatment: Must interrupt vicious cycle: Pruritis, then scratch trauma, then lichenification, then increased pruritis. Treat with high-potency topical steroids under occlusive dressing. May benefit from oral histamines or phototherapy. Refractory cases may benefit from 100 mg/d thalidomide. Credits: Bartlett, John G and Gallant, Joel E Medical Management of HIV Infection, pp

Prurigo nodularis An atopic diathesis (characterized by personal or family history of atopic dermatitis, asthma, and allergic rhinitis), which exists in up to 20% of the general population, may become manifest in individuals with advanced HIV disease and pruritis. Changes secondary to chronic rubbing and scratching include excoriations, atopic dermatitis, lichen simplex chronicus, and prurigo nodularis. From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1122, picture from p

Noninfectious Dermatoses: Pruritic and Papular Diseases- Drug Eruptions
.

Most commonly develop within 1 to 2 weeks of starting the drug.
Noninfectious Dermatoses: Pruritic and Papular Diseases- Drug Eruptions- General Exanthematous (Morbilliform, maculopapular) reactions are the most frequently encountered adverse drug reactions. Patients who have infectious mononucleosis are particularly at risk of developing an exanthematous reaction following therapy with ampicillin or amoxicillin. Most commonly develop within 1 to 2 weeks of starting the drug. Penicillins, sulfonamides, trimethoprim, and phenytoin are especially incriminated. Credits: Ferri, Atlas, p. 47. .

Noninfectious Dermatoses: Pruritic and Papular Diseases- Drug Eruptions- PE and Clinical
Fig (Right) Exanthematous drug reaction. These more extensive lesions on abdomen were associated with amoxicillin therapy. Clinical presentation: pts. present with erythematous macules and papules that with progression may become confluent or even acquire gyrate or polycyclic features. Credits: Ferri, Atlas, p. 47. .

Noninfectious Dermatoses: Pruritic and Papular Diseases- Drug Eruptions- PE and Clinical
Fig 14-4 Minocycline Pigmentation- typical pigmentation affecting the shin. Pruritis, low-grade fever, and eosinophilia are sometimes present, The eruption is often symmetrical and usually presents on the trunk and extremities or sites of pressure and trauma. Credits: Ferri, Atlas, pp .

Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV- Drug Eruptions- HIV
Cause: Most common are antibiotics, especially sulfonamides (TMP/SMX), beta-lactams, anticonvulsants, NNRTIs, and fosamprenavir and tipranavir, both of which include sulfa moities. Credits: Bartlett, John G and Gallant, Joel E Medical Management of HIV Infection, pp

Presentation: Most common- morbilliform, exanthematous, usually pruritic +/- low grade fever; usually within 2 weeks of new drug and days of re-exposure. Less common and more severe forms: 1) Urticaria: Intensely pruritic, edematous, and circumscribed 2) Anaphylaxis: Laryngeal edema, nausea, vomiting +/- shock 3) Hypersensitivity syndrome: Severe reaction with rash and fever +/- hepatitis, arthralgias, lymphadenopathy, and hematologic changes with eosinophilia and atypical lymphocytes, usually at 2 to 6 weeks after drug is started. Note especially abacavir and nevirapine 4) Stevens-Johnson Syndrome: Fever, erosive stomatitis, disseminated erosions +/- blisters dark red macules, ocular involvement; mortality -5%. 5) Toxic epidermal necrolysis: Epidermal necrosis with scalded skin appearance +/- mucous membrane involvement; mortality -50%. Credits: Bartlett, John G and Gallant, Joel E Medical Management of HIV Infection, pp

Treatment: In severe and very symptomatic reactions, discontinue implicated agent Pruritic unclomplicated drug rashes: antihistamines, topical antipruritics, and topical corticosteroids Stevens-Johnson and toxic epidermal necrolysis: Severe cases are managed as burns with supportive care; corticosteroids are not indicated Credits: Bartlett, John G and Gallant, Joel E Medical Management of HIV Infection, pp

HIV-related Drug Eruption
Description: Nonnucleoside reverse transcriptase inhibitor (NNRTI)-associated rash on a 12-year-old girl who had begun antiretroviral therapy with efavirenz (Sustiva) 1 week previously. Rash is one of the most common side effects observed with NNRTIs. Credits: Pediatric AIDS Pictoral Atlas, Baylor International Pediatric AIDS Initiative; Nat’l Library of Medicine.

HIV-Related Drug Eruption
Description: Drug eruption from Sulfa drugs (Septrin) in an HIV+ Kenyan male; patient died several days later. Credit: Dr. Thor Swanson, MD; Siouxland Medical Education Foundation, 2008.

Description: Drug eruption in an HIV+ Kenyan male following HAART, incl. D4T, 3TC and NVP Credits: Thor Swanson, MD: Siouxland Medical Education Foundation, Sioux City, Iowa, 2008.

Description: HIV-related Drug Eruption in an HIV+ Kenyan following HAART commencement with D4T, 3TC and NVP Credits: Thor Swanson, MD: Siouxland Medical Education Foundation, IA.

Noninfectious Dermatoses: Pruritic and Papular Diseases- Acne
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Noninfectious Dermatoses: Pruritic and Papular Diseases- Acne- General
Acne vulgaris is a chronic disorder of the pilosebaceous apparatus caused by abnormal desquamation of follicular epithelium leading to obstruction of the pilosebaceous canal resulting in inflammation and subsequent formation of papules pustules, nodules, comedones, and scarring. Acne can be classified by the type of lesion (comedonal, papulopustular, nodulocystic). Credits: Ferri, Atlas, p. 72.

The American Academy of Dermatology classification scheme of acne has denoted the following 3 levels. 1. Mild 2. Moderate 3. Severe PE- open comedones (blackheads), closed comedones (whiteheads), greasiness (oily skin), presence of scars from prior acne cysts, various stages of development and severity may be present concomitantly. Common distribution- face, back and upper chest Inflammatory papules, pustules, and ectatic pores. Credits: Ferri, Atlas, p. 72.

Fig Acne vulgaris. There are widespread blackheads that develop as a result of blockage of the pilosebaceous canal by keratotic debris. Credits: Ferri, Atlas, pp

Treatment- 1. Retinoids or retinoid analogues for comedones. 2. Benzoyl peroxide gel (2.5 % or 5%) may be added for inflamed papules or pustules. 3. Drying agents (sulfacetamide, sulfa lotions) are also effective when used in combination with benzoyl peroxide. 4. Oral antibiotics (doxycycline or erythromycin) are effective for pts. With moderate to severe pustular acne. 5. Pts. with nodular cystic acne can be treated with agents- antibiotics, isotretinoin (Accutane), or oral contraceptives. Oral contraceptives reduce androgen levels and therefore sebum production. Credits: Ferri, Atlas, p. 72.

Noninfectious Dermatoses: Pruritic and Papular Diseases of HIV- Acne- Frequency- HIV
Frequency-Exacerbations of acne are common in HIV infection, particularly as HAART-treated patients are immune reconstituted and become more capable of producing an inflammatory response. Credits: AAHIVM Fundamentals of HIV Medicine, 2007 ed., pp

Noninfectious Dermatoses: Pruritic and Papular Diseases- Acne- HIV-Presentation and Diagnosis
As in the HIV-negative, acne in the HIV-infected patients commonly presents with papulopustular lesions located predominantly on the face and back. It is important to distinguish acne from eosinophilic folliculitis since the latter is too often misdiagnosed as acne. The presence of comedones or “blackheads” between pustules with acne usually allows this distinction. In addition, eosinophilic folliculitis often causes extreme pruritis while acne does not. Credits: 2007 Medical Management of HIV Infection, AAHIVM, pp

In severe cystic cases, isoretinoin (Accutane) is required.
Noninfectious Dermatoses: Pruritic and Papular Diseases- Acne- HIV- Treatment Management does not differ from that for HIV-negative patients, with initial use of topical antibiotics and keratolytic agents, progressing to systemic antibiotics such as tetracycline or minocycline. In severe cystic cases, isoretinoin (Accutane) is required. Credits: 2007 Medical Management of HIV Infection, AAHIVM, pp

Fungal Diseases and Mycoses

Mycoses Superficial Mycosis Pseudomycosis Subcutaneous Mycosis
Systemic Mycosis Mycosis by Opportunists

Mycoses- Superficial Mycoses
Dermatophytoses- Tinea corporis (ringworm), Tinea capitis (ringworm of scalp), Tinea pedis (fungus of feet) , Tinea cruris (fungus of groin) Pityriasis Versicolor (Tinea versicolor) Onychomycosis Candidiasis Tinea Nigra Tricosporonosis

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses
Superficial mycoses are caused by parasitic fungi of the keratin. They are called dermatophytes. They belong to the gender Trichophyton, Microsporum and Epidermophyton. They infect the skin, the hair and nails, and occasionally, they involve deep tissue. Credits: Arenas and Estrada, Tropical Dermatology: Arenas and Estrada, 2001 ed..

Tropical Dermatology:Mycoses- Superficial Mycoses Dermatophytosis
GEOGRAPHIC DISTRIBUTON: Dermatophytosis, especially tinea capitis, tinea corporis and tinea cruris, occursworldwide but is very common in tropical countries. Ninety-eight percent of tinea capitis is seen in children. Credits: Arenas et al., Tropical Dermatology, 2001 edition.

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Tinea Corporis
Fig 26-1 Tinea corporis. Note the annular configuration and erythematous margin. Tinea corporis (ringworm) is a dermatophyte fungal infection caused by the Trichophyton or Microsporum sp. Typically it appears as a single or multiple annular lesions with an advancing scaly border; the margin is slighly raised and reddened and may be pustular. (See right) The central area becomes hypopigmented. Antifungal creams are effective Credits: Ferri, Atlas, p. 110.

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Tinea Capitis
Fig 26-2 Tinea capitis. There is marked hair loss. In this example, scaling and crusting are pronounced. Tinea capitis (ringworm of the scalp) is a dermatophyte infection of the scalp. Presents with triad of scalp scaling, alopecia (see right) and cervical adenopathy. Treatment- griseofulvin, oral terbinafine, itraconazole, or fluconazole. Credits: Ferri, Atlas, p

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Kerion
Fig (Right) Non-scarring patchy alopecia and boggy inflammation in Celsus’ kerion. Children manifest scalp infections under the kerion clinical form with patches of non-scarring alopecia and boggy inflammation of the skin. Credits: Cook et al., Manson’s Tropical Medicine, p. 348.

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Tinea Cruris
Fig 26-3 Tinea cruris This is much more common in men than women. In this example, pustulation is evident. Tinea cruris (jock itch) is a dermatophyte infection of the groin. Erythematous plaques have a half-moon shape and scaling border. Treatment- keep infected area clean and dry. Topical antifungals include miconazole, terbinafine, clotrimazole. Credits: Ferri, Atlas, p

Tinea Cruris 999 Tinea cruris This infection, which is very common in young males in hot, humid areas, is usually caused by Epidermophyton floccosum, Trichophyton rubrum or Trichophyton mentagrophytes var. interdigitale. The red, slightly raised margin of the lesion in this patient can be seen to be advancing down the inner thigh. Peters et al., Atlas of Tropical medicine, 2007.

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Tinea Pedis
Fig 26-4a (Right) Tinea pedis. Maceration between the toes Tinea pedis (athlete’s foot ) is a dermatophyte infection of the feet. Typical presentation is variable an ranges from erythemaous scaling plaques and isolated blisters to interdigital mmaceration. Most common dermatophyte infection (in West). Credits: Ferri, Atlas, p

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Tinea Pedis
Fig 26-4b (Right) Tinea pedis. Severe dermal edema has resulted in this bullous variant. Treatment includes keeping infected area clean and dry. Treatment also includes antifungal creams (clotrimazole, butenafine, naftifine). Credits: Ferri, Atlas, p

Tinea Imbricata 998 Tinea imbricata Trichophyton concentricum produces characteristic, superficial, scaly lesions in parallel lines and concentric circles. While it is common in the south Pacific and parts of the Far East, it is occasionally seen in other hot, humid areas. Peters et al., Atlas of Tropical Medicine

HIV-Related Onychomycosis
Fungal infection of the toe nails is most commonly caused by Trichophyton rubrum. In this individual who had been treated with zidovudine but no antifungal for four weeks, some clearing of the infection in the proximal toe nail with residual distal infection may be seen. Credits: Fig. 892 on p. 300 in Peters and Pasvol, Atlas of Tropical Medicine and Parasitology, 6th ed., (Philadelphia: Elsevier, 2007).

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Pityriasis versicolor/Tinea versicolor Fig (Right) Tinea versicolor. Hyperpigmented macules, many of which have coalesced, are present on the chest, which is a commonly affected site. Tinea versicolor is a fungal infection of the skin caused by the yeast Pityrosporum orbiculare (Malassezia furfur) Most lesions begin as multiple small, circular macules of various colors. The macules may be darker or lighter than the surrounding normal skin and will scale with scraping. Treatment: selenium sulfide 2.5% suspension; oral fluconazole, oral ketoconazole. Credits: Ferri, Atlas, p

Pityriasis versicolor
1000 Pityriasis versicolor Infection with Malassezia furfur is a common cause of hypopigmentation in dark-skinned young adults. Fluorescence of the patches in Wood’s light helps to differentiate the condition from vitiligo and other depigmenting lesions. Peters et al., Atlas of Tropical Medicine

Tropical Dermatology: Mycoses- Superficial Mycoses Dermatophytoses- Cutaneous candidiasis
Fig (Right) Cutaneous candiditais. Superficial mycotic infection of the skin usually caused by the yeast Candida albicans. The affected area has a red glistening surface with an advancing border and cigarette paper-like scaling. The intertriginous skin folds such as the inner thighs or other moist occluded sites such as underneath the breasts are most frequently affected. Treatment includes antifungal products (miconazole, clotrimazole, econazole) and oral therapies in resistant cases. Credits: Ferri, Atlas, p

Candidiasis in Child with AIDS
Oral thrush and candidal diaper dermatitis in child with AIDS. Credits: Fig on p. 505 from Zitellis, Atlas of Pediatric Physical Diagnosis, 5th ed., (Philadelphia:Elsevier, 2007).

Oral Thrush in HIV Pt. Thrush appears as a white, cheesy exudate, often on an erythematous mucosa in the posterior oropharynx. While most commonly seen of the soft palate, early lesions are usually found along the gingival border. From Fauci, Anthony et. al. Harrison’s Principles of Internal Medicine, 2008, p

Candidiasis: Balanoposthitis with HAART
Cutaneous Candida infections such as intertrigo, are common in adults with HIV disease; concomitant diabetes mellitus associated with HAART may increase the prevalence. Candidiasis of moist, keratinized cutaneous sites such as the anogenital region occurs with some frequency in up to 90% of HIV-infected patients. From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1131, picture from p

Tropical Dermatology:Mycoses- Superficial Mycoses Tinea Nigra
Tinea nigra is an infection of palmar or plantar skin caused by a black yeast, Phaeoannelomyces werneckii. Mainly seen in the tropics but can present in Europe and the USA. Tinea nigra responds to a variety of treatments including Whitfield’s ointment and azole creams. Credits: Cook et al., Manson’s Tropical Medicine, p. 71.

Tropical Dermatology:Mycoses- Superficial Mycoses Trichosporonosis
White piedra is a chronic infection of the hair shafts caused by a yeast Trichosporon beigelii. Generally sporadic and rare and the infection is mainly seen in genital hair. It may also affect axilla and scalp. The disease can be seen in temperate and tropical areas. Credits: Cook et al., Manson’s Tropical Diseases, p

Mycoses- Pseudomycoses
.

Mycoses- Pseudomycosis
Erythrasma Pitted Keratolysis Trichomycosis Protothecosis Actinomycosis Botryomycosis

Mycoses- Pseudomycosis- Erythrasma
Definition- Bacterial infection caused by Cornybacterium minutissimum, a gram-positive bacillus. Physical Findings- Characteristically presents as symptomatic, well-defined, scaly red patches on the inguinal and intergluteal skin. It has a predilection for obese and diabetic patients and is more common in regions with a humid and hot climate. Diagnosis- Diagnosed by demonstration of coral red flourescence under Wood’s light. It is caused by production of coproprophyrin II by the organism. Treatment- antifungal creams (miconazole, clotrimazole, econazole) Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine 2009, pp. 137.

Mycoses- Pseudomycosis- Erythrasma
Fig Erythrasma. Note the well-demarcated axillary scaly red path. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine 2009, pp. 137.

Mycoses- Pseudomycosis- Actinomycosis
Definition- Actinomycosis is an indolent, slowly progressive infection caused by both anaerobic or microaerophilic bacteria that normally colonize the mouth, vagina, and colon. Actinomycosis is characterized by the formation of painful abscesses, soft tissue infiltration, and draining sinuses. Physical Findings and Clinical Presentation- Actinomycosis can affect any organ. Although not typically considered as opportunistic pathogens, Actinomyces species capitalize on tissue injury or mucosal breach to invade adjacent structures in the head and neck regions. As a result, dental infections and oromaxillofacial trauma are common antecedent events. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine 2009, pp

Cause- Actinomycosis is most commonly caused by Actinomyces israelii. Other causes are A. naeslundii, A. odontolyticus, A. viscosus, A. meyeri, and A. Gerencseriae. Laboratory Tests- Isolating “sulfur ganules” from tissue specimens or draining sinuses confirms the diagnosis of actinomycosis. Actinomyces are noted for forming characteristic sulfur granules in infected tissue by not in vitro. Treatment- Incision and drainage of abscesses, excision of sinus tract, penicillin 10 to 20 million units per day in 4 divided doses for 4 to 6 weeks. In PCN-allergic pts., erythromycin, tetracycline, clindamycin, or cephalosporins are reasonable alternatives. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine 2009, pp

Fig Actinomycosis; Extensive intrathrothoracic disease has resulted in involvement of the anterior chest wall. Numerous sinuses are evident. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009

Sulfur granule of actinomycosis with well-demarcated sulfur granule composed of thin, delicate branching bacilli visible on HANDE. The bulk of the granule is composed of amorphous material (HANDEx 450). Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009.

Mycoses- Subcutaneous Mycoses
Mycetoma (Madura Foot) Sporotrichosis Chromoblastomycosis Lobomycosis (Jorge Lobo’s Disease) Entomophtoromycosis Rhinosporidiosis

Tropical Dermatology: Mycoses- Subcutaneous Mycosis Mycetoma- Introduction
Mycetoma is a non-contagious chronic infection of the skin and subcutaneous tissue which can involve deeper structures like the fasciae, muscles, and bones; it is acquired by traumatic inoculation of the etiologic agent. Clinically it is characterized by an increased volume of the affected area, fibrosis, tumefaction, and the formation of abscesses that drain pus-containing grains through fistulae. Credits:Tyring et al., Tropical Dermatology, 2006 edition.

Tropical Dermatology: Mycoses- Subcutaneous Mycosis Mycetoma-General
Mycetoma is an infectious disease caused by fungi or aerobic actinomycetes and characterized by an increased volume of involved areas with fibrosis, abscesses, and fistulae. It is mainly found in farmers of tropical and subtropical regions of the Americas, India, and Africa. The causative agents are identified by direct examination, histopathology, and culture. Treatment of actinomycetoma includes sulfamethoxazole, trimethoprim, and amikacin. Therapy of eumycetoma includes itraconazole, terbinafine, and surgical resection of the lesions. Credits: Tyring et al., Tropical Dermatology, 2006 edition.

Tropical Subcutaneous Mycosis Mycetoma- Epidemiology
This infection is more commonly found in young to middle-aged males from rural areas (3:1 ratio), probably reflecting occupational contact with the causative agents. This microorganism lives saprophytically in nature, in soil and plants, deriving nutrition from organic material in decomposition. The infection is more common in tropical and subtropical areas, and is endemic in India and various countries in Africa and the Americas. However, both forms of mycetoma have been reported in areas with a temperate climate such as the USA. Credits: Tyring et al, Tropical Dermatology, 2006 edition.

Tropical Dermatology: Mycoses- Subcutaneous Mycosis Mycetoma-Pathogenesis
Saprophytic fungi or bacteria from the soil or plants penetrate the skin and subcutaneous tissue by traumatic implantation. The infection evolves slowly by contiguity and can invade deeper structures like fasciae, muscles, tendons, bones, and exceptionally adjacent organs. The most frequently reported agents of actinomycetoma are species of Nocardia, especially N. brasiliensis, which is the most frequent agent in many countries of the Americas. Credits: Tyring et al., Tropical Dermatology:, 2006 edition.

Tropical Dermatology: Mycoses- Subcutaneous Mycosis Mycetoma- Clinical Features
At the inoculation site, after a variable incubation period (weeks or months), a nodule appears, generally painless, which suppurates and drains a serosanguineous or sepopurulent secretion through fistulae. Contiguous and similar lesions appear, and after a period of one to several years, the affected areas present an increased volume, and numerous fistulae draining secretion with grains. Credits: Tyring et al., Tropical Dermatology, 2006.

Tropical Dermatology:Mycoses- Subcutaneous Mycosis Mycetoma- Treatment
Actinomycetoma with Nocardia are treated successfully with a combination of sulfamthoxazole (1200 mg) trimethoprim (240) (SXT) b.i.d., and occasionally dapsone at a dose of mg/day for months. Treatment response in eumycotic mycetoma is variable, and in many cases shows poor results. The drugs of choice are itraconazole ( mg/day) or ketoconazole (400 mg/day) for 1 or 2 years or even for longer periods. Corticosteroids can be combined with antifungals for a short period to improve the inflammatory process. A combination of surgery and drug therapy is the best option. Credits: Tyring et al., Tropical Dermatology, 2006 edition.

Madura Foot 1003 Dorsum of Madura foot in an African patient Discharging sinuses and distortion of some of the toes are seen in this patient’s left foot. Peters et. al., Atlas of Tropical Medicine, 2007.

Chronic Maduromycosis
1008 Chronic maduromycosis due to Streptomyces somaliensis infection Extensive sinus formation and osteitis have led to gross disfigurement in this Sudanese man. Peters et. al., Atlas of Tropical Medicine, 2007

Radiographs of Madura Foot
1004 Radiographs of Madura foot Infiltration of the tarsals and metatarsals occurs in late cases. 1004 Radiographs of Madura foot Infiltration of the tarsals and metatarsals occurs in late cases. Peters et. al., Atlas of Tropical Medicine.

Tropical Dermatology: Mycoses- Subcutaneous Mycosis Sporotrichosis- Key Features
Worldwide infection caused by the dimorphic fungus Sporothri schenckii is mainly found in temperate warm and tropical areas. After cutaneous inoculation, ulcers, and verrucous plaques with or without lymphangitic spread occur in immunocompetent individuals. Pulmonary and disseminated disease can occur by conidia inhalation associated with immunosuppression. The S. schenckii infection is confirmed by immunohistochemical techniques and culture. Treatment includes the use of saturated solution of potassium iodide, and in pulmonary and disseminated cases itraconazole and amphotericin B are indicated. Credits: Tyring et al., Tropical Dermatology, 2006 ed.

FIGURE A, Sporotrichoid rash of Mycobacterium marinum infection showing typical location on the superficial cooler body tissues of the extremities. B, A similar rash in a patient with classical sporotrichosis due to the fungal pathogen Sporothrix schenckii. Credits: Guerrant et. al., Tropical Infectious Diseases, 2nd ed., 2006, p Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Tropical Dermatology: Mycoses- Subcutaneous Mycosis Chromoblastomycosis- Key Features
Chromoblastomycosis is a chronic cutaneous and subcutaneous fungal infection which predominates in exposed areas and is caused by several dematiaceous fungi implanted by traumatic injury. It is found worldwide but predominates in tropical climates to Central and South America, and Madagascar. Skin lesions are characterized by paules, nodules, plaques, verrucoid, and papillomatous slow-growing lesions. Thick-walled septated brown cells (muriform cells) located inside multinucleated cells and extracellularly are present in the granulomatous tissue. Treatment includes surgery, cryosurgery, carbon dioxide laser excision, topical heat application, amphotericin B, itraconazole, and terbinafine. Credits: Tyring et al., Tropical Dermatology, 2006.

Early Chromomycosis 1009 Early chromomycosis The early lesions show a violet discoloration. The primary ulcer spreads slowly and is followed by verrucous lesions. This condition is seen in many tropical areas, including Queensland, where this man was infected. Peters et. al., Atlas of Tropical Medicine, 2007

Verrucous Dermatitis 1010 Verrucous dermatitis This is the late stage of chromomycosis. The lesions are very chronic, and are usually painless but irritating. Lymphoedema follows lymphatic stasis. Peters et. al, Atlas of Tropical Medicine, 2007.

Chromomycosis of the Hand
1011 Chromomycosis of the hand The infection can also cause severe but usually superficial lesions on the hands, as in this man from the north-east of Brazil. Peters et. al., Atlas of Tropical Medicine, 2007

Tropical Dermatology: Mycoses- Subcutaneous Mycosis Lobomycosis- Key Features
Lobomycosis is a chronic granulomatous localized subcutaneous mycosis caused by Lacazia loboi. It is characterized by variably sized nodular (keloid-like) plaques, verrucoid and ulcerative skin lesions. It commonly develops on the ear, face, and extremities of humans with no visceral dissemination. Diagnosis made by observing globose yeast-like fungal cells in the histological study of the lesions.Culture is not available. Wide and deep excision for localized lesions is the treatment of choice. Credits: Tyring et al., Tropical Dermatology, 2006.

Loboa Loboi 1013 Loboa loboi The typical spores of this fungus are seen in this biopsy specimen from the keloidal lesions. (H&E × 350) Peters et. al, Atlas of Tropical Medicine, 2007.

Lobo’s Disease 1012 Lobo’s disease This condition, usually presenting with shiny, keloid-like lesions, produces a general picture similar to late chromoblastomycosis and occurs in the north-east of Brazil. It is caused by Loboa loboi. Peters et. al., Atlas of Tropical Medicine, 2007.

Mycoses- Systemic Mycoses

Mycoses- Systemic Mycoses
Coccidioidomycosis Paracoccidioidomycosis Histoplasmosis Cryptococcosis Blastomycosis Penicillium

Systemic Mycoses- Coccidioidomycosis
Definition- Coccidioidomycosis is an infectious disease cause by the fungus Coccidioides immitis. It is usually asymptomatic and characterized by a primary pulmonary focus with infrequent progression to chronic pulmonary disease and dissemination to other organs. Cause- Coccidiodies immitis is endemic to North and South America. Physical Exam Can affect many organ systems including pulmonary, CNS and musculo-skeletal systems. Cutaneous involvement: variable lesions- pustules, papules, plaques, nodules, ulcers, abscesses, or verrucous proliferative lesions. Ferri, Ferri’s Color Atlas of Tropical Medicine, 2009, pp

Tropical Dermatology:Mycoses- Systemic Mycosis Coccidioidomycosis
. Coccidioidomycosis Credits: Fig , Ferri’s Clinical Medicine,

Fig Coccidioidomycosis: ulcerated nodules are present on the knee and ankle. Ferri, Ferri’s Color Atlas of Tropical Medicine, 2009, pp

Fig Coccidioidomycosis, showing hilar lymphadenopathy and a cavity in the left lung. Ferri, Ferri’s Color Atlas of Tropical Medicine, 2009, pp

Paracoccidioidomycosis- General
Paracoccidioidomycosis, Brazilian blastomycosis or South American blastomycosis is a deep and systemic mycosis caused by the thermally dimorphic fungus Paracoccidioides brasiliensis. Before sulfonamides were introduced in 1940 it was invariably fatal. This therapy results in improvement or cure in more than 60% of the cases. Credits: Arenas et al,, Tropical Derrmatology, 2001 edition.

PLATE 126-2 A, Tropical phagedenic ulcer. B, Buruli ulcer
PLATE A, Tropical phagedenic ulcer. B, Buruli ulcer. C, Myiasis extruding larva. D, Granuloma inguinale. E, South American blastomycosis (paracoccidioidomycosis). Credits: Guerrant et. al. , Tropical Infectious Diseases, 2nd edition,, 2006 (A–C, Courtesy of Jay S. Keystone, MD. D and E, Courtesy of R. L. Guerrant, MD, Charlottesville, VA.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Mucocutaneous Lesions in Paracoccidioidomycosis
1014 Mucocutaneous lesions in paracoccidioidomycosis In adults, gross infiltration of mucocutaneous and mucous surfaces by Paracoccidioides brasiliensis may spread to the pharynx and larynx. The diagnosis is made by demonstrating the fungi in smear or biopsy preparations, or by serological testing. Peters et. al., Atlas of Tropical Medicine, 2007.

Radiograph of Chest in Paracoccidioidomycosis
Chronic pulmonary infiltration may result in fibrosis and eventual death from respiratory insufficiency in infections with P. brasiliensis. Peters et al., Atlas of Tropical Medicine, 2007.

Pseudotumoral form of Paracoccidioidomycosis
1016 Computed tomography (CT) scan of the abdomen of a 57-year-old Brazilian man who presented with right lumbar pain and massive weight loss 15 years after having oropharyngeal infection. Physical examination suggested the presence of a colonic carcinoma but radiography and a CT scan revealed the presence of abscesses involving the psoas muscle as well as calcification and thickening of the ileocaecal region of the intestine. Material removed during radical surgery confirmed that the lesions were caused by infection with P. brasiliensis. Peters, Atlas of Tropical Medicine, 2007.

Paracoccidioidomycosis in a Brazilian Child
1017 In children, P. brasiliensis infection is a widely disseminated disease affecting macrophages and causing generalised lymphadenopathy and hepatosplenomegaly. Although it is uncommon prior to adolescence, this boy was aged only 41⁄2 years. Ultrasound may help to locate intra-abdominal lymphadenopathy, which was present in this case. Infection of the macrophages results in a state of immunodeficiency, which was reflected here by a negative skin test. Note the general emaciation associated with an enlarged abdomen, generalised lymphadenopathy and ulcerating cervical lymph nodes. In this boy, a titre of 1/1 280 against P. brasiliensis was recorded. Peters et al., Atlas of Tropical Medicine, 2007.

Tropical Dermatology: Mycoses- Systemic Mycosis Histoplasmosis- Key Features
Histoplasmosis is a respiratory and systemic mycosis caused by a thermally dimorphic fungus Histoplasma capsulatum. Histoplasmosis infection occurs in immunocompetent individuals, and rarely causes significant clinical symptoms. Histoplasmosis manifests as a progressive, disseminated disease that can be fatal if not treated promptly in individuals with an impairment in the immune system. Credits: Tyring et al., Tropical Dermatology, 2006.

Histoplasmosis Fig Endemic Distribution of histoplasmosis in the Americas. This is based on skin testing surveys. Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009.

Cutaneous Histoplasmosis
891 The typical lesions of cutaneous histoplasmosis are shown in this individual with HIV infection who came from the Caribbean. Histoplasma capsulatum is a dimorphic fungus existing as a mould in organic matter and as a yeast in tissue. Disseminated infection occurs especially in the immunosuppressed. Peters et. al, Atlas of Tropical Medicine, 2007.

Tropical Dermatology: Mycoses- Systemic Mycosis Histoplasmosis
Cutaneous Histoplasmosis in pt. with HIV Credits: Ferri’s Clinical Medicine, Fig

Histoplasmosis in HIV Patient
FIGURE Histoplasmosis. Credits: Fig from Mandell et. al., Infectious Diseases, (Courtesy of Stephen Raffanti, MD, MPH.)

African Histoplasmosis
1023 Histoplasmosis caused by Histoplasma duboisii commonly produces large destructive lesions of the skin and subcutaneous tissues. Bones are often involved in the invasive process. Credits: Peters et al., Atlas of Tropical Medicine, 2009.

African Histoplasmosis
1024 Histoplasma duboisii in biopsy. The typical giant-cell reaction to the presence of H. duboisii spores seen in this figure. Credits: Peters et al., Atlas of Tropical Medicine, 2009.

Cryptococcosis- General
Description- Cryptococcosis is an infection caused by the fungal organism Cryptococcus neoformans. Physical Exam- More than 90% present with meningitis; almost all have fever and headache. Skin lesions include- cellulitis, papular eruption, erythematous nodules. Skin lesions confused with bacterial cellulitis or molluscum contagiosum. Credits: Ferri’s Clinical Medicine, 2009.

Cutaneous Cryptococcosis
Cryptococcosis: Multiple erythematous nodules are present Credits: Fig Ferri’s Clinical Medicine, 2009.

Systemic Mycoses-Cryptococcosis
Cryptococcus neoformans infection of lung. Patient with acquired immunodeficiency syndrome and pulmonary infiltrates. Many round yeast are present and who thick capsules and narrow-based budding (Diff-Quik stain, x600) Credits: Fig Ferri’s Clinical Medicine, 2009.

Cutaneous Cryptococcosis
An AP chest film demonstrates a fine reticular interstitial pattern, right paratracheal and hilar adenopathy, and left pleural fluid. Although the interstitial pattern may simulate that seen with pneumocystis penumonia, the present of adenopathy and pleural fluid should direct attention toward another diagnosis Credits: Fig Ferri’s Clinical Medicine, 2009.

HIV-Related Cutaneous Cryptococcus
Description: 9 year old HIV-infected girl with Cutaneous Cryptococcus neoformans. Credits: Pediatric AIDS Pictoral Atlas, Baylor International Pediatric AIDS Initiative; Nat’l Library of Medicine

Cutaneous cryptococcosis
This lesion is typical of the skin lesions of most endemic mycoses that occur in patient who have AIDS, and such a lesion may therefore also be seen in an AIDS pt. who has disseminated histoplasmosis or penicilliosis From Ferri, Fred. Ferri’s Color Atlas and Text, 2009, p

Forehead ulcer in an HIV-infected host with Cryptococcus neoformans seen in histopathology
FIGURE Forehead ulcer in an HIV-infected host with Cryptococcus neoformans seen in histopathology. Credits: Fig in Mandell et. al, Infectious Diseases, 2005.

Cryptococcosis in HIV Patient
Credits: Fig from Mandell et. al, Infectious Diseases, (Courtesy of Stephen Raffanti, MD, MPH.)

Blastomycosis- General
Blastomycosis is a systematic pyogranulomatous disease caused by a dimorphic fungus, Blastomyces dermatitidis. Credits- Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Blastomycosis Fig a. Numerous ulcerated and crusted nodules are visible on the chest; the patient had systemic involvement. Credits- Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Blastomycosis Fig b. Severe facial involvement in this pt. with blastomycosis. Note the sepiginous border. Credits- Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Blastomycosis Fig Localized blastomycosis was a incidental finding in an autopsy. Yeast cells of Blastomyces dermatitidis demonstrate muliple nuclei, thick cell walls, broad-based budding, and an artificial separation of the cytoplasm from the cell wall (HANDE x1000) Credits- Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Blastomycosis Fig Blastomycosis pneumonia showing nonspecfic widespread areas of severe consolidation in both lungs. Credits- Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Penicillium- Key Points
Penicillium marneffei is a fungus which is a pathogen of bamboo rats of the genus Canomys, found in China and South-east Asia. Causes a disease which grossly resembles histoplasmosis in both healthy and immunocompromised patients. It is common in AIDS patients. The endemic areas extend from parts of Malaysia through Thailand to Myanmar and Assam and north to South China, Taiwan and Hong Kong. The main sites affected are the lungs, skin, liver, spleen and bone marrow. Skin lesions occur in about 60% of cases with AIDS and consist of umbilicated papules, small ulcers of nodules. They are prominent on the face. Main therapeutic agents are itraconazole or amphotericin B. Credits: Cook et al., Manson’s Tropical Diseases, p

Penicilliosis in a man with AIDS
890 Penicillium marneffei is a facultative invader of human macrophages in immunocompromised individuals. Lesions resembling those of molluscum contagiosum seen in this patient are indicative of the presence of disseminated infection. (From Hoepelman AIM. Opportunistic Fungi. In: Cohen J and Powderly W, eds. Infectious Diseases, 2nd edn. Edinburgh: Mosby 2004; 2341–2362.) Peters et al., Atlas of Tropical Medicine, 2007.

FIGURE 82-1 Molluscum contagiosum–like lesions in a patient with penicilliosis marneffei.
Credits: Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006. (From Supparatpinyo K, Khamwan C, Baosoung V, et al: Disseminated Penicillium marneffei infection in Southeast Asia. Lancet 344:110, 1994.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Credit: Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006.
FIGURE 82-2 A, Small budding yeast of Histoplasma capsulatum (arrow). B, Larger elongated yeastlike form of Penicillium marneffei with central septum (arrow). Credit: Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006. Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Mycobacterial Diseases

Leprosy Cutaneous Tuberculosis Atypical Mycobacteria/ Environmental Mycobacteria

Leprosy at a Glance Highly curable infectious disease with acute and chronic manifestations that may result in life-long disability. Primarily infects skin and peripheral nerves. Transmission and infectivity easily interrupted by antibiotics. Limited susceptibility in human populations; only 3-5% of people capable of active infection. Prolonged incubation is the rule; may require up to 20 years to present clinically.- this is why we sometimes see it in immigrants years after they arrive. Walker, Patricia et al. Immigrant Medicine, p. 455.

Leprosy Leprosy is a chronic granulomatis infection of humans that primarily affects the skin and peripheral nerves. It is caused by Mycobacterium leprae, on obligate intracellular acid-fast rod. The mode of transmission remains elusive. Spread in humans is thought to occur via the respiratory route or entry through broken skin. Ferri, Color Atlas of Clinical Medicine, 2009; p

Leprosy Clinical Findings include: Skin lesion (most common presentation), sensory loss, anhidrosis, neuritic pain, palpable peripheral nerves, nerve damage (most commonly affected nerves are ulnar, median, common peroneal, posterior tibial, radial cutaneous nerve of the wrist, facial and posterior auricular), muscle atrophy and weakness, foot drop, claw hand and claw toes, lagophthalmos, nasal septal perforation, collapse of bridge of nose, loss of eyebrows resulting in “leonine”facies (Fig ). Leprosy can present along a spectrum from simple cutaneous skin lesions with minimal sensory loss to severe extensive skin involvement (Fig ), painful neuritis, muscle wasting and contractures, and multiple peripheral nerve damage. Ferri, Color Atlas of Clinical Medicine, 2009; p

Leprosy Leprosy has been classified according to the WHO into:
1. Paucibacillary leprosy defined as fewer than five skin lesions with no bacilli on skin smear. 2. Multibacillary leprosy defined as six or more skin lesions and may be skin-smear positive. Leprosy has been classified according to type of skin lesions, sensory and motor deficits, and biopsy into: 1. Indeterminate leprosy 2. Tuberculoid leprosy (Fig ) (paucillary [few organisms], intense inflammatory reaction; few, well-demarcated skin lesions). 3. Borderline tuberculoid leprosy (Fig ) 4. Borderline lepromatous leprosy 5. Lepromatous leprosy (Fig 340-5) (multibacillary [numerous organisms], inadequate host response; diffuse poorly organized skin lesions) Ferri, Color Atlas of Clinical Medicine, 2009; p

Cutaneous Tuberculosis May include: 1. Skin infection from autoinoculation or dissemination 2. Nodules or abscesses 3. Tuberculids 4. Erythema nodosum Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 546.

Primary (Dermal) Tuberculosis
This form of tuberculosis is found in patients who are non-primarily infected. The initial infection can take place as a result of the bacteria coming into contact with a patient’s skin but this is unusual. This form of the disease manifests itself 3 to 4 weeks after infection, appearing as a papule, becoming a plaque, or in a nodular inflammatory form which evolves into an ulceration. (See next page) Credits, Fig and text, Cook, Manson’s Tropical Diseases, 2009, pp

Chronic large verrucous plaque with erythematous islets in chronic tuberculosis verucosa cutis.
Credits, Fig and text, Cook, Manson’s Tropical Diseases, 2009, pp

Chronic large verrucous plaque with erythematous islets in chronic tuberculosis verucosa cutis.
M. Marinum frequently infects freshwater fish and, hence, individuals handling fish. Also known as “fish tank granuloma” Credits, Fig and text, Cook, Manson’s Tropical Diseases, 2009, pp

Cutaneous TB in HIV pt. Description: Cutaneous M. TB in an HIV+ pts.
Credits: Paul A. Volberding, MD, UCSF: Nat’l Library of Medicine Images

Runyon classification of environmental Mycobacteria
Group 1- Photochromogens- M Kansasii, M marinum Group 2- Scotochromogens- M scrofulaceum, M gordonae Group 3- Nonchromogens- M avium complex, M malmoense, M nonchomogenicum Group 4- Rapid Growers- M chelonae, M fortuitum, M vaccae Credits: Cook et al., Manson’s Tropical Medicine, p

Mycobacterium avium-intracellulare- Definition
Mycobacterium avium-intracellulare (MAI) is a group of slow-growing nontuberculous mycobacteria present widely in dust, soil, and water. It is one of the most common causes of bacterial infection in AIDS pts. Credits: Ferri, Ferri’s Atlas of Tropical Medicine, 2009, . 142

Mycobacterium avium-intracellulare
Physical Findings Cervical adenitis, disseminated infection in immunocompromised hosts. Generally skin infections present as panniculitis, often in relation to affected lymph nodes, or as nodules progressing to abscesses and ulcers. Credits: Ferri, Ferri’s Atlas of Tropical Medicine, 2009, . 142

Mycobacterium avium-intracellulare
Fig Nodules caused by Mycobacterium avium-intracellulare. These multiple nodules on the thigh resemble panniculitis. Credits: Ferri, Ferri’s Atlas of Tropical Medicine, 2009.

Mycobacterium ulcerans- General
M ulcerans, the causative organism of Buruli ulcer, is emerging as the third most prevalent mycobacterial disease in the world after TB and leprosy. Four stages of the Buruli ulcer have been described Subcutaneous nodule Vasculitis and spreading cellulitis Ulceration Healing with gross fibrosis Credits: Cook et al., Manson’s Tropical Diseases, pp

Mycobacterium ulcerans
Physical Findings Cervical adenitis, disseminated infection in immunocompromised hosts. Generally skin infections present as panniculitis, often in relation to affected lymph nodes, or as nodules progressing to abscesses and ulcers. Credits: Ferri, Ferri’s Atlas of Tropical Medicine, 2009, p

Mycobacterium ulcerans- Geography
Fig 57.1 Buruli ulcer: global distribution Credits: Cook et al., Manson’s Tropical Diseases, pp

Buruli ulcer-Mycobacterial ulcerans
Fig 971 Typical Buruli ulcer in a Nigerian child. The condition is characterized by gross, necrotising skin ulcers in which numerous acid-fast bacilli are present (M. ulcerans). The disease occurs in localised tropical areas in al continents. While the mode of transmission remains unknown, there is a clear association with moist vegetation and infection by aquatic insects has been postulated. Some cross-protection against multiple lesions in children appears to be affected by vaccination with BCG as used against tuberculosis. Credits: Peters et al., Atlas of Tropical Medicine, 2009.

FIGURE 37-2 Nodular form of Buruli ulcer with incipient ulceration in a child in Ghana. Credits: Guerrant et. al, Tropical Infectious Diseases, 2nd edition, 2006, Vol. 1, p. 429.

FIGURE 37-3 Minor ulcerative lesion of Buruli ulcer on the leg of a 3-year-old child in Benin. The lesion has nearly healed without treatment. Credits: Guerrant et. al, Tropical Infectious Diseases, 2nd edition, 2006, Vol. 1, p. 430.

FIGURE 37-4 Major ulcerative form of Buruli ulcer in an Angolan man covering entire epigastrium. Note the central slough and undermined and indurated borders. Credits: Guerrant et. al, Tropical Infectious Diseases, 2nd edition, 2006, Vol. 1, p. 430.

FIGURE 37-5 Movat-stained section of edge of ulcer from lesion in Figure 37-4 (x2.5). There is re-epithelialization of the undermined flap, with contiguous coagulation necrosis of the subcutaneous tissue. Credits: Guerrant et. al, Tropical Infectious Diseases, 2nd edition, 2006, Vol. 1, p. 430.

Mycobacterium ulcerans in section of ulcer
Fig 972 Acelllular necrosis occurs involving the dermal layers and subcutaneous fat. Acid-fast bacilli are found in the necrotic material. Application of the PCR procedure greatly improves the ease and speed of diagnosis in material from exudates and biopsies when organisms are difficult to find with classical staining (Z-N x1,000). Credits: Peters et al., Atlas of Tropical Medicine, 2009.

Fishtank Granuloma- Mycobacterium marinum
The purplish lesion of a patient who kept tropical fish as a hobby. Mycobacterium marinum was grown from a biopsy of the chronic, nodular lesion. Credits: Peters et al., Atlas of Tropical Medicine, 2009.

Nodular verrucous violaceous lesions with proxinal dissemination by Mycobacterium Marinum
M. Marinum frequently infects freshwater fish and, hence, individuals handling fish. Also known as “fish tank granuloma” Credits, Fig and text, Cook, Manson’s Tropical Diseases, 2009, pp

M marinum FIGURE A, Sporotrichoid rash of Mycobacterium marinum infection showing typical location on the superficial cooler body tissues of the extremities. B, A similar rash in a patient with classical sporotrichosis due to the fungal pathogen Sporothrix schenckii. Credits: Guerrant et. al., Tropical Infectious Diseases, 2nd ed., 2006, p Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Pyodermas

Pyodermas Impetigo Folliculitis/Furunculosis Hidradenitis
Ecthyma/Erysipelas Necrotizing Fasciitis (Streptococcal Gangrene) Staphylococcal Scalded Skin Syndrome (Ritter’s Disease) Anthrax Batronelloses Tularemia Rhinoscleroma Lyme Borreliosis

Pyodermas-Impetigo- General
Impetigo is a superficial skin infection generally secondary to Staph aureus and/or Strep spp. Common presentations are bullous impetigo (generally secondary to staph disease) and nonbullous impetigo (secondary to streptococcaly infection and possible staph infection; the bullous formm is cause by an epidermolytic toxin produced at the site of the infection. Multiple lesions with golden yellow crusts and weeping areas are often found on the skin around the nose, mouth, and limbs. Creditis: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 138

Pyodermas-Impetigo- Treatment
Remove crusts by soaking with wet cloth compresses; crusts block the penetration of antibacterial creams. Application of 2% mupirocin ointment (Bactroban), three times daily for 10 days to the affected area until all lesions have cleared. Oral antibiotics are used in severe cases; commonly used agents are dicloxacillin, cephalexin, and azithromycin. Creditis: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 138.

Pyodermas- Impetigo Fig 28-13a and 28-13b. Impetigo. Note that the vesicles are covered by a golden crust. These perioral lesions are at a characteristic site. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 138

Impetigo Left- Erythematous plaque of superificial impetigo with satellite lesions Right- Circular plaque of staphylococcal pustular impetigo on the chin with satellite lesions. Credits, Figs and 19.3, Cook, Manson’s Tropical Diseases, 2009.

Folliculitis Definition- Folliculitis is the inflammation of the hair follicle as a result of infection, physical injury, or chemical irritation. A deep folliculitis caused by S. aureus may affect the beard area; this form is termed sycosis or follliculitis barbae. Staphylococcal folliculitis is the most common form of infectious folliculitis; it occurs most commonly in those with diabetes. Physical Examination- The lesions generally consist of painful yellow pustules surrounded by erythema; a central hair may be present in the pustules. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 139.

Pyoderma- Folliculitis
Cause: Staphylococcus infection (e.g. sycosis barbae), Pseudomonas aeruginosa (hot tub folliculitis) Gram negative follicullitis (Klebsiella, Enterobacter, Proteus spp.) associated with antibiotic treatment of acne Chronic irritation of the hair follicle. Initial use of systemic corticosteroid therapy (steroid acne) Pityrosporum orbiculare Treatment- Cleansing of the area with chlorhexidine and application of saline compresses to involved area. Treatment of Pseudomonas folliculitis with ciprofloxacin Treatment of S. aureus folliculitis with dicloxacillin, 250 mg QID, for 10 days Treatment of carrier Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 139.

Pyoderma- Folliculitis
Fig Folliculitis- characteristic small pustules with surrounding erythema. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009.

Pyoderma- Furunculosis
Furunculosis- Definition- A furuncle is a more exuberant form of suppurative folliculitis Presentation and Physical Findings- More common in young adults and usually affects the skin of the face, neck, buttocks, and axillae. Lesions can be up to 2 cm across and the inflammation is not confined within the follicle, but is associated with surrounding erythema and often systemic symptoms. After discharge of the pustular necrotic core, the lesions heals rapidly, but with scarring. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 139.

Furunculosis Diagnosis- Treatment
Culture and sensitive of pus, nasal swab, CBC Treatment Incision and drainage, systemic antibiotics, topical antibiotics Eradication of nasal carriage of staphylocci. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 139.

Pyoderma- Furuncle Fig Furuncle. Shown are multiple erythematous nodules in the axilla, which is a commonly affected site. The lesions are exquisitely painful. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009.

Pyoderma- Furunculitis
Fig Furuncle. Early lesion characterized by edema and erythema. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009.

Pyoderma- Hidradenitis
Chronic relapsing condition that occurs in the terminal follicular epithelium of the apocrine glands (axilla, inguinal folds, perineum, genitalia) and periareolar region where keratinous materials occlude the follicles. This causes secondary inflammation of the apocrine glands, resulting in chronic infection and draining abscesses, which lead to scarring. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 52.

Pyodermas- Hidradenitis
Physical Findings- Initially there is a firm painful nodule in the groin or axilla. The nodule may involute slowly or discharge pus through the skin, which is often foul-smelling. In the late stages a complex interconnecting system of sinuses extends deeply into the dermis and subcutaneous fat with extensive dense fibroses. There is a strong tendency toward relapse and recurrence. Treatment- Antibiotics (Erythromycin, clindamycin, cephalexin), surgical interventions, intralesional corticosteroids, hormone therapy. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Hidradenitis Fig Hidradenitis suppurativa. This early lesion presented as an erythematous nodule discharging clear fluid. The axilla is a commonly affected site. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Hidradenitis Fig In this very severe case, there is marked scarring, and numerous sinuses are present Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Bacterial Infections-Erysipelas
Cellulitis- a superficial inflammatory condition of the skin characterized by erythema, warmth, and tenderness of the area involved. Erysipelas- Cellulitis with superficial spreading, warmth, erythematous lesion distinguished by its indurated and elevated margin; lymphatic involvement and vesicle formation. Credits: Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, pp

Pyodermas- Ecthyma Ecthyma is a deeper from of impetigo caused by staphylococci or streptococci, with ulceration and scarring. It occurs frequently in the extremities. Credits; McPhee et al., Current Medical Diagnosis and Treatment, p. 124.

Necrotizing Fasciitis (Streptococcal Gangrene)
Definition Necrotizing Fasciitis (NF) is a bacterial infection of the subcutaneous soft tissues. There is an intense acute inflammation of the fascia, with involvement of the adjacent muscle (see fig 28-8) and presence of bacteria (see fig 28-9). NF may evolve following a surgical procedure, with minor trauma, or even apparently intact skin. Cause NF is often a polymicrobial condition Pts. with underlying diabetes mellitus and iatrogenic immunosuppression are particularly susceptible. It can also occur as a complication of childhood varicella. Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, pp

Physical Findings and Clinical Presentation Staph aureus is the most frequently cultured organism. The clinical presentation may be fulminant, acute or subacute. NF occurs mainly on the extremities, although almost any site can be affected. It usually commences as an ill-defined area of erythema and is often mistaken for cellulitis or an insignificant wound infection. Severe pain, indurated edema, skin necrosis, cyanosis, bullae, crepitation, muscle weakness, and malodorous exudates can develop rapidly (Fig ). Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, pp

Physical Findings and Clinical Presentation Fournier’s gangrene is a clinical variant of NF that involves the penis, scrotum, perineum and abdominal wall in men and less often the vulva in women. Pts. Often have other systemic manifestations of severe sepsis, including hypotension, tachycardia, tachypnea, oliguria, and impaired mental function. Radiographs may reveal gas in affected tissues. Treatment IV antibiotics, debridement Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, pp

Staphylococcal Scalded Skin Syndrome (Ritter’s Disease)
Definition Staphylococcal scalded skin syndrome (SSSS) is a disorder usually occurring in neonates and young children, who first develop a macular scarlatiniform eruption in association with a staphylococcal infection. Physical Findings and Clinical Presentation Often associated with fever, irritability, and skin tenderness Eruption spreads from its usual original sites on the face, axillae, and groins to involve large areas of skin surface. Conjunctivitis is often also present. Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, p. 136.

Staphylococcal Scalded Skin Syndrome (Ritter’s Disease)
Physical Findings and Clinical Presentation Mucous membranes, however, are not affected. Traction pressure on intact skin causes bullae formation (Nikolsky’s sign). At the same time, the skin becomes edematous and the surface fragile so that it can be sheared off in thin wrinkled sheets, similar to peeling wet wallpaper, leaving a glistening red surface, and the child becomes sick and feverish (Fig 28-7). Diagnostic Investigation CBC, blood cultures, nose and throat swabs, histologic examination of frozen section of blister roof, skin biopsy Treatment Treatment: IV penicillinase-resistant penicillin, IV macrolide, cephalosporins, vancomycin Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, p. 136.

Pyodermas-Anthrax Definition Cause
Anthrax is an acute infectious disease cause by the spore-forming bacterium Bacillus anthracis. Cause The disease is caused by Bacillus anthracis, a gram-positive, spore-forming bacillus. The microbe is aerobic, nonmotile, nonhemolytic on sheep’s blood, and grows readily at 37 C, forming large colonies with irregularly tapered outgrowths ( a Medusa’s head appearance or joint bamboo rod; Fig ). In the host, it appears as single organisms or chains of 2 or 3 bacilli. Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, pp

Pyodermas-Anthrax Cutaneous Anthrax
Characterized by a skin lesion evolving from a papule, through a vesicular stage (Fig ) to a depressed black eschar (Fig ). The incubation period ranges from 1 to 12 days. The lesion is usually painless, but patients also may have fever, malaise, headache, and regional lymphadenopathy. The eschar dries and falls off in 1 to 2 weeks, with little scarring. Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, pp

Pyodermas-Anthrax Physical Findings and Clinical Presentation
Symptoms of disease vary depending on how the disease was contracted, but usually occurs within 7 days after exposure. The serious forms of human anthrax are inhalation anthrax, cutaneous anthrax, and intestinal anthrax. Inhalation anthrax-Initial symptoms include mild fever, muscle aches, and malaise and may progress to respiratory failure and shock; meningitis often develops. Gastrointestinal anthrax- characterized by severe abdominal pain followed by fever and signs of septicemia. Bloody diarrhea and signs of acute abdomen may occur. Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, pp

Pyodermas-Anthrax Laboratory Tests Treatment
Presumptive ID is base on Gram stain of material from skin lesion, CSF, or blood showing encapsulated gram-positive bacilli. Confirmatory tests are performed. Treatment Most strains sensitive to penicillin. The FDA has approved PCN, doxycyline, and ciprofloxacin for tx. of inhalational anthrax infection. Credits: Ferri, Ferri’s Color Atlas Clinical Medicine, 2009, pp

Cutaneous Anthrax 978 Four discrete lesions on the arm of an African patient infected with Bacillus anthracis. The black eschars are associated with direct inoculation through a break in the skin after contact with infected animal material or from transmission by biting flies such as tabanids. The lesion is painless without pus but is often surrounded by an arc of oedema and ultimately heals, leaving a scar. Anthrax-infected game or domestic animals that are eaten have also been recorded as the source of human infection, for example in Namibia in 2004. Credits: Peters et al., Atlas of Tropical Medicine, 2007.

Extensive Erythema and Hemorrhagic Bullae in Cutaneous Anthrax
979 This condition may be seen 2–4 days after the initial infection. People who work with potentially contaminated animals or animal skins are especially liable to this type of infection by anthrax spores. Although about 95% of all human anthrax lesions are located in the skin, infection acquired by the ingestion or inhalation of spores may cause life-threatening disease of the internal organs. Peters et. al, Atlas of Tropical Medicine, 2007.

Pyoderma-Bartonelloses
Infection caused by Bartonella bacilliformis Condition endemic in the higher altitude regions of Peru Initial stage of infection (hematic phase) is referred to as Oroya fever. Pts. are acutely ill with pyrexia, rigors, myalgia, and severe hemolytic anemia. The later is attributable to infection of the circulating erythrocytes and can be confirmed by a blood smear. Later, the disease enters an eruptive phase characterized by the evolution of numerous popular, nodular, or verrucous vascular skin lesions, referred to as verruga peruana (Peruvian wart, cutaneous verrucous diease). These occur predominantly on the face and extremities (fig ). Ferri, Color Atlas of Clinical Medicine, 2009, p. 141

Pyodermas- Bartonelloses
FIGURE 40-1 Verruga peruana skin lesions on the foot and leg of a patient from Peru infected with B. bacilliformis. Credits: Guerrant et. al., Tropical Infectious Diseases, 2nd ed., Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Bartonella- Oroyo Fever
FIGURE 40-2 Peripheral blood smear of a Peruvian patient with Oroya fever. A high portion of erythrocytes contain Bartonella bacilliformis. Credits: Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006; Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Tropical Dermatology: Pyodermas Tularemia
Definition: Tularemia is a zoonosis caused by small, facultative gram-negative intracellular coccobacillus Francisella tularensis. Clinical Presentation: Ulceroglandular and glandular: account for 75% to 80% of cases. Fever and a single erythematous papuloulcerative lesion with a central eschar accompanied by tender lymphadenopathy. Credits: Chapter 347, Ferri’s Clinical Medicine, 2009.

Tropical Dermatology: Pyodermas Tularemia
Figure 81. Primary ulcer of tularemia. Francisella (Pasteurella) tularensis is a Gram-negative coccobacillus that affects a wide range of wild rodents and rabbits but that can also occur in carnivores and some species of birds. Zoonotic infection in humans- tularemia- a plague-like illness, is usually acquired by contact with infected animals. Credits: Peters et. al, Atlas of Tropical Medicine,

Tropical Dermatology: Pyodermas Lyme Borreliosis
Lyme disease is a multisystem inflammatory disorder caused by the transmission of a spirochete, Borrelia burgdorferi. Lyme disease is spread by the bite of infected Ixodes ticks. Credits: Ferri, Ferri’s Clinical Medicine, 2009.

Treponematosis, Genital Ulcers and Miscellaneous STDs

Treponematosis and Genital Ulcers and Miscellaneous STDs
Syphilis Pinta Yaws (Pian, Frambesia) Endemic Syphilis (Bejel) Chancroid (Soft Chancre) Granuloma Inguinale (Donovanosis) Lymphgranuloma Venereum Gonorrhea

History and PE reveal genital lesion or ulcer
Algorithm for evaluation of patients with genital lesions or ulcers. From: Ferri’s Color Atlas and Text of Clinical Medicine, 2009; Available at .

Syphilis- General Intro
Syphilis is a complex infectious disease caused by Treponema pallidum, a spirochete capable of infecting almost any organ or tissue in the body and causing many clinical manifestations. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis- US Public Health Info
Most cases of syphilis in the US continue to occur in MSM. From 2008 to 2009, the rates of primary and secondary syphilis decreased slightly in white men and women and hispanic women, but increased among black men and women and Hispanic men. The highest rates were in black men, with 31 cases/100,000 population. In 2009, 53% of primary and secondary syphilis cases were reported from the South. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis- General Intro
Transmission occurs most frequently during sexual conduct (including oral sex), through minor skin or mucosal lesions; sites of inoculation are usually genital but may be extragenital. The risk of acquiring syphilis after unprotected sex with an individual with infectious syphilis is approximately 30-50%. Rarely syphilis can be transmitted through nonsexual contact, blood transfusion, or via the placenta from mother to fetus (congenital syphilis). McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis- Disease The natural history of acquired syphilis is generally divided into two major clinical stages: 1) Early (Infectious )2) Late The two stages are separated by a symptom-free latent phase during the first part of which (early latency) infectious lesions are liable to recur. Infectious syphilis includes the primary lesions (chancre and regional lymphadenopathy), the secondary legions (commonly involving skin and mucous membranes, occasionally bone, CNS or liver), relapsing lesions during early latency, and congenital lesions. The hallmark of these lesions is an abundance of spirochetes; tissue reaction is usually minimal. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis- Disease The typical lesion of primary syphilis is the chancre at the site or sites of inculation. An initial mall erosion days (average 3-4 weeks) after inoculation appears then rapidly develops into a painless superficial ulcer with a clean base and firm, indurated margins. This is associated with enlargement of regional lymph nodes. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis- Disease The secondary stage of syphilis usually appears a few weeks (or up to 6 months) after development of the primary chancre, when dissenimation of T pallidum produces systemic signs (fever, lymphadenopathy) or infectious lesions at sites distant from the site of inoculation. The skin lesions are nonpruritic, macular, papular, pustular, or follicular (or combinations of these type), though the the maculopapular rash is the most common. The skin lesions usually are generalized; involvement of the palms and soles occurs in 80% of cases. Specific lesions- condyloma lata- are fused, weeping papules on the moist areas of the skin and mucous membranes and sometimes mistaken for genital warts. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis-Disease Late syphilis consists of so-called benign (gummatous) lesions involving skin, bones, and viscera; cardiovascular disease (principally aortitis); These late forms of syphilis are not contagious. The lesions contain few demonstrable spirochetes, but tissue reactivity (vasculitis, necrosis) is severe and suggestive of hypersensitivity phenomena. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis- Disease In early (infectious) syphilis, darkfield microscopic exam by a skilled observer of fresh exudate from lesions or material aspirated from regional lymph nodes is up to 90% sensitive for diagnosis. There are 2 general categories of serologic tests for syphilis: 1) Non-treponemal tests detect antibodies to lipoidal antigens present in the host after modification by T. pallidum. (VDRL, RPR). Generally become positive 4-6 weeks after infection or 1-3 weeks after the appearance of a primary lesion. 2) Treponemal tests use live or killed T. Pallidum as antigen to detect antibodies specific for pathogenic treponemes. Value principally in determining with a posititive non-trep. test is a false positive or is indicative of syphilis. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Syphilis- Treatment Penicillin remains the preferred treatment for syphilis. For Early (Primary, secondary or early latent)- Benathine PCN G 2.4 million units IM once. Alternatively: Doxycyline 100 BID for 14 days, tetracycline 500 QID for 14 days or Ceftriaxone 1 gm IM or IV daily for 8-10 days. For late latent or uncertain duration, or for tertiary w/o neurosyphilis-, Benzathine PCN G 2.4 million units IM weekly for 3 weeks, or alternatively: Doxy 100 BD for 28 days or tetracycline 500 QID for 28 days. Neurosyphilis- Aq Pen G million units IV daily, given every 3-4 hours or as continuous infusion for days. Alternatively, procaine PCN 2.4 million units IM daily with probenicid 500 QID for days, or Ceftriaxone 2 gm IM or IV daily for days. McPhee et al., 2012 Current Medical Diagnosis and Treatment, p

Treponematosis and Genital Ulcers Syphilis
Description: Treponema pallidum Dark field examination of exudate from a penile ulcer (x1000) in a patient with syphilis. The spirochete Treponema pallidum, which is too small to be seen using ordinary microscopy, appears as a delicate spiral rod when dark field illumination is employed. Credit: uptodate. Courtesy of Harriet Provine

Treponema pallidum through dark-field microscope
The spirochetes can usually be seen in scrapings from serous fluid exuding from the chancre by simple dark-field examination. Their detection is facilitated by the use of a direct flourescent antibody test for T. pallidum. The DFAA-TP employs a flourescein-labelled anti-T. pallidum globulin (x 400).

Figure 8-37 Treponema pallidum (dark-field microscopy) showing several spirochetes in scrapings from the base of a chancre. (Courtesy of Dr. Paul Southern, Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX.) Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 6 December :12 PM) © 2005 Elsevier

Figure 8-39 Syphilitic chancre in the scrotum (see Figure 8-8 for the histopathology of syphilis). (Courtesy of Dr. Richard Johnson, Beth Israel-Deaconess Hospital, Boston, MA.) Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 6 December :12 PM) © 2005 Elsevier

Primary Syphilis Primary syphilis. A typical chancre is present on the left labium majus. In Ferri’s Color Atlas and Text of Clinical Medicine, 2009; Available at .

Primary Syphilis The chancre is a painless ulcer with an indurated edge. The base is yellow and harbors large numbers of spirochetes. As seen in Ferri’s Color Atlas and Text of Clinical Medicine, As available at .

Syphilis: primary chancre
(Courtesy of D. Mabey) in Manson’s Tropical Diseases, 22nd edition, As available in .

Primary Syphilis on Penis
Primary Syphilitic chancre on penis- ulcer with a clean, non-purulent and smooth, regular, sharply defined border

HIV-Related Syphilis Description: Palmar Rash of Secondary Syphilis
Credits: Paul A. Volberding, MD, UCSF; Nat’l Library of Medicine Images

Secondary Syphilis Secondary syphilis. The face is commonly affected. Note the numerous papules. In Ferri’s Color Atlas and Text of Clinical Medicine, Available at .

Secondary Syphilis Note the widespread papules and nodules, many of which have a hypertrophic appearance. As seen in Ferri’s Color Atlas and Text of Clinical Medicine, As available at .

Secondary syphilis: typical palmar rash
(Courtesy of D. Mabey) in Manson’s Tropical Diseases, 22nd edition, As available in .

Secondary syphilis: condyloma abutting on ala nasi
(Courtesy of J. Richens) in Manson’s Tropical Diseases, 22nd edition, As available in .

Secondary Syphilis- Condyloma Lata in a female
The condition is readily diagnosed by the demonstration of spirochetes in a dark-field preparation.

Secondary Syphilis- Corona veneris
Discoid lesions may develop on the face and head in secondary syphilis. The condition seen in this man is known as “corona veneris.”

Secondary syphilis: condyloma lata
(Courtesy of J. Richens) in Manson’s Tropical Diseases, 22nd edition, As available in .

Tertiary Syphilis- Asymptomatic exudative gummata of the penis in Syphilis
Tertiary gummata of syphlilis may be localized on the forehead, scalp, lips, tongue, genitals (see here) or any part of the body. Morphologically, the gummata are various shades of red and may ulcerate and heal with extensive scarring. Credits, Figs. 19.5, Cook, Manson’s Tropical Diseases, 2009, pp

Figure 12-69 Congenital syphilis
Figure Congenital syphilis. A and B, Desquamation of the foot and hand are seen in this infant with congenital syphilis. C, This 3-month-old who presented with untreated congenital syphilis had diffuse periosteal reaction of the tibias and generalized demineralization. D, Wimberger sign, the osseous destruction of the proximal tibial metaphysis, is seen in another affected infant. (A and B, Courtesy Pablo Sanchez, MD, and Walid Salhab, MD, University of Texas South-western Medical Center; D, courtesy Manuel P. Meza, MD, Children's Hospital of Pittsburgh.) Downloaded from: Atlas of Pediatric Physical Diagnosis, 5e (on 3 March :41 PM) © 2007 Elsevier

Treponematosis- Pinta
Definition- This is a nonsexually transmitted treponematosis characterized by depigmented skin lesions. It is caused by Treponema pallidum, subsp. Carateum. Children are primarily affected and transmission is thought to be by direct cutaneous or mucous membrane contact, possibly via minute abrasions. The lesions present as small, scaly, erythematous indurated papules and plaques on exposed skin, usually on the hands and feet. Late stages of pinta are characterized by disfiguring hyperpigmentation, achromia, hyperkeratosis, and atrophy. Unlike syphilis and yaws, there is no evidence of systemic disease. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 142.

Fig Pinta. This is a late lesion showing characteristic complete loss of pigmentation surrounded by a hyperpigmented border. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p. 142.

Fig 988 Depigmented lesions of pinta. Pinta is endemic in the New World from Mexico to the Amazon. ‘Pintids’ start as small papules and develop into plaques with actively growing edges that become confluent. In the late stages the pintids become depigmented. The causative organism of pinta, Treponema caroteum, is morphologically indistinguishable from that of syphilis and bejel. Credits: Peters et al., Atlas of Tropical Medicine, 2009.

Circumscribed patches of hypopigmented truncal skin in ‘Mal de Pinto’
Endemic and caused by Treponema carateum. It is characterized by chronic skin lesions only, with no systemic involvement, and occurs mainly in young adults. There are 4 stages: primary, secondary, latent, tertiary. These are the tertiary areas that develop years after initial infection.. Credits, Figs. 19.6, Cook, Manson’s Tropical Diseases, 2009, pp

Treponematosis- Yaws (Frambesia)
Definition- This is a tropical disease caused by infection by the spirochete Treponema pallidum, subsp. Pertenue. It is not transmitted sexually but rather by close contact- for example inoculation of skin previously traumatized by insects or scratching. Yaws is most common in children 6 to 10 years of age, who present with lesions on the feet, legs, and buttocks. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p

Treponematosis- Yaws (Frambesia)
Physical Findings- Generally it is divided into early and late yaws. The initial lesion, known as a mother yaw, develops 3 to 5 weeks after inoculation. It starts as a nontender papilloma, which ulcerates and is then covered with a yellow crust. It resembles a raspberry- hence the alternative designation of framboesia (from the Dutch framboos, raspberry) Subsequently, other lesions develop daughter yaws. They eventually resolve to leave a depressed and hyperpigmented scar. Late lesions may develop in 10% of patients and are destructive ulcers and gummatous nodules that affect the skin, bones, and joints. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p

Treponematosis- Yaws Fig Early yaws- typical framboesiform mother yaw. Note the yellow crust and surrounding hypopigmentation. Credits- Ferri, Ferri’s Color Atlas of Clinical Medicine, 2009, p

FIGURE 44-1 Initial, solitary yaws papilloma (frambesioma) on the upper thigh.
Credits: Guerrant et. al., Tropical Infectious Diseases, 2nd ed., 2006. (From Perine PL, Hopkins DR, Niemel PLA, et al: Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, World Health Organization, 1984.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

PLATE 44-1 Initial axillary papilloma of yaws.
Credit: Guerrant et. al., Tropical Infectious Diseases, 2006. (From Perrine PL, Hopkins DR, Niemel PLA, et al: Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, World Health Organization, 1984.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

FIGURE 44-2 Bony deformity of the tibiae due to yaws osteoperiostitis.
Credit: Guerrant et. al., Tropical Infectious Diseases, 2nd ed., 2006. (From Perine PL, Hopkins DR, Niemol PLA, et al: Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, World Health Organization, 1984.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Treponematoses- Yaws Fig Secondary framboesiform yaws. Thanks to the mass penicillin-based eradication campaign of the 1950s, yaws is now a relatively rare disease in the humid tropics, although a new outbreak was recently recorded in Ghana. This Papuan child shows classic framboesiform lesions, caused by Treponema pertenue. Secondary lesions are frequent also at mucocutaneous junctions. Credits: Peters et. al, Atlas of Tropical Medicine, 2009.

Treponematoses- Yaws Fig Hyperkeratosis of feet and hands is a common secondary phenomenon in yaws. This man’s feet were seriously eroded. Credits: Peters et. al, Atlas of Tropical Medicine, 2009.

Treponematoses- Yaws Fig. 986 Gangosa. The most advanced and destructive lesions (of yaws) affect the maxillary bones and hard palate, resulting in a condition known as ‘gangosa’. Credits: Peters et. al, Atlas of Tropical Medicine, 2009.

Endemic Syphilis (Bejel)
Endemic syphilis is an acute or chronic infectious caused by T pallidum subspecies endemicum. Reported in a number of countries, particularly in the eastern Mediterranean area, often with local names: bejel in Syria, Saudi Arabia, and Iraq,and dichuchwa, njovera and siti in Africa. It also occurs in Southeast Asia. The local forms have distinctive features. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Moist ulcerated lesions of the skin or oral or nasopharyngeal mucosa are the most common manifestations. Generalized lymphadenopathy and secondary and tertiary bone and skin lesions are also common. Deep leg pain points to periostitis or osteomyelitis. In the late stages of disease, destructive gummatous lesions similar to those seen in yaws can develop, resulting in loss of cartilage and saber skin deformity. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Fig. 989 Secondary rash in endemic syphilis. These novenereal spirochetes (‘endemic syphilis’) occur mainly in dry parts of Africa, the Balkans and Australia. A florid, secondary, maculopapular eruption and associated adenitis is usually the first sigh. In the Middle East, the tertiary form is known as Bejel. Credits: Peters et al., Atlas of Tropical Medicine, 2009.

Gummatous Lesions in Endemic Syphilis (Bejel)
Fig. 990 Gummatous lesions in bejel. If left untreated, bejel can produce severe, gummatous changes of the bone, cartilage and skin as seen in this unfortunate sufferer from the Middle East. Credits: Peters et al., Atlas of Tropical Medicine, 2009.

Chancroid (Soft Chancre)
Definition: Chancroid is a sexually transmitted disease characterized by painful genital ulcerations and inflammatory inguinal adenopathy. The initial lesion is usually a transient vesicular tender papule, which rapidly ulcerates with copious suppuration. The ulcer is sharply circumscribed, with an undetermined edge, and is typically not indurate. Cause: Haemophilus ducreyi, a bacillus. Credits: Ferri’s Clinical Medicine, chapter 226, 2009.

Chancroid (Soft chancre)
A single dose of either azithromycin 1 g orally, or ceftriaxone 250 mg IM is effective treatment. Effective multiple-dose regimens are erythromycin 500 mg orally QID for 7 days, or ciprofloxacin 500 mg orally BD for 3 days. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Chancroid (Soft Chancre)
Credits: Ferri’s Clinical Medicine, 2009.

Chancroid Ulcer of Penis with Inguinal Lymphadenopathy
Chancroid (soft chancre, ‘ulcus molle’) is a veneral condition caused by haemophilius ducreyi. It occurs most commonly among the poorer populations of developing countries, in whom it is the commonest cause of genital ulcers. Although it occurs in both sexes it is most commonly observed in males. Papule formation commences after a short incubation period (often 4-10 days) after exposure, the papule developing into a deep, very painful ulcer associated with inguinal lymphadenopathy. This also is painful and may be bilateral. The buboes may suppurate, as seen here. In the female, the lesions, usually on the vulva or cervix, are frequently asymptomatic. The severe pain helps to differentiate chancroid form lymphgranuloma venereum, granuloma inguilnale and syphilis. Credits: Fig. 913, Peters, Tropical Medicine, 2007

Indirect fluorescent antibody test of Haemophilus ducreyi
The small, Gram negative bacteria may be seen on a smear or after cultivation on specialised media. They may also be identified by staining smears with a fluorescein-labelled, specific monoclonal antibody as seen here (Indirect flourescent antibody test (IFAT) x 300). Credits: Fig. 914, Peters, Tropical Medicine, 2007

Granuloma Inguinale (Donovanosis)
GI is a chronic, relapsing granulomatous anogenital infection due to Calymmatobacterium (Donovania) granulomatis. The pathognomonic cell, found in tissue scrapings or secretions, is large (25-90 mcm) and contains intracytoplasmic cyts filled with bodies (Donovan bodies) that stain deeply with Wright stain. McPhee, 2012 Current Medical Diagnosis and Treatment, p. 414.

Granuloma Inguinale- Course (Donovanosis)
The incubation period is 8 days to 12 weeks. The onset is insidious. The lesions occur on the skin or mucous membranes of the genitalia or perineal area. They are relatively painless infiltrated nodules that soon slough. A Shallow, sharply demarcated ulcer forms, with a beefy-red friable base of granulation tissue. The lesion spreads by contiguity. The advancing border has a characteristic rolled edge of granulation tissue. Large ulcerations may advance onto the lower abdomen and thighs. Scar formation and healing occur along one border while the opposite border advances. McPhee, 2012 Current Medical Diagnosis and Treatment, p. 414.

Granuloma Inguinale- Treatment (Donovanosis)
Several therapies are available. Due to the indolent nature of the disease, duration of therapy is relatively long. The following therapies should be given for 3 weeks or until lesions heal: doxycyline 100 BD, azithromycin 1 g orally once weekly, ciprofloxacin 750 BD, erythromycin 500 QID. McPhee, 2012 Current Medical Diagnosis and Treatment, p. 414.

Donovanosis of Penis and Adjacent Skin of Leg
This venereal infection, which occurs mainly in the tropics and subtropics, is caused by a Gram-negative coccobacillus, Calymmatobacterium granulomatis. In the male it produces deep, punched-out ulcers of the penis. These are clean and painless initially but, with secondary bacterial infection, may become covered with a thick, offensive, purulent exudate and develop a marked granulomatous reaction; such lesions are painful. As seen here, secondary luceration may appear on adjacent skin. Credits: Fig. 915, Peters, Tropical Medicine, 2007

Donovanosis of Female Genitalia
The disease runs a very chronic course. As in LGV, mutilating ulceration of the genitalia may occur and anorectal involvement is common. In comparison with LGV, the lymphatics are not primarily involved. Credits: Fig. 916, Peters, Tropical Medicine, 2007

Donovan Bodies in Exudate
The encapsulated coccobacilli of C. granulomatosis can be seen in Romanowsky-stained smears within the cytoplasm of macrophages. These are the so-called ‘Donovan bodies’ in which the bipolar staining gives the appearance of a closed safety pin (Wright-Geimsa x 650) Credits: Fig. 917, Peters, Tropical Medicine, 2007

FIGURE 29-1 Inguinal lesions of donovanosis.
Credit: Guerrant et.. al., Tropical Infectious Diseases, 2nd edition, 2006. Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

FIGURE 29-2 Typical penile donovanosis lesion.
Credit: Guerrant et. al., Tropical Infectious Diseases, 2nd ed., 2006. Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Credit: Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006.
FIGURE 29-3 Tissue smear stained by rapid Giemsa (RapiDiff) technique showing numerous Donovan bodies in a monocyte. Credit: Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006. Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Lymphogranuloma Venereum
LGV is an acute and chronic STD cause by Chlamydia trachomatis types L1-L3. The disease is acquired during intercourse or through contact with contaminated exudate from active lesions. The incubation period is 5-21 days. After the genital lesion disappears, the infection spreads to lymph channels and lymph nodes of the genital and rectal areas. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Lymphogranuloma Venereum- Lesions
In men, the initial vesicular or ulcerative lesion (on the external genitalia) is evanescent and often goes unnoticed. Inguinal buboes appear 1-4 weeks after exposure, are often bilateral, and have a tendency to fuse, soften, and break down to form multiple draining sinuses, with extensive scarring. In women, the genital lymph drainage is to the perirectal glands. Early anorectal manifestations are proctitis with tenesmus and bloody purulent discharge; late manifestations are chronic cicatrizing inflammation of the rectal and perirectal tissue. These changes lead to obstipation and rectal stricture and, occasionally, rectovaginal and perianal fistulas. They are also seen in homosexual men. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Lymphogranuloma Venereum- Treatment
The antibiotic of choice is doxycyline (contraindicated in pregnancy), 100 mg BD for 21 days. Erythromycin, 500 mg QID for 21 days is also effective. Azithromycin, 1 g orally once weekly for 3 weeks, may also be effective. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Lymphgranuloma Venereum (lymphgranuloma inguinale, climactic bubo, esthiomene)
The organisms enter the body through epithelial abrasions and are passed to the draining lymphatics. Thus inguinal lymphadenitis is a common feature, resuting in large, sausage-shaped masses such as those seen here, over which the skin is shiny and puplish in color. Urethritis may develop in males or females. Serious genitoanorectal lesions can result from this infection. Credits: Fig. 911, Peters, Tropical Medicine, 2007

Lymphgranuloma Venereum in a female adult
The patient seen here had unilateral vulval edema and inguinal buboes. Credits: Fig. 912, Peters, Tropical Medicine, 2007

Gonorrhea- Essentials of Diagnosis
Purulent and profuse urethral discharge, especially in men, with dysuria, yielding positive smear. Men: epididymitis, prostatitis, periurethral inflammation, proctitis. Women: cervicitis with purulent discharge, or asymptomatic, yielding positive culture; vaginitis, salpingitis, proctitis also occur. Fever, rash, tenosynovitis, and arthritis with disseminated disase. Gram-negative intracellular diplococci seen in a smear or cultured from any site, particularly the urethra, cervix, pharynx, and rectum. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Urethral Discharge in Gonorrhea
Although gonorrhea is prevalent worldwide, it is especially widespread in the tropics where between 4% and 10% of the population may be infected. Chronic gonococcal salpingitis is a common cause of infertility in women. Gonorrheal urethral strictures are often seen in men.. Credits: Fig. 918, Peters, Tropical Medicine, 2007

Neisseria gonorrhoeae in Urethral Exudate
The Gran-negative diplococci are readily seen in smears of the purulent exudate in the cytoplasm of polymorphs. (Gram x 900) Credits: Fig. 919, Peters, Tropical Medicine, 2007

FIGURE 126-11 Disseminated gonococcal infection
FIGURE Disseminated gonococcal infection. Cutaneous lesions showing characteristic discrete pustules and papules with subcutaneous hemorrhage. Credits: Guerrant et. al., Tropical Infectious Disease, 2nd ed., 2006, p. 1528/ (Courtesy of Kenneth J. Tomecki, MD, Cleveland, OH.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Parasitic Dermatoses

Parasitic Dermatoses Pediculosis Scabies (Sarna)
Larva Migrans (Larva Migrans Syndrome) Tungiasis Myiasis Leishmaniasis Cutaneous Amebiasis Trypanosomiasis Onchocerciasis Trichinosis Dracunulosis Loiasis Cysticercosis

Pediculosis-General Pediculosis is a lice infestation.
Humans can be infected with three types of lice. 1) Pediculus capitis (head louse) 2) Pediculus corporis (body louse) 3) Pediculus pubis (pubic, or crab louse) Lice feed on human blood and deposit their eggs (nits) on the hair shafts (head lice and pubic lice) and along the seams of clothing (body lice). Nits generally hatch within 7 to 10 days. Lice are obligate human parasites and cannot survive away from their hosts for longer than 7 to 10 days. Ferri, Color Atlas of Clinical Medicine, 2009, p. 144.

Pediculosis- PE Pruritis with excoriation may be caused by hypersensitivity reaction, inflammation from saliva, and fecal material from the lice. Nits can be identified by examining hair shafts. The presence of nits on clothing is indicative of body lice. Lymphadenopathy may be present (cervical adenopathy with head lice, inguinal lymphadenopathy with pubic lice). Head lice is most frequently found in the back of the head and neck, behind the ears. Scratching can result in pustules and crusting. Pubic lice may affect the hair around the anus. Ferri, Color Atlas of Clinical Medicine, 2009, p. 144.

Pediculosis- Diagnosis
Lice are transmitted by close personal contact or use of contaminated objects (e.g. combs, clothing, bed linens, hats). Diagnosis is made by seeing the lice or their nits. Combing hair with a fine-toothed comb is recommended because visual inspection of the hair and scalp may miss more than 50% on infestations. Wood’s light exam is useful to screen a large number of children; live nits flouresce, empty nits have a gray fluorescence, and nits with unborn lice reveal a white fluorescence. Ferri, Color Atlas of Clinical Medicine, 2009, p. 144.

Pediculosis- Treatment
Patients with body lice should discard infested clothing and improve their hygiene. Combing out nits is a widely recommended but unproved adjunctive therapy. Personal items such as combs and hairbrushes should be soaked in hot water for 15 to 30 minutes. Close contacts and household members should also be examined for the presence of lice. The hollowing products are available for treatment of lice: permethrin, lindane, pyrethrin S, malathion, ivermectin. Ferri, Color Atlas of Clinical Medicine, 2009, p. 144.

Pediculosis- Body Louse Feeding
The body louse Pediculus corporis, transmits typical epidemic typhus due to Rickettsia prowazekii and trench fever. Credits: Peters et. al, Atlas of Tropical Medicine, 2007, Image 43 with explanation.

Pediculosis- 1045 Pediculus capitis The head louse, P. capitis, is very common, and heavy infestations such as that seen here in an Indian girl can cause severe irritation. The eggs (‘nits’) are attached to the hairs and appear as masses of white dots. Unlike Pediculus corporis, P. capitis is not known to be a disease vector. DNA fingerprinting has recently confirmed the specific identity of head and body lice. The evolutionary origin of the two species and that of their hosts are still being debated by geneticists. Credits: Peters et. al, Atlas of Tropical Medicine, 2007, Image 1045 with explanation.

Pediculosis- 1046 Severe pediculosis corporis Heavy infestation is common where people live in unhygienic conditions. Body lice spread rapidly wherever suitable ecological conditions prevail and are common in soldiers and refugees during wartime, in institutions for the mentally subnormal, prisons, etc. Formerly known also as ‘vagabond’s disease’, severe dermatitis due to the presence of heavy louse populations and the scratching that the bites stimulate, especially at night, is often accompanied by pigmentation of the affected areas, restlessness causing loss of sleep and, in chronic cases, lichenification and eczema. As in this patient, thousands of lice may be present on the patient’s body and in his clothes. Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1046 with explanation.

Figure 8-72 Microscopic appearance of lice
Figure 8-72 Microscopic appearance of lice. A, The crab louse has a short, broad body, with claws spaced far apart. B, The head louse has a long, thin body, with claws spaced close together. Downloaded from: Atlas of Pediatric Physical Diagnosis, 5e (on 3 March :00 PM) © 2007 Elsevier

Figure 8-73 Head lice. A, Nits appear as tiny white dots that adhere to the hair shafts. They are typically found 1 to 3 cm from the scalp above and behind the ears. B, Microscopic appearance of the nit of a head louse attached to a scalp hair. Microscopic examination distinguishes nits from hair casts and other artifacts. (A, Courtesy Michael Sherlock, MD, Lutherville, Md.) Downloaded from: Atlas of Pediatric Physical Diagnosis, 5e (on 3 March :00 PM) © 2007 Elsevier

Scabies-Definition Scabies is a contagious disease caused by the mite Sarcoptes scabiei. It is generally acquired by sleeping with or in the bedding of infested individuals. Ferri, Color Atlas of Clinical Medicine, 2009, p. 143.;

Scabies-Clinical Primary lesions are caused when the female mite burrows within the stratum corneum, laying eggs within the tract she leaves behind; burrows (linear or serpinginous tracts) end with a minute papule or vesicle. Primary lesions are most commonly found in the web spaces of the hands, buttocks, scrotum, penis, breasts, axillae, and knees. Secondary lesions result from scratching or infection. Intense pruritis, especially nocturnal, is common; it is caused by an acquired sensitivity to the mite or fecal pellets and is usually noted 1 to 4 weeks after the primary infestation. Examination of the skin may reveal burrows, tiny vesicles, excoriations, and inflammatory papules. Widespread and crusted lesions (Norwegian or crusted scabies) may be seen in older and immunocompromised patients. Ferri, Color Atlas of Clinical Medicine, 2009, p. 143.;

Scabies-Diagnosis and Treatment
Diagnosis is made on the clinical presentation and on the demonstration of mites, eggs, or mite feces. Microscopic demonstration of the organism, feces, or eggs; a drop of mineral oil may be placed over the suspected lesion before removal; the scrapings are transferred directly to a glass slide; a drop of KOH is added and a cover slip is added. Skin biopsy is rarely necessary to make the diagnosis. The following products are available for treatment of scabies mites: permethrin, lindane, ivermection. Ferri, Color Atlas of Clinical Medicine, 2009, p. 143.

Scabies-Clinical Ferri, Color Atlas of Clinical Medicine, 2009, p. 143.

Scabies 1032 Male and female scabies mites The gravid female Sarcoptes scabiei burrows into the epidermis, lays its eggs and dies at the end of the tunnel. It is cosmopolitan in distribution. (1032 left, ventral view × 115; 1033 dorsal view × 85) Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1032 with explanation.

Scabies 1033 Male and female scabies mites The gravid female Sarcoptes scabiei (1033, right) burrows into the epidermis, lays its eggs and dies at the end of the tunnel. It is cosmopolitan in distribution. ( 1033 dorsal view × 85) Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1033 with explanation.

Scabies 1034 Scabies burrows These are seen here on the instep of the foot of an infant. The foot is the second commonest site of early infection at this age, with the axillae and neck also being invaded in some cases. The darker colouring represents the inflammatory reaction to the mites and their detritus. Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1034 with explanation.

Scabies 1035 Infected scabies in a Papuan boy Intense local pruritus and dermatitis appear within a few days of infection. The tortuous tunnels may extend for several centimetres. Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1035 with explanation.

Scabies 1037 Chronic eczematous scabies in a Gambian woman The backs of the hands and arms are heavily infested in this woman. Constant scratching due to the intense itching may result in lichenification of the dry skin. The condition would need to be differentiated from onchocerciasis where both conditions are present. Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1037 with explanation.

Scabies 1038 Hyperkeratotic (‘Norwegian’) scabies in a patient who had suffered a 70% burns injury This condition is often associated with immunosuppression, which may result, among other causes, from severe burns and includes HIV infection. The dorsum of the hands and fingers are most affected in this patient. Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1038 with explanation.

Scabies 1039 Norwegian scabies in an old man This 91-year-old man had had pruritus with crusty skin lesions, some over 1 cm thick, for 6 months prior to admission to hospital. In addition to the discovery of a heavy scabies infection he was found to have carcinoma of the bladder. The skin condition improved rapidly following anti-mite treatment. (Courtesy of A Biglino, D Casabianca and A Mastinu.) Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1039 with explanation.

Scabies 1040 Section of biopsy from patient with Norwegian scabies This skin section shows some of the cuticular spines and internal organs of a female mite which lies within a subepidermal pocket under a thick layer of dead epidermis. The mites can be present in such patients in vast numbers. (H&E × 40) Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1040 with explanation.

Scabies 1036 Secondary erythema in scabies Secondary infection is common, and erythema may be associated with bacterial invasion of the sarcoptic tracks. Credits: Peters et. al, Atlas of Tropical Medicine, 2009, Image 1036 with explanation.

HIV- Related Scabies Description: Scabies in an HIV-infected infant; Exaggerated scabies with a generalized, papular, pruritic eruption. Credits: Pediatric AIDS Pictoral Atlas, Baylor International Pediatric AIDS Initiative

HIV- Related Scabies Description: Norwegian (Crusted) scabies in an HIV-infected boy. Generalized scaling and hyperkeratotic, crusted plaques are present. Credits: Pediatric AIDS Pictoral Atlas, Baylor International Pediatric AIDS Initiative

Figure 8-69 Scabies. A, Multiple pruritic papules, some excoriated and a few with central black dots, are seen on the wrist and dorsum of the hand. B, A pathognomonic scabies burrow is present in the finger web space of another child. Downloaded from: Atlas of Pediatric Physical Diagnosis, 5e (on 3 March :00 PM) © 2007 Elsevier

Figure 8-70 Infantile scabies
Figure 8-70 Infantile scabies. Widespread, pruritic papules, pustules, and vesicles are seen over the trunk and axilla (A); the soles, dorsal, lateral, and instep portions of the feet (B and C), where burrows are also evident; the palm of the hand (D); and the lateral aspect of the wrist (E). F, Infants are also more likely to develop an intense nodular reaction to the mite. Downloaded from: Atlas of Pediatric Physical Diagnosis, 5e (on 3 March :00 PM) © 2007 Elsevier

Figure 8-71 A, Microscopic appearance of an adult scabies mite obtained by scraping off the black dot at the end of a burrow. Note the small oval egg within the body. B, In a second specimen, no mite is seen but multiple eggs and mite feces are evident. Downloaded from: Atlas of Pediatric Physical Diagnosis, 5e (on 3 March :00 PM) © 2007 Elsevier

Larva Migrans (Larva Migrans Syndrome; Creeping Eruption; Cutaneous Larva Migrans)
This dermatitis results from penetration of and migration through the skin by infectious nematode larvae, usually of animal origin. The condition is most prevalent in warm humid tropical regions, especially along the coastline. The larval forms of Ancylostoma braziliensis (the cat and dog hookworm) are the most frequent cause of cutaneous larva migrans. The larvae evolve in the soil from eggs passed via the feces of infected hosts. These metamorphose into infectious filariofrm larvae capable of penetrating human skin on contact. The larvae appear to enter the skin via the ostia of hair follicles or sweat glands, usually on the feet, buttocks, or abdomen, in decreasing order of frequency. Ferri, Color Atlas of Clinical Medicine, 2009, p. 145.

An intensely pruritic erythematous papule or vesicle develops at the site of larval penetration. Migration of the larvae commences 2 to 4 days later, and is associated with the development of a characteristic erythematous, serpiginous tract. The larvae may migrate at a rate of 2 to 5 cm/day. Biopsy specimens obtained from the advancing tract confirm the presence of tunneling larvae. CBC reveals a high eosinophil count. Chest x-ray may reveal a patchy infiltrate. Treatment: 1) Ivermectin 200 microgrms/kg, single dose 2) Albendazole is also effective 3) Antibiotics may be needed for secondary infection. Ferri, Color Atlas of Clinical Medicine, 2009, p. 145.

Ferri, Color Atlas of Clinical Medicine, 2009, p. 145.

Tungiasis Tungiasis is due to the burrowing flea known as Tunga penetrans and is found in Africa, the West Indies, and South and Central America. The female burrows under the skin, sucks blood, swells to 0.5 cm, and then ejects her eggs onto the ground. Ulceration, lymphangitis, gangrene, and septicemia may result, in some cases with lethal effect. Simple surgical removal is usually performed. McPhee, 2012 Current Medical Diagnosis and Treatment, p. 151.

Tungiasis 1053 Male Tunga penetrans The ‘jigger’ or ‘chigoe’ flea, which is common in tropical areas of South America and Africa, is only 1 mm long and the smallest flea known. The male, which has a characteristically angular head, is free-living. (× 28) Credits: Peters et al., Atlas of Tropical Medicine,

Tungiasis 1054 Female jigger flea penetrating the skin of a toe The gravid female (arrow) burrows into the epidermis, where it settles with its posterior end facing the entrance hole. The periungual region is a favoured site of entry. Here two lesions are visible near the rim of the nail. There is inflammation and desquamation of the adjacent skin. Secondary infection is common when pathogenic microorganisms enter through the entry hole. (Courtesy of Professor H Feldmeier and Dr M Eisele.) Credits: Peters et al., Atlas of Tropical Medicine,

Tungiasis 1055 Section of female Tunga penetrans in the skin Having buried itself in the skin, often under the toenails, the female swells up to the size of a small pea within 8–10 days as its eggs mature. (H&E × 75) Credits: Peters et al., Atlas of Tropical Medicine,

Tungiasis 1056 Female Tunga penetrans laying eggs Some 150–200 eggs per day are actively ejected through the entry hole as seen in this photograph showing a line of recently projected eggs. Oviposition continues over a period of about 5 weeks, after which the flea dies. The eggs mature in 3–4 days in the dust and dirt covering the floors of dwellings. (Courtesy Professor H Feldmeier and Dr M Eisele. Reproduced by permission of Springer-Verlag from Eisele M, Heukelbach J, Van Marck E et al 2003 Investigations on the biology, epidemiology, pathology and control of Tunga penetrans in Brazil: I Natural history of tungiasis in humans. Parasitology Research 90: 94, Fig. 15). Credits: Peters et al., Atlas of Tropical Medicine,

Tungiasis 1057 Living egg of Tunga penetrans The oval egg, which is readily seen macroscopically as a tiny pearly object (see 1056), is about 0.5 mm long and 0.3 mm in diameter. (× 70) Credits: Peters et al., Atlas of Tropical Medicine,

Parasitic Dermatosis: Myiasis
Clinically, maggots that cause myiasis may attack 3 parts of the body. 1. Cutaneous tissue. Some species of maggots cause furuncles (subcutaneous myiasis), invade sores and wounds (wound myiais), burrow under the skin (dermal myiasis, a cause of creeping eruption) or suck blood. 2. Body cavities. Other species invade the nasal passages (nasal myiasis), mouth, ears and accessory passages, enter the orbit of the eye (ocular myiasis), or penetrate the anus or vagina. 3. Gut lumen. If accidentally ingested, fly eggs or larvae may survive passage through the stomach and bowel to emerge in the stool (intestinal myiasis) Credits: Cook et al., Manson’s Tropical Disease, 26th ed., 2009, p

Pathologically, myiasis-producing flies can be divided into three categories. 1. Obligatory myiasis producers. For some fly species, it is essential for the larvae to develop in living tissue because they are unable to develop elsewhere. These obligate parasites are highly specialized insects, the larvae of which have developed highly sophisticated mechanisms to avoid the host’s immune system. 2. Facultative myiasis producers. These larvae usually devlop on carrion but may invade wounds. They may be primary invaders which initiate myiasis; secondary invaders, entering tissue only when the animal has become infested; or tertiary, which become involved later, only once decomposition is advanced. 3. Accidental myiasis producers. These eggs or larvae are accidentally ingested and are not killed in the intestine. Credits: Cook et al., Manson’s Tropical Disease, 26th ed., 2009, p

Cutaneous tissue myiasis- Blood suckers (Congo floor maggot) Subcutaneoous myiasis- the maggot penetrates the skin; no previous lesion is necessary; 2 species of fly are the cause; both are obligatory myiasis producers: Cordylobia anthropophaga (family Calliphoridae) in Africa and Dermatobia hominis (family Cuterebridae) in South America. Dermal myiasis or creeping eruption- caused by maggots of horse and cattle bot flies; obligatory myiasis producers, producing tunnels in the epidermis in which they may wander for some time; Species: Gasterophilus spp. (horse bots, warble flies), Hypoderma spp. (cattle bots) Credits: Cook et al., Manson’s Tropical Disease, 26th ed., 2009, p

PLATE 126-2 A, Tropical phagedenic ulcer. B, Buruli ulcer

C) Myiasis PLATE A, Tropical phagedenic ulcer. B, Buruli ulcer. C, Myiasis extruding larva. D, Granuloma inguinale. E, South American blastomycosis (paracoccidioidomycosis). Credits: Guerrant et. al. , Tropical Infectious Diseases, 2nd edition,, 2006 (A–C, Courtesy of Jay S. Keystone, MD. D and E, Courtesy of R. L. Guerrant, MD, Charlottesville, VA.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Leishmaniasis Leishmaniasis is an infectious disease caused by a heterogenous group of protozoan parasites belonging to the genus Leishmania and resulting in a variety of different clinical syndromes. Ferri, Color Atlas of Clinical Medicine, 2009, p ;

Leishmaniasis- Physical Findings
Cutaneous Syndrome Localized cutaneous leishmaniasis (Fig ) Mucosal leishmaniasis Leishmania recidivans Diffuse Cutaneous leishmaniasis (Fig ) Visceral Syndrome Viscerotrophic leishmaniasis: fever, chronic fatigue, malaise, cough, intermittent diarrhea, and abdominal pain. Signs include adenopathy, hepatosplenomegaly (Fig ), hyperpigmentation of skin, petechiae, jaundice, edema, and ascites. Post kala-azar dermal leishmaniasis: generalized cutaneous rash that is often papular or nodular; severe forms with desquamation of skin and mucosa. Ferri, Color Atlas of Clinical Medicine, 2009, p ;

Leishmaniasis- Cause Cause: Laboratory Tests
1. Old world parasite: Leishmania tropica, L. major, L. aethiopica, L. donovani, L. infantum 2. New World parasite: L. braziliensis and L. mexicana complex, L. chagasi, L. b. guyanensis, L. b. paramensis Laboratory Tests 1. CBC: anemia, neutropenia, thrombocytopenia, and eosinophilia 2. LFTs: hypergammaglobulinemia, hypoalbuminemia, and hyperbilirubinemia. 3. Elevated BUN and creatinine 4. Specific diagnosis confirmed by intracellular amastigote in Giemsa-stained impression smears or sectioned tissue or culture performed in NMN (novy, MacNeal, Nicolle) or Schneider’s medium. 5. Serologic diagnosis: ELISA, direct agglutination tests, K39 ELISA, PCR, and monoclonal antibody staining of tissue smears. 6. Montenegro skin test. Ferri, Color Atlas of Clinical Medicine, 2009, p ;

Leishmaniasis- Treatment
Nonspecific or supportive care: 1. Nutritional diet. 2. Antimicrobial agents for concurrent infections 3. Blood transfusions 4. Iron and vitamins Specific antileishmanial therapy 1. Pentavalent antimonials: Na stibogluconate and NA antimonygluconate 2. Miltefosine 3. Amphotericin B 4. Pentamidine 5. Aminosidine 6. Other agents: allopurinol, ketoconazole, paromomycin (combined with other regimens) Immunotherapy: IFN-g; Local or topical treatments and physical therapy including thermal treatments; plastic surgery. Ferri, Color Atlas of Clinical Medicine, 2009, p ;

Parasitic Dermatosis: Leishmaniasis
Fig. 258 Reaction to sandfly bites- A persistent macule appears at the site of each bite, even from an uninfected fly; this may be the starting point of the lesion in simple cutaneous leishmaniasis. Multiple primary lesions occur when the sandfly probes repeatedly in the course of feeding. Creditis: Peters, Tropical Medicine, 2007.

Visceral Leishmaniasis-Distribution
,Fig. 259 Peters et. al, Atlas of Tropical Medicine, 6th ed., 2007.

Visceral L.- Village in the kala-azar endemic area of Bihar, India
This is the typical habitat of L. donovani where new epidemics of kala-azar have occurred in recent years. The close association between humans and domestic animals in this village favours the growth of populations of the local vector, Phlebotomus argentipes. This has a wide geographical range in south-east Asia and is suspected to be a species complex, since many areas where it occurs are free of Leishmania. ,Fig. 260 Peters et. al, Atlas of Tropical Medicine, 6th ed., 2007.

Parasitic Dermatosis: V. Leishmaniasis
Fig. 264 Infantile kala-azar-Children present with chronic, irregular fever, anaemia, leukopenia and thrombocytopenia, a moderately enlarged, nontender liver and a greatly enlarged, firm spleen. If left untreated, the infection is often fatal, commonly from secondary infections. This infant was infected in the northeast of Brazil with L. chagasi (regarded by some as synonymous with L. infantum of the Old World). Credits: Peters, Tropical Medicine, 2007.

Fig. 265 Purpura in kala-azar- The condition may present as a petechial rash if the thrombocytopenia is severe, as in this Indian boy with L. donovani, sensu stricta. Petechial haemorrhages of the retina also occur not infrequently. Credits: Peters, Tropical Medicine, 2007.

Parasitic Dermatosis: Old World Cutaneous Leishmaniasis
Fig.277 Distribution- Cutaneous leishmaniasis in the Old World is caused by L. major, L. tropica, L. aethiopica and certain zymodemes of the L. infantum complex . With the possible exception in some localities of L. tropica, these infections are essentially zoonoses that occur in scattered foci throughout the tropical and subtropical belts. Depending upon the area, cutaneous leishmaniasis is known as Oriental sore, Aleppo button, bouton de Biskra, Baghdad boil, Delhi sore, etc. Credits: Peters, Tropical Medicine, 2007.

Parasitic Dermatosis: OWC Leishmaniasis
Fig. 281 Wet lesion of mouth- L. major occurs most commonly in rural areas, causing moist, ulcerative lesions that may be extensive and sometimes involve the epithelium of lips and nose. Credits: Peters, Tropical Medicine, 2007

Fig. 282 Nodulo-ulcerative lesion of Leishmania major--These are the commonest types of lesion caused by L. major. The prominent ‘rolled’ edge of the lesions is the best area in which to demonstrate the parasites, which are present in macrophages or are free in surrounding tissue, often in small numbers. Credits: Peters, Tropical Medicine, 2007.

Cutaneous OW Leishmaniasis
Fig. 283 Invasive ulcerative lesion of Leishmania major--The extensive lesion on the lower leg of this Sudanese woman near Khartoum has exposed deep tissues, including a tendon sheath. (Courtesy of Dr S El-Safi.) Credits: Peters, Tropical Medicine, 2007.

Amebiasis- Essentials of Diagnosis
Organism or antigen present in stools or abscess aspirate. Positive serologic tests with colitis or hepatic abscess but may represent prior infections./ Mild to moderate colitis- recurrent diarrhea Severe colitis- severe bloody diarrhea with fever, abdominal pain, and tenderness; prostration, progression to hemorrhage or perforation. Hepatic Abscess- fever, abdominal pain, hepatomegaly, hepatic abscess on imaging studies. McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Amebiasis- General Information
The Entamoeba complex contains 3 morphologically identical species: Entamoeba dispar and Entamoeba moshkovskii, which are avirulent, and Entamoeba histolytica, which may be an avirulent intestinal commensal or lead to serious disease. Disease follows penetration of the intestinal wall, resulting in diarrhea, and with severe involvement, dysentery or extraintestinal disease, most commonly liver abscess. E. histolyica infections are present worldwide but are most prevalent in subtropical and tropical areas under conditions of crowding, poor sanitation, and poor nutrition. McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Amebiasis- General Information
Of the estimated 500 million persons worldwide infected with Entamoeba, most are infected with E dispar and an estimated 10% with E histolytica. The prevalence of E moshkovskii is unknown. Mortality from invasive E histolytica infections is estimated at 100,000 per year. Humans are the only established E histolytica host. Transmission occurs through ingestion of cyts from fecally contaminated food or water, faciliated by person-to-person spread, flies and other arthropods as mechangical vectors, and use of human excrement as fertilizer. McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Intestinal Amebiasis- Clinical Findings
In most infected persons, the organism lives as a commensal, and the carries with without symptoms. With sympomatic disease, diarrhea may begin within a week of infection, although an incubation period of 2-4 weeks is more common, with gradual onset of abdominal pain and diarrhea. Fever is uncommon. Periods of remission and recurrence may last days to weeks or longer. Abdominal exam may show distension, tenderness, hyperperistalsis, and hepatomegaly. Microscopic hematochezia is common. McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Intestinal Amebiasis- Clinical Findings
More severe presentations include colitis and dysentery, with more extensive diarrhea (10-20 stools per day) and bloody stools. With dysentery, physical findings include high fevers, prostration, vomiting, abdominal pain and tenderness, hepatic enlargement, and hypotension. Severe presentations are more common in young children, pregnant women, and those who are malnourished, and those receiving corticosteroids. Thus, in endemic areas, corticosteroids should not be started for presumed inflammatory bowel disease without first ruling out amebiasis. Fulminant amebic colitis can progress to nectrotizing colitis, intestinal perforation, mucosal sloughness, and severe hemorrhage, with mortality rates over 40%. More chronic complications of intestinal amebiasis include chronic diarrhea with weight loss, which may last for months to years; bowel ulcerations; and amebic appendicitis. McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Extraintestinal Amebiasis- Clinical Findings
The most common extraintestinal manifestation is amebic liver abscess. This can occur with colitis, but more frequently presents without history of prior intestinal symptoms. Patients present with the acute or gradual onset of abdominal pain, fever, an enlarged and tender liver, anorexia, and weight loss. Diarrhea is present in a small number of patients. Abscesses are most commonly single and in the right lobe of the liver, and they are much more common in men. Without prompt treatment, amebic abscesses may rupture into the pleural, peritoneal, or pericardial space, which is often fatal. Amebic infections may rarely occur throughout the body, including the lungs, brain, and genitourinary system. McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Extraintestinal Amebiasis- Diagnosis
Diagnosis is by finding E histolytica or its antigen or by serologic tests. Intestinal amebiasis- Diagnosis is most commonly made by identifying organisms in the stool; however, E histolytica and E dispar cannot by distinguished, but the identification of amebic trophozoites or cyts in a symptomatic patient is highly suggestive of amebiasis. Stool evaluation for organisms is not highly sensitive (about 30 to 50% for amebic colitis), and at least 3 stool specimens should be evaluated. Hepatic abscesses- Liver abscesses can be identified by US, CT or MRI. McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Extraintestinal Amebiasis- Treatment
Treatment of amebiasis generally entails the use of metronidazole or tinidazole to eradicate tissue trophozoites and a luminal amebicide to eradicate intestinal cysts. Treatment of intestinal amebiasis requires metronidazole (750 mg orally 3x per day for 10 days) or tinidazole (2 grams orally for 3 days and 5 days for serious disease) plus a luminal agent (Diloxanide furoate or iodoquinol or paromomycin) Amebic liver abscess is also treated with metronidazole or tinidazole plus a luminal agent. Needle aspiration may be helpful for large abscesses (over 5 to 10 cm), in particular if the diagnosis remains uncertain, if there is an initial lack of response, or if a patient is very ill, suggesting imminent abscess rupture. With successful therapy, abscesses disappear slowly (over months). McPhee et al., Current Medical Diagnosis and Treatment, 2012, p

Cutaneous Amebiasis Fig 673 Amoebiasis of the Skin. Amoebic infection of the skin may arise by direct spread from a primary abscess. This pt. was erroneously operated on for a perforated duodenal ulcer and no antiamoebic durgs were given. Sloughing of the skin occurred and amoebae were recovered from the skin lesion. Peters et. al, Atlas of Tropical Medicine, 6th ed., 2007.

Cutaneous Amoebiasis Fig 674 Amoebic balanitis. Amoebic infection
Peters et. al, Atlas of Tropical Medicine, 6th ed., 2007.

Trypanosomiasis Definition: Trypanosomiasis (Chaga’s disease) is an infection caused by the protozoan parasite Trypanosoma cruzi. This is a vector-borne disease transmitted by reduviid (“kissing”) insects from multiple wild and domesticated animal reservoirs. The disease is characterized by an acute nonspecific febrile illness that may be followed, after a variable latency period, by chronic cardiac, GI and neurologic sequlae. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Trypanosomiasis-Cause
T. Cruzi, causative agent, found only in the Americas, ranging from the southern half of the US to southern Argentina. Transmitted to humans by the various species of bloodsucking reduviid insects, primarily those of the genera Triatoma, Pantrongylus, and Rhodnius. Usually found in burrows and trees, where infected insects transmit the parasite to nonhuman mammals (e.g. opossums and armadillos), which constitute the natural reservoir. Intrusion into enzootic areas for farmland, allowing insects to take up residence in rural dwellings, thus including humans and domestic animals in the cycle of transmission. Ferri’s Atlas of Clinical Medicine, 2009, pp

Trypanosomiasis-Cause (2)
Multiplication of ingested parasites in the insect midgut as epimastigotes, then differentiation into infective metacyclic trypomastigotes in the hindgut whereby the parasites are discharged with the feces during subsequent blood meals. Transmission to the second mammalian host through contamination of mucous membranes, conjunctivae, or wounds with insect feces containing infected forms. In the vertebrae host- movement of parasites into various cell types, intracellular transformation and multiplication in the cytoplasm as amastigotes, and thereafter differentiation into trypomastigotes. Following rupture of the cell membrane, parasitic invasion of local tissues or hematogenous spread to distant sites, maintaining a parasitemia infective for vectors. Ferri’s Atlas of Clinical Medicine, 2009, pp

Trypanosomiasis- Clinical
Inflammatory lesion that develops about 1 week after contamination of a break in the skin with infected insect feces (chagoma). Presence of Romana’s sign (see Fig ), which consists of unilateral painless palpebral and periocular edema, when conjunctiva is portal of entry. Constitutional symptoms of fever, fatigue, and anorexia, along with edema of the face and lower extremities, generalized lymphadenopathy, and mild hepatosplenomegaly after the appearance of local signs of disease. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Trypanosomiasis- Clinical (2)
Myocarditis in a small portion of patients, sometimes with resultant congestive heart failure (CHF). Uncommonly, CNS disease, such as meningoencephalitis, which carries a poor prognosis. Symptoms and signs of disease persisting for weeks to months, followed by spontaneous resolution of the acute illness: patient then in the indeterminate phase of the disease (asymptomatic with attendant subpatient parasitemia and reactive antibodies to T. cruzi antigens. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Chronic disease may become manifest years to decades after the initial infection. Most common organ involved: heart, followed by GI tract and, to a much lesser extent the CNS Cardiac involvement takes the form of arrhythmias or cardiomyopathy, but rarely both. Cardiomyopathy (fig ) is generally bilateral but may affect either ventricle and is often accompanied by apical aneurysms (fig ) and mural thrombi. Arrhythmias are a consequence of involvement of the bundle of HIS and have been implicated as the leading cause of sudden death in adults in highly endemic areas. Right-sided heart failure, thromboembolization, and rhythm disturbances associated with symptoms of dizziness and syncope are characteristic. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Patients with megaesophagus (Fig ): dysphagia, odynophagia, chronic cough, and regurgitation, frequently resulting in aspiration pneumonitis Megacolon (Fig ): abdominal pain and chronic constipation, which, when severe, may lead to obstruction and perforation CNS symptoms: most often secondary to embolization from the heart or varying degrees of peripheral neuropathy. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Trypanosomiasis- Workup
For acute diagnosis: Demonstration of T. cruzi in wet preparation of blood, buffy coat, or Giemsa-stained smears (Fig ) Xenodiagnosis, a technique involving laboratory-reared insect vectors fed on subjects with suspected infection thereafter examined for parasites and culture of body fluids in liquid media to establish diagnosis. Recent advances in serologic testing include immunoblot assay, in situ indirect fluorescent antibody, PCR-based techniques, and an immunochromatographic assay (Chagas Stat Pak). For chronic diagnosis: Traditional serologic tests including: complement fixation (CF), indirect immunofluorescence (IIF), indirect hemaglutination, enzyme-linked immunosorbent assay (ELISA), and radioimmune precipitation assay. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Trypanosomiasis- Treatment
Chronic chagasic heart disease: mainly supportive Megaesophagus: symptoms usually amenable to dietary measures or pneumonic dilatation of he esophagogastric junction. Chagasic megacolon: in its early stages responsive to a high-fiber diet, laxatives, and enemas. Nifurtimox: only drug available in the US for the treatment of acute, congenital, or laboratory-acquired infection. Parasitologic cure in approximately 50% of those treated, should be begun as early as possible. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Oncocerciasis- Essentials of Diagnosis
1) Severe pruritis, skin excoriations, thickening, and depigmentation; and subcutaneous nodules. 2) Conjunctivitis progressing to blindness 3) Microfilariae in skin snips and on slit-lamp examination; adult worms in subcutaneous nodules. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Onchocerciasis- General
Onchocerciasis, or river blindness is caused by Onchocerca volvulus. An estimated 18 million persons are infected, of whom 3-4 million have skin disease, 500,000 have severe visual impairment, and 300,000 are blinded. Over 99% of infections are in subsaharan Africa, especially the West African savana, with about half of cases in Nigeria and Congo. In some hyperendemic Africa villages, close to 100% of individuals are infected, and 10% or more of the population is blind. The disease is also prevalent in the southwestern Arabian peninsula and Latin America, including southern Mexico, Guatemala, Venezuela, Columbia, Ecuador, and northwestern Brazil. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Onchocerciasis- Cause
Onchocerciasis is transmitted by simulium flies (black flies). These insects breed in fast-flowing streams and bite during the day. After the bite of an infected blackfly, larvae are deposited in the skin, where adults develop over 6-12 months. Adult worms live in subcutaneous connective tissue or muscle nodules for a decade or more. Microfilariae are released from the nodules and migrate through subcutaneous and ocular tissues. Disease is due to responses to worms and to intracellualar Wolbachia bacteria. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Onchocerciasis- Clinical
After an incubation period of up to 1-3 years, the disease typically produces an erythematous, papular, pruritic rash, which may progress to chronic skin thickening and depigmentation. Itching may be severe and unresponsive to medications, such that more disability-adjusted life years are lost to onchocercal skin problems than to blindness. Numerous firm, non-tender, movable subcutaneous nodules of about cm, which contain adult worms, may be present. Due to differences in vector habits, these nodules are more common on the lower body in Africa but on the head and upper body in Latin America. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Onchocerciasis- Clinical (2)
Inguinal and femoral lymphadenopathy is common, at times resulting in a “hanging groin.” Patients may have systemic symptoms such as weight loss and musculoskeletal pain. The most serious manifestations of onchocerciasis involve the eyes. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Onchocerciasis- Treatment
The treatment of choice is ivermectin. Treatment is with a single oral dose of 150 mcg/ml, but schedules for re-treatment have not been standardized. McPhee, 2012 Current Medical Diagnosis and Treatment, p

FIGURE Onchocercal dermatitis demonstrating characteristic pruritic papules due to cutaneous microfilaria. Credits: Guerrant et. al., Tropical Infectious Diseases, 2nd ed., 2006, p Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Trichinosis Trichinosis is an infection by one of various species of Trichinella. The nematode responsible for this illness is an obligate intracellular parasite belonging to the genus Trichinella. It is one of the most ubiquitous parasites in the world and may be found in virtually all warm-blooded animals. Infection in humans occurs by the ingestion of contaminated animal meat that is raw or partially cooked and contains viable cysts. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Trichinosis Symptoms may vary widely depending on the time from ingestion of contaminated meat and on worm burden. Most persons are aymptomatic. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Trichinosis Enteral Phase Migratory Phase Severe Complications
Correlates with penetration of ingested larvae into the intestinal mucosa; may last 2 to 6 weeks; mild transient diarrhea and nausea, abdominal pain, malaise, low-grade fevers. Migratory Phase Maturing and mating in intestine; Newborn larvae penetrate into lymphatic and blood vessels and then migrate to muscles where they penetrate into muscle cells, enlarge, coil, and develop a cyst wall (see Fig ); Pts. May present with fever, myalgias, periorbital or facial edema, headache, skin rash. Severe Complications Brain damage and cardiac involvement Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Trichinosis Workup Labs Treatment
Antibody assay of serum is usually positive by approximately 2 weeks after infection. Muscle biopsy is used to detect the larvae in muscle tissue if diagnosis is unclear. Labs CBC shows leukocytosis with prominent eosinophilia, ESR usually normal; Elevation of muscle enzymes common (i.e. CPK, aldolase) Treatment Albendazole, mebendazole, Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Dracunculiasis/Dracunculiosis
Disease caused by the nematode Dracunculus medinensis, or Guinea worm. Causes chronic cutaneous ulcers with protruding worms in rural Africa. Occurs only in humans and is a major cause of disability. Annual incidence dropped from 3.5 million in late 1980s to 3185 reported cases in 2009. Eradicated from Asia, but remains endemic in 6 countries in West and Northeast Africa, most notably in South Sudan. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Infectious occurs after swallowing water containing the infected intermediate host, the crustacean Cyclops (known as copepods or water fleas). In the stomach, larvae escape from the copepods and migrate through the intestinal mucosa to the retroperiotoneum, where mating occurs. Females then migrate to subcutaneous tissue, usually of the legs, over about a year. A subcutaneous ulcer then forms. Upon contact with water, the parasite discharges large numbers of larvae, which are ingested by copepods. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Patients are usually asymptomatic until the time of worm extrustion. At that time, a painful papule develops, with erythema, pruritis, and burning, usually on the lower leg. The skin lesion(s) usually vesiculate over a few days, followed by ulceration. The ulcer is tender, often with a visible worm. The worm is then extruded or absorbed over a few weeks, followed by ulcer healing. Treatment- no drug cures the infection; worms are typically removed by sequentially rolling them out over a small stick. McPhee, 2012 Current Medical Diagnosis and Treatment, p

FIGURE A, Blister caused by emerging nematode parasite Dracunculus medinensis. B, After the blister ruptures, the worm is exposed. Credits: Guerrant et. al., Tropical Infectious Diseases, 2nd ed. , 2006. (A, Courtesy of Stephen Fitzgerald; B, Courtesy of WHO Collaborating Center for Research, Training, and Eradication at the Centers for Disease Control and Prevention.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Dracunculiasis FIGURE Pyogenic organisms invade the superficial lesion and worm tract, aggravating the condition. (Dracunculiasis) Credit: Guerrant et. al., Tropical infectious Diseases, 2nd ed., 2006. (Courtesy of WHO Collaborating Center for Research, Training, and Eradication at the Centers for Disease Control and Prevention.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Loiasis- Essentials of Diagnosis
Subcutaneous swellings, adult worms migrating across the eye. Encephalitis, which may be brought on by treatment. Microfilariae in the blood. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Loiasis- General Chronic filarial disease caused by infection with Loa loa. Infection occurs in humans and monkeys in rainforest areas of West and central Africa. An estimated 3-13 million persons are infected. The disease is transmitted by chrysops flies, which bite during the day. Over 6-12 months after infection, larvae develop into adult worms, which migrate through subcutaneous tissues, including the subconjunctiva (leading to the term ‘eye worm’). Adult worms can live for up to 17 years McPhee, 2012 Current Medical Diagnosis and Treatment, p

Loiasis- Clinical Many infected persons are aymptomatic, although they may have high levels of microfilaremia and eosinophilia. Transient subcutaneous swellings (Calabar swellings) develop in symptomatic persons. The swellings are nonerythematous, up to 20 cm in diameter, and may be preceded by local pain or pruritis. The usually resolve after 2-4 days but occasionally persist for several weeks. Calabar swellings commonly seen around joints. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Loiasis- Clinical Adult worms may be seen to migrate across the eye with eithr no symptoms or conjunctivitis, with pain and edema. Most serious complication is encephalitis. Symptoms may range from headache and insomnia to coma and death. Treatment is diethylcarbamazipine which eliminates microfilariae and has some activity against adult worms. McPhee, 2012 Current Medical Diagnosis and Treatment, p

FIGURE Calibar swelling in the left (upper) forearm of an expatriate patient with loiasis. Eosinophilia of 60% was coincident with this rash. Credits: Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006, p Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Cysticercosis/Tapeworm
Four species of adult tapeworms may infect humans as the definitive host: Taenia saginata (beef tapeworm) (fig 333-1), Taenia solium (pork tapeworm), Diphyllobothrium latum (fish tapeworm), and Hymenolepis nana. In addition, T. solium may infect humans in its larval form (cysticercosis), and several animal tapeworms may cause infection in an analogous manner. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Cysticercosis Occurs when humans ingest eggs of T. solium in food contaminated with human feces that contain the eggs (as opposed to eating infected pork, which results in colonization). Eggs hatch into larvae in gut. Larvae disseminate through tissues (Fig ) (particularly soft tissue and CNS) forming cystic lesions (Fig 333-7) containing either viable or nonviable larvae. Soft tissue and visceral lesions also can form. Mass lesions of brain (neurocysticercosis) may cause seizures and hydrocephalus. Therapies for symptomatic cysticercosis: may regress spontaneously, surgery, albendazole and/or praziquantel. Credits: Ferri’s Atlas of Clinical Medicine, 2009, pp

Viral Dermatoses Herpes Simplex HHV-8/Kaposi sarcoma-associated HV
Aphthous Ulcer Varicella and Zoster Viral Warts/Focal Epithelial Hyperplasia Molluscum Contagiosum Dengue HIV/AIDS

Viral Dermatoses

Viral Dermatoses Herpes Simplex

Herpes Simplex- Essentials of Diagnosis
Recurrent small grouped vesicles on an erythematous base, especially in the orolabial and genital areas. May follow minor infections, trauma, stress, or sun exposure; regional lymph nodes may be swollen and tender. Viral cultures and direct flourescent antibody tests are positive. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Herpes Simplex- General
Over 85% of adults have serologic evidence of herpes simplex as type 1 (HSV-1) infections, most often acquired asymptomatically in childhood. Occasionally, primary infections may be manifested as severe gingivostomatitis. Thereafter, the patient may have recurrent self-limited attacks, provoked by sun exposure, orofacial surgery fever, or a viral infection. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Herpes Simplex- General
Over 85% of adults (in US) have serologic evidence of herpes simplex as type 1 (HSV-1) infections, most often acquired asymptomatically in childhood. Occasionally, primary infections may be manifested as severe gingivostomatitis. Thereafter, the patient may have recurrent self-limited attacks, provoked by sun exposure, orofacial surgery fever, or a viral infection. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Herpes Simplex About 25% of the United States population has serologic evidence of infection with herpes simplex type 2 (HSV-2). HSV-2 causes lesions whose morphology and natural history are similar to those caused by HSV-1 on the genitalia of both sexes. Genital herpes may also be due to HSV-1. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Herpes Simplex- Clinical Findings
The principal symptoms are burning and stinging. Neuralgia may precede or accompany attacks. The lesions consist of small, grouped vesicles that can occur anywhere, but most often occur on the vermillion border of the lips, the penile shift, the labia, the perianal skin, and the buttocks. Regional lymph nodes may be swollen and tender. The lesions usually crust and heal in 1 week. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Herpes Simplex- Treatment
Three systemic agents are available for the treatment of herpes infections: acyclovir, valacyclovir, and famciclovir. Only acyclovir is available for IV use. In pts. with frequent or severe recurrences, suppressive therapy is most effective in controlling disease. McPhee, 2012 Current Medical Diagnosis and Treatment, p

HIV-related Herpes Simplex
Description: Herpes on oral mucous membranes Credits: Arthur Amman, MD, Global Strategies for HIV Prevention; Nat’l Library of Medicine.

Description: Extensive Herpes Simplex Infection. In children, it occurs primarily on the oral mucous membranes but also may be systemic Credits: Arthur Amman, MD, Global Strategies for HIV Prevention; Nat’l Library of Medicine.

Description: HSV infection in an HIV-infected girl. Chronic or progressive herpetic skin lesions are observed occasionally in HIV-infected children. Credits: Pediatric AIDS Pictoral Atlas, Baylor International Pediatric AIDS Initiative; National Library of Medicine.

HSV in HIV: Chronic Genital Ulcer
With more advanced immunocompromise, HSV lesions tend to be subacute or chronic, indolent, atypical, and respond less promptly to oral antiviral therapy. Chronic herpetic ulcers of greater than 1 months’ duration are an AIDS-defining illness. Clinically, reactivated latent infections (ulcers) are larger and deeper. Ulcerated, crusted lesions at perioral, anogenital, or digital locations are usually HSV in etiology, in spite of atypical clinical appearances. From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1134, picture from p

Severe, erosive perirectal herpes simplex in an pt. with AIDS
Rectal lesions are common in HIV-infected patients, particularly the perirectal ulcers and erosions due to the reactivation of HSV. These may appear quite atypical, as denuded skin without vesicles, and they respond well to treatment with acyclovir, famciclovir, or foscarnet. From Fauci, Anthony et. al. Harrison’s Principles of Internal Medicine, 2008, p

HHV-8/Kaposi sarcoma-associated Virus
Viral Dermatoses HHV-8/Kaposi sarcoma-associated Virus

Viral Dermatoses- HHV-8
Identified in 1994 and considered to be the etiologic agent for all forms of Kaposi sarcoma (KS) including classic KS, African endemic KS, iatrogenic immunosuppression-related KS, and AIDS endemic KS. KS is a tumor that involves blood and lymphatic vessels. Each type of KS is clinically distinct, but histopathologically similar. Several subtypes of HHV-8, including subtypes A, B, C, and D. These subtypes have a geographical distribution, with subtypes A and C common in Europe, subtype B found in Africa, and the rare subtype D found in aborigines in Polynesia and Australia. The highest prevalence of KS is in sub-Saharan Africa, where endemic KS is found. Tyring et. al, Tropical Dermatology, 2006, pp

HHV-8 likely infects a B-lymphoid precursor or KS precursor cell, which is endothelial, but it is not known if it is vascular, lymphatic, or both. HHV-8 integrates into the cells and becomes latent until reactivation through immunosuppression or genetic, endocrine, metabolic, microbiologic, and social stimuli. Tyring et. al, Tropical Dermatology, 2006, pp

Classic KS is mostly a chronic skin disease of elderly Mediterranean, east European, or Jewish Men and presents as multiple firm purple-red plaques and nodules on the lower extremities. African endemic KS, generally an indolent tumor in HIV-seronegative adults, has the following four clinical subtypes: 1) Benign cutaneous nodular disease that is similar to classic KS, seen mostly in young adults that runs a mean duration of 5-8 years. 2) Aggressive infiltrative cutaneous disease that invades the dermis, subcutaneous tissue, muscle, cone and usually becomes fatal in 5-7 years. 3) Florid disseminated visceral and mucocutaneous disease, in which an extensive number of cutaneous lesions involves one or more extremities 4) Fulminant lymphadenopathic disease without cutaneous manifestations that disseminates to lymph nodes and multiple organs and is found in children. Tyring et. al, Tropical Dermatology, 2006, pp

In general, pts. with classical KS respond to local therapy, like excision, alitretinoin, and intralesional chemotherapy. Endemic KS responds to systemic therapies, like chemotherapy with vinca alkaloids or paclitaxel and interferon-a. Immunosuppression-related KS usually regresses after decreasing or discontinuing the immunosuppressive drugs. There is no curative therapy for AIDS-related KS, but highly active antiretroviral therapy can prevent and treat the lesions. In those HIV- seropositive pts. already receiving HAART, KS has a less aggressive presentation but its natural history and outcome are not affected. Tyring et. al, Tropical Dermatology, 2006, pp

Neoplastic Dermatoses of HIV- Kaposi’s Sarcoma
Description: Kaposi’s Sarcoma in an HIV+ Kenyan Woman. Credit: Thor Swanson, MD; Siouxland Medical Education Foundation, 2008.

Description: Kaposi’s Sarcoma in an HIV+ Kenyan Woman; she died just minutes before the picture was taken. Credit: Thor Swanson, MD; Siouxland Medical Education Foundation, 2008.

Description: Kaposi’s Sarcoma in an HIV+ Kenyan Woman, she died several weeks later. Credit: Thor Swanson, MD; Siouxland Medical Education Foundation, 2008.

Description: Kaposi’s Sarcoma in an HIV+ Kenyan woman Credits: Thor Swanson, MD: Siouxland Medical Education Foundation, IA.

Description: Kaposi’s Sarcoma in an HIV+ Kenyan Woman Credits: Thor Swanson, MD; Siouxland Medical Educational Foundation, IA.

Description: KS in an HIV+ Kenyan woman. Credits: Thor Swanson, MD; Siouxland Medical Educational Foundation, IA.

Description: Kaposi’s Sarcoma in an HIV+ Kenyan Woman Credits: Dr. Thor Swanson, MD; Siouxland Medical Educational Foundation, Sioux City, IA.

Neoplastic Dermatoses of HIV- Kaposi’s Sarcoma- KS in an African
Many patients with AIDS develop disseminated KS, thought to be due to human herpesvirus 8. In most AIDS sufferers, the terminal stages are accompanied by a plethora of different infections (including KS). Credits: Figure 904 on p. 303 in Peters and Pasvol, Atlas of Tropical Medicine and Parasitology, 6th edition, (Philadelphia: Elsevier, 2007).

KS: arm and hand KS may regress, or can expand and coalesce into larger lesions and then ulcerate (as seen here). From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1139, picture from p

Kaposi’s Sarcoma Cutaneous manifestations of Kaposi sarcoma. The purplish hyperpigmented plaques and nodules are characteristic. Credits: Fig on p. 506 from Zitellis, Atlas of Pediatric Physical Diagnosis, 5th ed., (Philadelphia:Elsevier, 2007).

KS management: before and after intralesional vinblastine
Individual lesions may be treated with destructive methods like cryotherapy, intralesional chemotherapy (as here), alitretinoin gel, radiotherapy, and interferon. From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1140, picture from p

Description: Kaposi’s Sarcoma in an HIV+ Kenyan Woman Credits: Dr. Thor Swanson, MD; Siouxland Medical Educational Foundation, Sioux City, IA.

KS: arm and hand KS may regress, or can expand and coalesce into larger lesions and then ulcerate (as seen here). From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1139, picture from p

Aphthous Ulcers/Stomatitis
Viral Dermatoses Aphthous Ulcers/Stomatitis

Viral Dermatoses-Aphthous Ulcer
Aphthous ulcers are very common and easy to recognize. Their cause remains uncertain, although an association with human herpes 6 has been suggested. Found on freely moving, nonkeratinized mucosa, they may be single of multiple, are usually recurrent, and appear as painful small, round ulcerations with yellow-gray fibrinoid centers surrounded by red halos. Minor are less than 1 cm and major greater than 1cm. Treatment- nonspecific- topical corticosteroids, topical diclofenac, mouthwashes, etc. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Aphthous Ulcer in patient with HIV
FIGURE Aphthous ulcer. (Courtesy of Stephen Raffanti, MD, MPH.) Credits: Fig from Mandell et al, Infectious Disease, 2005.

Viral Dermatoses Varicella/Zoster

Varicella (Chickenpox) and Zoster (Shingles)
Varicella zoster virus (VZV) is HHV-3. Disease manifestations include chickenpox (varicella) and shingles (herpes zoster). Chickenpox has an incubation period of days (average 2 weeks) and his highly contagious, spreading by inhalation of infective droplets or contact with lesions. The incidence and severity of herpes zoster affects up to 25% of persons during their lifetime and increases with age due to an age-related decline in immunity against VZV. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Varicella (Chickenpox)
Fever and malaise are mild in children and more marked in adults. The pruritic rash begins prominently on the face, scalp, and trunk, an later involves the extremities. Maculopapules change in a few hours to vesicles that become pustular and eventually form crusts. New lesions may erupt for 1-5 days, so that different stages of the eruption are usually present simultaneously. The crusts slough in 7 to 14 days. Although the disease is often mild, complications such as secondary bacterial infection, pneumonitis and encephalitis occur in about 1% of cases and often lead to hospitalization. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Herpes Zoster (Shingles)
After the primary infection, the virus remains dormant in cranial nerves sensory ganglia and spinal dorsal root ganglia. Herpes zoster usually occurs among adults, but cases are reported among infants and children. Skin lesions resemble those of chickenpox. Pain is often severe and precedes the appearance of rash. Lesions follow a dermatomal distribution, with thoracic and lumbar roots being the most common. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Herpes Zoster A painful linear-zosteriform eruption of vesicles on an erythematous base is characteristic of herpes zoster. The eruption may be persistent, and verrucous lesions are not uncommon. From Ferri, Fred. Ferri’s Color Atlas and Text, 2009, p

Kenyan Girl with Herpes Zoster with Secondary Infection
Credits: Dr. Thor Swanson, Sioux City

HIV-related Herpes Zoster
This women with advanced AIDS had severe herpes zoster lesions. Her infant was also HIV positive. Credits: Fig. 879 in Peters, Atlas of Tropical Medicine 2007.

Description: Herpes Zoster (Shingles) in an HIV-infected boy. Such cases can be complicated by chronicity or dissemination. Credits: Pediatric AIDS Atlas, Baylor International Pediatric AIDS Initiative; Nat’l Library of Medicine

Description: Herpes Zoster (Shingles) in an HIV+ Kenyan patient Credits: Thor Swanson, MD; Siouxland Medical Educational Foundation, IA.

Description: Shingles in an American HIV+ patient. Credits: Thor Swanson, MD: Siouxland Medical Education Foundation, 2008.

Description: Shingles in an American HIV+ patient Credits: Thor Swanson, MD; Siouxland Medical Education Foundation, 2008.

HIV-Related Herpes Zoster
Description: Shingles in an American HIV+ patient Credits: Thor Swanson, MD; Siouxland Medical Education Foundation, 2008

VZV: Zoster with dissemination
Disseminated Herpes Zoster is defined as cutaneous involvement by greater than 3 contiguous dermatomes of more than 20 lesions scattered outside the initial dermatome, or systemic infection (hepatitis, pneumonitis, encephalitis). From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1136, picture from p

Warts/Human Papilloma Virus
Viral Dermatoses Warts/Human Papilloma Virus

Viral Dermatoses-Warts-General
Warts are caused by human papillomaviruses (HPVs). Typing of HPV lesions is not a part of standard medical evaluation except in the case of genital dysplasia. Genital HPV types are divided into low-risk and high-risk depending on the likelihood of their association with cervical and anal cancer. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Warts-Clinical There are usually no symptoms.
Tenderness on pressure occurs with plantar warts. Itching occurs with anogenital warts. Flat warts are most evident under oblique illumination. Periungal warts may be dry, fissured, and hyperkeratotic and may resemble hangnails or other nonspecific changes. Plantar warts resemble plantar corns or calluses. Treatment- Liquid nitrogen, keratolytic agents, Podophyllum, Imiquimod, operative removal, laser therapy, and other agents. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Warts-Essentials of Diagnosis
Verrucous papules anywhere on the skin or mucous membranes, usually no larger than 1 cm in diameter. Prolonged incubation period (average 2-18 months). Spontaneous “cures” are frequent (50% at 2 years for common warts). “Recurrences” (new lesions) are frequent. McPhee, 2012 Current Medical Diagnosis and Treatment, p

HIV-Related Condyloma Accuminata
Description: Condyloma Accuminata in an HIV+ patient Credits: Dr. Thor Swanson, MD, Siouxland Medical Educational Foundation

HIV-Related Warts Description: Severe cutaneous warts in a boy with HIV infection. Credits: Pediatric AIDS Pictoral Atlas, Baylor International Pediatric AIDS Initiative

HIV-Related Condyloma Accuminata
Description: Condyloma Accuminata in an HIV+ Kenyan Woman Credits: Dr. Thor Swanson, MD, Siouxland Medical Educational Foundation

Human papillomavirus infection
Human papillomavirus infections are common in HIV-infected patients. They may have unusual features, as demonstrated here, and may be refractory to therapy. From Ferri, Fred. Ferri’s Color Atlas and Text, 2009, p

HPV: Giant perianal condyloma
From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1131, picture from p

Molluscum Contagiosum
Viral Dermatoses Molluscum Contagiosum

Viral Dermtoses-Molluscum Contagiosum
Molluscum contagiosum, caused by a pox virus, presents as single or multiple dome-shaped, waxy papules 2-5 mm in diameter that are umbilicated. Lesions first are firm, solid and flesh-colored but upon reaching maturity become soft, whitish, or pearly gray and may suppurate. The principal sites of involvement are the face, lower abdomen, and genitals. The best treatment is by curettage or applications of liquid nitrogen. Molluscum is common in pts. with AIDS, usually with a CD4 count less than After starting ART, molluscum will usually spontaneously clear. McPhee, 2012 Current Medical Diagnosis and Treatment, p. 143.

HIV-Related Molluscum
Credits: Pediatric AIDS Pictoral Atlas, Baylor Int’l Pediatric AIDS Initiative; Nat’l Library of Medicine

HIV-Related Molluscum
The numerous lesions with the classical, umbilicated appearance seen here bear a superficial resemblance to those caused by smallpox. The condition is caused by infection with a DNA poxvirus that is spread by direct person-to-person contact and by fomites. Molluscum contagiosum can be extensive, as shown in this patient who is immunosuppressed with HIV infection. Credits: Figure 878, p. 276 in Peters and Pasvol, Atlas of Tropical Medicine and Parasitology, 6th ed., (Philadelphia: Elsevier, 2007).

Molluscum in AIDS Severe molluscum contagiosum in a pt. with AIDS.
Credits: Fig on p. 505 from Zitellis, Atlas of Pediatric Physical Diagnosis, 5th ed., (Philadelphia:Elsevier, 2007).

Molluscum contagiosum: giant
Molluscum contagiosum (MCV) commonly infects keratinized skin subclinically, can cause lesions at sites of minor trauma and in the infundibular portion of the hair follicle. From Dolin, Raphael et al. AIDS Therapy, 3rd edition, Info from p. 1131, picture from p

Molluscum contagiosum
FIGURE Molluscum contagiosum. (Courtesy of Stephen Raffanti, MD, MPH.) Credits: Fig in Mandell et. al, Infectious Diseases, 2005.

Molluscum in Pediatric HIV Patient
From Zitelli, Atlas of Pediatric Physical Diagnosis, 2007.

Viral Dermatoses Dengue Fever

Viral Dermatoses-Dengue- Cause
Dengue is due to a flavivirus transmitted by the bite of the Aedes mosquito. An estimated million cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever occur each year with numbers growing in both dengue fever and dengue hemorrhagic fever as a consequence of climactic factors, travel, and urbanization. Dengue is the second most common cause of fever (after malaria) in travelers returning from developing countries. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Dengue- Essentials of Diagnosis
Exposure 3-15 days (usually 7-10) days before onset. Sudden onset of high fever, chills, severe myalgias and arthralgias, headache, sore throat, and depression. Biphasic fever curve: initial phase, 3-7 days; remission, few hours to 2 days; second phase 1-2 days. Biphasic rash: evanescent, then maculopapular, scarlatiniform, morbilliform, or petechial changes from extremities to torso. Leukopenia and thrombocytopenia in the hemorrhagic form. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Dengue Lab Findings include: leukopenia, elevated transaminases, thrombocytopenia. Complications include: pneumonia, bone marrow failure, hepatitis, iritis, retinal hemorrhages, maculopathy, orchitis, oophoritis and more. Treatment entails: appropriate use of volume support (with Ringer lactate) in moderately severe shock and colloids in more severe cases), blood products, and pressor agents, and acetaminophen rather than nonsteroidal anti-inflammatory drugs for analgesia. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Distribution map of Dengue and Dengue Hemorrhagic Fever
The distribution of dengue is expanding regularly. Countries with outbreaks between 1975 and 1996 (Circles) and localities with imported cases during that period (Triangles). Credits: Fig 25 in Peters et al. Atlas of Tropical Medicine and Parasitology, 6th ed.

Dengue- Dengue Temperature Chart
Dengue is an Aedes (Stegomyia)-borne disease of wide distribution in the tropics and subtropics, and is caused by four serotypes of a species of positive, single-stranded RNA flavivirus. The incubation period is short, on average about 5 days. The illness is often of short duration, with a characteristic ‘saddle-back’’ fever. Credits: Fig. 23, Peters et. al, Atlas of Tropical Medicine

Dengue- Rash The figure shows the characteristic blanching rash of dengue fever. The rash is thought to be due to capillary vasodilatation in the skin and occurs shortly after defervescence on about day 5 of the infection. The rash lasts 1-5 days, sparing the palms and soles. It may be followed by a transient morbilliform or scarlatiniform rash that spreads centrally from the extremities during the second bout of fever. Credits: Fig. 24, Peters et. al, Atlas of Tropical Medicine.

Dengue- Breeding Site Breeding site of Aedes (Stegomyia) aegypti in a Thai cemetery. Numerous larvae of this vector were detected in flower pots decorating this altar in a Thai cemetery during an extensive outbreak of dengue. Credits: Fig. 26 Peters et. al., Atlas of Tropical Medicine and Parastiology, 6th ed.

Dengue- Vector Female Aedes (Stegomyia) polynesiensis. An important vector of dengue in the Pacific region. (x4). Credits: Fig. 27, Peters et al., Atlas of Tropical Medicine, 6th ed.

Dengue-Marked Ecchymoses in a Chinese Boy
Dengue Hemorrhagic Fever is believed to arise as a result of a second infection, possibly with a different serotype, following an initial attack of uncomplicated dengue via antibody- mediated enhancement. Immune complex formation leads to increased capillary permeability, which may be followed by hypovolemia and even disseminated intravascular coagulation. Cutaneous manifestations ranging from petechiae to gross ecchymoses characterise the infection, esp. in children. Credits: Fig. 28, Peters et. al., Tropical Medicine, 6th ed.

Dengue- Subcutaneous Hemorrhage
Subcutaneous hemorrhage in Dengue Hemorrhagic Fever. This Thai pt. had a large hemorrhagic lesion on the upper arm. Credits: Fig. 29, Peters et. al., Tropical Medicine, 6th ed.

Dengue- Scleral Hemorrhage
Scleral hemorrhage in Dengue Hemorrhagic Fever. Scleral hemorrhages often accompany the skin rash in this condition. Credits: Fig. 30, Peters et. al., Tropical Medicine, 6th ed.

Dengue- Cutaneous Manifestations
Cutaneous manifestations of dengue. A, Early maculopapular nonpruritic rash usually seen at the time of defervescence. B, Late hemorrhagic and purpuric skin changes of a patient with dengue hemorrhagic fever. Credits: Fig , Guerrant et. al, Tropical Infectious Diseases, 2nd ed., 2006, p (Courtesy of James H. Maguire, MD, Centers for Disease Control and Prevention, Atlanta, GA.) Copyright © 2006, 1999 by Elsevier Inc. All rights reserved.

Viral Dermatoses-Dengue- Key Points
Dengue is due to a flavivirus transmitted by the bite of the Aedes mosquito. An estimated million cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever occur each year with numbers growing in both dengue fever and dengue hemorrhagic fever as a consequence of climactic factors, travel, and urbanization. Dengue is the second most common cause of fever (after malaria) in travelers returning from developing countries. Exposure 3-15 days (usually 7-10) days before onset. Sudden onset of high fever, chills, severe myalgias and arthralgias, headache, sore throat, and depression. McPhee, 2012 Current Medical Diagnosis and Treatment, p

Conclusion 1. Discussed the importance of knowing tropical and HIV dermatology in general. 2. Reviewed common dermatological manifestations of tropical fungal diseases. 3. Reviewed common dermatological manifestations of HIV-related diseases. 4. Recounted atypical dermatological signs of mycobacterial and bacterial diseases. 5. Spoke about the dermatological appearances of viral diseases. 6. Used pictures and clinical cases from around the world, including the US, South Asia, Africa, and Central America to do the above.

References AAHIVM Fundamentals of HIV Medicine. Washington: American Academy of HIV Medicine, 2007. Arenas, Roberto and Roberto Estrada, Tropical Dermatology, 2001 edition. Published by Landes Bioscience. Bartlett John et al., Medical Management of HIV, 2007 ed., Baltimore: Johns Hopkins University Press 2007. Cook, Gordon C. et al., Manson’s Tropical Medicine , 6th ed.,Philadelphia: Elsevier, 2009, pp Fauci, Anthony et. al., editors; Harrison’s Principles of Internal Medicine, 17th ed. New York: McGraw-Hill, 2008. Fred F. Ferri, Ferri’s Color Atlas and Text of Clinical Medicine. Philadelphia: Saunders, 2009; p Guerrant , Richard et. al., Tropical Infectious Diseases, 2nd ed., Philadelphia: Elsevier, 2006. Habif, Thomas. Clinical Dermatology, 4th ed., New York: Mosby, 2003. Hay, William Jr. et al., editors; Pediatrics: Current Diagnosis and Treatment, 19th ed. New York: McGraw Hill, 2009. Kumar et. al, Robbins, 6th Edition, 2005. Mandell, Gerald et al., Principles and Practice of Infectious Disease, Philadelphia: Elsevier, 6th ed., 2005. Markle, William H. et. al., eds; Understanding Global Health, New York: McGraw-Hill, 2007. Peters, Wallace et. al., eds: Atlas of Tropical Medicine and Parasitology, 6th edition, Philadephia: Elsevier, 2007. Tyring, Stephen et. al, Tropical Dermatology, 1st edition, New York: Churchhill Livingstone, 2006. Zitelli et. al., Atlas of Pediatric Physical Diagnosis, 6th ed., Philadelphia: Elsevier, 2012. National Library of Medicine Image Library. At

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