-Ensherah Mokheemer. 1 P a g e

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1 -5 -Ensherah Mokheemer P a g e

2 The pictures were not included in the sheet so please refer to the slides to see them. Cutaneous abscesses: It is basically abscess in the cutaneous tissue. Collections of pus within the dermis and deeper skin structures (below the epidermis). Usually polymicrobial containing skin/mucous membrane flora; Skin flora it is the most common, S. aureus is the sole pathogen in 25% of cases. Clinical features painful, tender, fluctuant nodules, usually with an overlying pustule and surrounded by a rim of erythematous swelling. How we differentiate an abscess from inflamed lymph node or hematoma or other skin lesions? from the presence of a white head. And since there is an abscess then there is inflammation, pain tenderness and so on. Fluctuant nodule: Capable of being moved or compressed. The cutaneous abscesses when palpated there is motion detected inside them since they contain abscess. As for inflamed nodes they are red and painful but they are not fluctuant nodules since they contain no abscess. Treatment is Incision and drainage Antibiotics are rarely necessary (except in extensive infection or systemic toxicity, or immunocompromised). *Incision and Drainage without giving antibiotics is usually enough for immunocompetent patient, but recurrence is lower with giving antibiotics. *If the person shows toxicity or he is immunocompromised then incision and drainage is done and giving an antibiotic is a MUST. raised lesion, White head Hair follicle might Be port of entry 2 P a g e

3 Diabetic foot infections: -Defined as any infection (lesion) in a patient with DM that is below the malleolus. Everything we mentioned in our previous lectures can be part of diabetic foot. The commonest of these lesion is an infected diabetic ulcer, however, as mentioned it is a broad spectrum of infections ranging from: Paronychia cellulitis, myositis abscess formation, necrotizing fasciitis, septic arthritis, tendonitis, osteomyelitis. It is the most common cause of hospitalization in diabetic patients. -Because of the presence of several characteristic diabetic foot pathologies it is called Diabetic foot syndrome, and it requires a group of different practitioners to be dedicated for it. -Foot infections in DM are a common complication, they are often carry a high burden of morbidity and are notoriously difficult to manage (there are DF clinics!), there are other complications for DM, it affects the vision and the heart (atherosclerosis) but diabetic foot is more common. Why it affects the foot and not the hand??! The foot is the furthest form the heart so this is an indication of poor circulation, and less blood you have in certain area the more susceptible you are to get infection. Risk factors: Neural development of peripheral sensory, motor, and/or autonomic neuropathy, neuro-osteopathic deformity (e.g. Charcot joint*). *Charcot joint: refers to progressive degeneration of a weight bearing joint, in diabetic foot the destruction is most commonly in the ankle joint. Vascular vascular insufficiency (less white blood cells, less oxygen). Immune hyperglycaemia leading to poor immune function and wound healing. 3 P a g e

4 Other factors poor vision, limited mobility, previous amputations poor healthcare. The major underlying causes for diabetic foot are noted to be peripheral neuropathy and ischemia from peripheral vascular disease. -Patients with adequate healthcare are less likely to have lesions that are unnoticed, thus they are less likely to have infection in their foot. Etiology: We notice in the previous table the presence of 3 ulcers: 1- Infected ulcer (antibiotic-naϊve): Patients who have not had antibiotics for DFU in the previous month and it is the first ulcer and it is easily treated since it does not have resistance. 2- Infected ulcer chronic previous antibiotic therapy: Patients who have had antibiotics for DFU in the previous month, now the patient has been exposed in pathogens from the hospitals and he has gotten more diversity of pathogens. 3- Macerated ulcer: wet ulcers, it is filled with water and since pseudomonas prefers water it is the most common pathogen in this type of ulceration. 4 P a g e

5 Long-standing, non-healing wound with prolonged antibiotic: Infected wounds which takes long time to heal, the prolonged usage of antibiotic will lead to killing more and more normal flora and it will also lead to the emergence of resistant bacteria, so the antibiotic treatment is causing more harm than use in this case. But the guidelines still indicate on giving antibiotics to get rid of the invasive bacteria, surgical treatment in this case is effective, it is done by removing the necrotic tissue, because any wound which has necrotic tissue will never heal until this necrotic tissue is removed. Clinical features: Range from mild severe life threatening Please remember that the most aggressive pathogens are the obligate anaerobes. The stages of diabetic foot infection: 1-foot ulcer with no signs of infection. 2-foot ulcer with surrounding inflammation or cellulitis less than 2cm from the edge of the wound. 3-Local complications cellulitis more than 2cm from edge of wound, in addition to lymphangitis, spread beneath the superficial fascia, deep tissue abscess, gas gangrene (most aggressive because of the presence of obligate anaerobes), involvement of muscle, tendon, or bone. 4-systemic toxicity or metabolic instability fever, chills, tachycardia, hypotension, confusion, vomiting, leucocytosis, acidosis, hyperglycaemia, uraemia. Systemic toxicity occurs when the bacteria releases the toxin or antigens in the blood in amounts the overwhelms the immune system. -Note: Not every lesion in the leg is infected and requires antibiotic, the indication of infected lesion is erythema, if the erythema is less than 2cm it is less severe, but if it is more than 2cm then it indicates deeper infection meaning it is more aggressive. 5 P a g e

6 Diagnosis: Very Very important: 1-Clinical features: must assess perfusion (peripheral pulses), as well as sensation (using a mono filament), to check if there is vascular insufficiency of neuropathy. 2-Doppler ultrasound to determine ratio of ankle Vs brachial pressure index (ABPIs). Extra info: The ankle-brachial pressure index (ABPI) or ankle-brachial index (ABI) is the ratio of the blood pressure at the ankle to the blood pressure in the upper arm (brachium). Compared to the arm, lower blood pressure in the leg suggests blocked arteries due to peripheral artery disease (PAD). The ABPI is calculated by dividing the systolic blood pressure at the ankle by the systolic blood pressure in the arm. 3-Imaging (MRI) may help determine the extent of infection (osteomyelitis, fasciitis). In the diagnosis of diabetic foot MRI and CT are used not x-rays, we use MRI and CT to get detailed pictures of organs, soft tissues, bone and other internal body structures and see, whether there is swelling or how much the infection is spread. 4-Deep tissue specimens (not superficial swabs) need to be sent to microbiology lab for microscopy and culture before Antibiotics treatment. Note that superficial swabs are non-diagnostic, when superficial swabs are taken the pathogens in the deeper tissues will not be considered and thus will not be included in the treatment, for example if you take a superficial sample and your culturing for that sample showed s.aureus (since it is part of skin flora) you will give treatment only for that pathogen ignoring whether there are others in the deeper tissues and this will not help in the treatment of the foot infection. Management: 1-First you have to decide whether this patient is inpatient or outpatient. It is always preferable to keep the patients away from the hospital because the hospital contains many aggressive bacteria and pathogens so if you see that the patient s stat is manageable at home and can be treatd outside the hospital then this patient will be an outpatient. In case of the presence of severe ulcers or the ulcer is not responding to treatment or systematic toxicity signs then this patient is definitely an inpatient. 6 P a g e

7 2-Treatment: and it is divided to medical treatment and surgery. a) Medical treatment: initial infected ulcers empiric therapy Oral for mild cases and IV broad spectrum for severe cases. And do not give antibiotics for non-infected ulcers. b) Surgery: it is basically by debridement of dead, damaged, or infected tissue sever infections in deeper tissues, necrotizing fasciitis, gas gangrene, extensive tissue loss, critical limb ischemia. 3-Wound care plan following discharge. Papular and Nodular Lesions. Nodules are basically very large papules. Mycobacterium marinum: -infections of the skin may present as cellulitis or as raised erythematous nodules. It occurs because the body can t handle the presence of mycobacterium so the only way the body will contain them is by forming a tissue around them. It is red in colour (erythematous) because of inflammation. -Occupational hazard, usually for aquarium cleaners, fishermen, seafood handlers. -Organism growth requires lower temperatures than 37C (2432) and thus is limited only to skin. Diagnosis: needle aspiration, see acid fact bacilli. Treatment: rifampicin (rifampin)+ ethambutol for four months. 7 P a g e Cat-scratch disease: -It is caused by Bartonella henselae: Gram negative bacillus, usually grows on Columbia agar supplemented with 5% sheep blood. -Transmission cycle between cat and flea, then cats transmit to humans by bite or scratch. The transmission between the cat and human does not depend on the depth of the scratch, as long as you get scratched by an infected cat you will get infected.

8 -Symptoms: myalgia, arthralgia, malaise, anorexia, maybe low-grade fever. Signs: Lesions (papule, pustule or large vesicles) developing at the primary site of inoculation of Bartonella henselae. Then in (85-90%) of cases persistent painful regional IPSILATERAL Lymph adenopathy usually on the axillary region. Ipsilateral: on the same side of the body. Diagnosis: Serology (IgM, or IgG titers) or biopsy of lymph node. IgM appears first then IgG. Treatment: self-limited in immunocompetent, resolves within 8 weeks, there is increased risk of reaction if antibiotics given in first 48 hours. What we mean by a reaction is an adverse one, a not wanted reaction might occur if antibiotics were given in the first 28 hours, that is because the body will still not have made the appropriate antibodies and giving an antibiotic will release the foreign proteins from the break down of bacteria making the situation much worse and another disease will emerge. 8 P a g e Schistosomiasis: -Caused by Schistosoma a parasitic blood fluke (trematodes, life cycle in two hosts). -Multiple erythematous papules develop in schistosomiasis; each represents a cercarial invasion site (known as bilharzia), the parasite is found in contaminated water. If it is diagnosed early it can be easily treated by giving praziquantel. But if it is not caught early it will keep damaging the tissue causing liver and kidney damage in the end. - Acute phase (Katayama fever, whole body hypersensitivity fever malaise. Etc) Diagnosis: stool and urine microscopy (shows the presence of eggs).

9 Treatment: single dose Praziquantel (antiparasitic). Skin signs: Especially in S. cercariae but other parasites as well (called swimmers itch) due to allergic reaction at site of invasion by parasites. Swimmer s itch: is a short-term immune reaction occurring in the skin of humans that have been infected by water-borne schistosomiases. Symptoms, which include itchy, raised papules, commonly occur within hours of infection and do not generally last more than a week. It is usually due to a parasite from the freshwater penetrating the skin and causing nodule. Note that the parasite lives in freshwater not in sea water because they cannot survive in salty environment. Swimmer s itch The carrier of the parasite is the snails that lives in the contaminated water. 9 P a g e

10 Leprosy: -Leprosy is caused by Mycobacterium leprae (acid fast bacillus). - Skin nodules as well as thickened subcutaneous tissue are prominent features of lepromatous leprosy. - Chronic infection of the skin, causes granulomas at the body aims to contain the bacilli - Long incubation (years, 3upto 20 years), that means they well overpowered by the immune system but when immunity decreases usually as a result of aging it will be activated and nodules will start to appear. - Transmission mostly by nasal secretion of Untreated patients, however low risk from casual (direct) contact is present. - Skin changes: bilateral symmetrical macules and papules, progresses to nodules and even plaques, they are usually present on the nose, chin, the ears and eyebrows, this manifestation is called lion face. - Has two types: a) Tuberculoid patient has intact immunity, usually nerve changes predominate. b) Lepromatous where skin changes predominate (defect in cell immunity). - Usually hypopigmented in dark skinned people and seen on face, wrists, buttocks and kneed, but spares groin and axilla (folded skin has higher temp which doesn t favour its growth). Diagnosis: Acid fast stain skin smears and biopsy (stain especially +ve in lepromatous leprosy). Treatment: Anti-mycobacterial drugs (Dapsone and Rifampin), treatment at early stages is for 12 years, in leprosy treatment maybe lifelong. 10 P a g e

11 Syphilis: - Large nodules or gummas are features of tertiary syphilis (late untreated syphilis). - whereas flat papulosquamous lesions are characteristic of secondary syphilis. Primary syphilis is typically acquired by direct sexual contact with the infectious lesions of another person. Approximately 3 to 90 days after the initial exposure (average 21 days) a skin lesion, called a chancre, appears at the point of contact. Secondary syphilis occurs approximately four to ten weeks after the primary infection. The rash may become maculopapular or pustular. Tertiary syphilis may occur approximately 3 to 15 years after the initial infection. People with tertiary syphilis are not infectious. Condylomata lata or condyloma latum, is a cutaneous condition characterized by wart-like lesions on the genitals. They are generally symptoms of the secondary phase of syphilis, caused by the spirochete, Treponema pallidum. *Note: The difference between chickenpox and syphilis is the age of the patient. Human Papilloma virus: - Human papillomavirus may cause singular warts (verruca vulgaris) or multiple warts in the anogenital area (condylomata acuminata this is a major problem in HIV patients). Please differentiate between: *condyloma acuminata: a sexually transmitted infection caused by certain types of human papillomavirus (HPV) and it is a major problem in HIV patients. * Condylomata lata: are generally symptoms of the secondary phase of syphilis, caused by the spirochete, Treponema pallidum. -Human Papilloma virus it is the most common sexually transmitted disease. 11 P a g e

12 - HPV is an Sexually transmitted disease, and can cause cervical cancer (16, 18, 31,33..). How it causes cancer? the virus begins to make the proteins it encodes. Two of the proteins made by high-risk HPVs (E6 and E7) interfere with cell functions that normally prevent excessive growth, helping the cell to grow in an uncontrolled manner and to avoid cell death. As the persistently infected cells continue to grow, they may develop mutations in cellular genes that promote even more abnormal cell growth, eventually leading to cancerous tumors. - Verruca vulgaris: HPV 1,2,4, 7, and common in children and young adults. Warts are caused by infection with a type of human papillomavirus (HPV), They are not cancerous. - Transmitted by skin contact, sharing certain tools/cloth. - Usually on the hands and nail edges (digits), can auto inoculate face. -Management: Dermatologist Diagnosis of skin infections: As discussed, so far diagnosis of skin infections depends on three main clinical observation: the appearance of lesion (macule, papule, vesicle etc) location within the layers of soft tissues (stratum corneum, epidermis, dermis..etc) location relative to the body (trunk, face, extremities..etc). Aiding information that helps fine tune the pathogenesis of the infective agent are: The temporal progression of the lesions (e.g. appear in crops, or appear acutely..etc). the patient s travel history (for exogenous or exotic sources of pathogens). animal exposure or bite history. 12 P a g e

13 age of patient underlying disease status. Lifestyle. However, even the most experienced clinician will find it difficult to diagnose all infections of the skin and soft tissue by History and inspection alone. Thus, aiding diagnostic tests can help: Soft tissue radiography, CT, and MRI may be used to help determine the depth of infection They help in assessing deeper infections. For example: you might recall that serious ones like fasciitis are rapidly progressing. evidence of a systemic inflammatory response syndrome (to find a local infection that may be releasing toxins). another value for these tests is for defining a localized abscess or detecting gas in tissue (air pockets) where anaerobes are present (not GAS infection, which may only show swelling as shown in next figure). lab diagnostics: Aspiration (without saline better less dilution) or punch biopsy with frozen section might help if imaging is positive, however, there is a large false negative rate 80%. The left side is more swollen than the right side and this tell us the degree of fasciitis. Frozen sections are especially useful in distinguishing SSSS from TEN (?) also quite valuable in cases of necrotizing fasciitis (determining depth and level of involvement). 13 P a g e

14 Open surgical inspection (+debridement) is the optimal way to determine the extent and severity of infection, also is the superior method to obtain specimen for culture and Gram stain. Although surgical approach maybe an aggressive approach, it is an important step and maybe lifesaving in the course of fulminant infections where there is evidence of systemic toxicity. Treatment, overview. Furuncles, carbuncles, and abscesses caused by MRSA and MSSA are commonly encountered Rx here depends on the size of the lesion. Furuncles < 2.5 cm in diameter treated with moist heat. Furuncles > 4.5 cm of erythema + induration surgical drainage larger lesions + fever, chills, or leucocytosis drainage and antibiotic treatment. A study in children showed that surgical drainage of abscesses (mean diameter, 3.8 cm) was as effective when used alone as when combined with trimethoprim-sulfamethoxazole treatment. However, recurrence was less in groups that added antibiotics with incision and drainage. Myositis and Myonecrosis: Myositis - Muscle involvement (inflammation or infection). The muscle involvement depends on the type of the pathogen and the type of reactions that occurs. -It can occur with: viral infection (such as influenza, dengue, or coxsackievirus B infection). In case of viral infections, the muscle itself is not involved in the infection it is involved in the inflammation reactions. parasitic invasion (trichinellosis, cysticercosis, or toxoplasmosis). 14 P a g e

15 Myalgia (muscle pain) can occur in most of these infections, severe muscle pain is the hallmark of pleurodynia (coxsackievirus B), trichinellosis, and bacterial infection. - Acute rhabdomyolysis (active breakdown of damaged muscle) predictably occurs with clostridial and streptococcal myositis, as both these organisms have enzymes that breakdown muscle. Rhabdomyolysis is less so associated with influenza virus, echovirus, coxsackievirus, Epstein Barr virus, and Legionella infections. Myonecrosis (Necrotizing myositis) - S. pyogenes (GAS) may induce primary myositis (referred to as streptococcal necrotizing myositis) in association with severe systemic toxicity. this is basically necrotizing fasciitis (Type2) that involves the muscle tissue. - Myonecrosis occurs in about 50% of cases in typical necrotizing fasciitis without muscle involvement being the primary tissue infected. meaning muscles are affected by necrosis when the surrounding fascia is involved, even without the infection being active in the muscle itself! (The muscle is not infected by the pathogen but it is involved in the reactions of infection and inflammation). Pyomyositis: - Pyomyositis, or pus forming infection of the skeletal muscle tissue, is usually due to S. aureus (remember it is the typical pus former in skin). - Pyomyositis usually arises from haematogenous spread (deeper infections, muscle and bone, are typically more related with haematogenous spread rather direct inoculation). Muscles and bones are more likely to be infected by blood rather than direct inoculation because it is difficult to have a trauma that is so severe that it reached the muscles and the bone and broke through all the barriers and immunity reactions. So, bones and 15 P a g e

16 muscles are from hematogenous root rather than from direct inoculation. - Abscess formation is the usual consequence when these pyogenic bacteria reach the muscle tissue. - Pyomyositisis common in tropical areas, and generally has no known portal of entry (in contrast to necrotizing fasciitis). - Cases of pyomyositis caused by MRSA producing the PVL toxin have been described among children in the United States. - Muscle infection begins at the exact site of blunt trauma or muscle strain Pyomyositis infection usually remains localized, and shock does not develop unless organisms produce: toxic shock syndrome toxin 1 (which acts as a super antigen, that causes exaggerated immune response that is many fold the normal response shock. enterotoxins (exotoxins produced by S. aureus). If the patient lacks antibodies to the toxins above then they are prone to developing toxic shock when these toxins are produced. Epidemiology: Occurs in males more than females, and more in tropical climate in two main age groups: children (aged 2 5 years) adults (aged years). - In temperate climes: pyomyositis typically affects adults or the elderly (not children). - In temperate climates if it happened then the Patient usually has predisposing conditions such as HIV, infection, DM, malignancy, cirrhosis, renal insufficiency, organ transplantation (reduced cell immunity), immunosuppressive therapy. Other risk factors include trauma, IDU, and concurrent infections (toxocariasis roundworms, VZV). 16 P a g e

17 In case of pyomyositis there are two questions must be answered: First since it is mostly from haematogenous spread then why there is bacteria in the blood? Secondly in temperate climate what is the underlying cause (predisposing factor)? Microbiology: S. aureus 90% of tropical cases 75% of temperate cases. GAS account for 1 5% of cases all around. E. coli ST131 is an emerging cause in patients with haematological malignancy. Extra: Haematological malignancies are cancers that affect the blood and lymph system, Escherichia coli is the most common cause of gramnegative bacteraemia including the patient of cancer and since E.coli is in the blood of these patients it will spread to the muscles and cause pyomyositis. Uncommon causes B, C, and G streptococci and S. pneumoniae, and S. anginosus. Rare causes include Enterobacteriaceae, Y. enterocolitica, N. gonorrhoeae, H. influenzae, A. hydrophila, anaerobes, B. mallei, B. pseudomallei, A. fumigatus, Candida spp., MTB, and MAC. Clinical features : 20% and 50% of cases patient have had recent blunt trauma or vigorous exercise of the affected area myolysis- The muscle area is damaged and becomes susceptible for infections). Vigorous exercise: when you move your muscles very much in a way that will overwhelm the oxygen capacity of that muscle, lactic acid will form, and the blood supply for that muscle will decrease, this muscle will eventually become a prime location for bacteria. Seen more in the lower extremity (thigh, calf, gluteal muscles), but not limited to that area and can affect any muscle group. 17 P a g e

18 Multifocal infection occurs in up to 20% of cases! Since it is usually from a hematologic cause, the patient must be assessed for complications of bacteraemia (endocarditis) clinical stages: stage 1 (early invasive stage) crampy local muscle pain, swelling, and low-grade fever. Induration (hardening) of the affected muscle + leucocytosis may be present.this stage is usually undiagnostic or mistaken with other infections. stage 2 (suppurative stage) at days after onset of symptoms (most patients present at this stage). fever, very sharp muscle tenderness and swelling an abscess may be clinically apparent, aspiration of which yields pus. There is marked leucocytosis stage 3 (systemic stage) the affected muscle is fluctuant. Patients may present with complications of S. aureus bacteraemia, e.g. septic shock, endocarditis, septic emboli, pneumonia, pericarditis, septic arthritis, brain abscess, and ARF. Rhabdomyolysis may occur. Diagnosis : Early pyomyositis is difficult to distinguish from other Dx (thrombophlebitis, muscle haematoma, muscle rupture, fever of unknown origin osteomyelitis). Iliacus pyomyositis may mimic septic arthritis of the hip, and iliopsoas pyomyositis may mimic appendicitis. Imaging MRI is gold standard technique (may show muscle enhancement and intramuscular abscesses see the picture below). CT (may detect muscle swelling and well-defined abscesses). Ultrasound can be helpful for Dx and Rx. This is stage 1 pyomyositis as you can see it can be misdiagnosed as cellulitis 18 P a g e

19 Microbiology diagnostic aspirates before starting Abx to get a specific culture BCs are only positive in 10% of tropical cases and 35% of temperate cases Management: Antibiotics stage 1 antibiotics alone HOWEVER, most patients present with stage 2/3 disease and require antibiotics+ drainage. Empiric therapy for these stages: Directed against S. aureus and streptococci (flucloxacillin or vancomycin if MRSA is suspected or there is a risk of MRSA). Immunocompromised patients broader Abx such as piperacillin tazobactam ± vancomycin. Once culture is out Tailored Abx for 34 weeks. Drainage percutaneous drainage Dx and Rx (drainage and send drain sample for Micro) This may be CT guided or ultrasound guided. Sorry for any mistakes, and please do not curse me if you found this sheet very long. Good luck 19 P a g e