Infection Flashcards

Question

What are the signs and symptoms of malaria?

Answer 1

Headache, weakness, myalgia, arthralgia, diarrhoea, anorexia and loss of appetite, Less common = N+V, pallor, abdo pain P falciparum = seizures, jaundice and Anuria

Answer 2

Thick and thin blood film - seen in erythrocytes Malaria PCR blood FBC - variable WCC but possible anaemia ABG - metabolic acidosis in severe Urinalysis - mod protein increase LFTs/RFTs = variable but possibly abnormal

Answer 3

An infection caused by the varicella zoster virus, resulting in chicken-pox, generally characterised by fever, malaise and a generalised pruritic vesicular rash that begins on the face/scalp and spreads to the chest.

Answer 4

9-11yo, exposure, unimmunised

Answer 5

Generalised vesicular pruritic rash that begins on the face and spreads distally across the torso. Vesicles on mucosal membranes. Malaise fever <38 Preceding symptoms (by 1 week) - headache, sorethroat, tachycardia, fatigue.

Answer 6

Usually a clinical diagnosis Viral PCR/Culture can be done. ELISA for IgG ab can be done If pregnant perform USS.

Answer 7

Paracetamol + antihistamine (diphenhydramine) | Severe = acyclovir 10mg/kg IV 8hrly

Answer 8

Bacterial infection through breaks in skin 1/3 get reactivation -> shingles Reyes syndrome

Answer 9

Self-limiting LRTI Inflammation of the bronchioles. CRITERIA: (a) an acute illness of <21 days; (b) cough as the predominant symptom (c) at least 1 other lower respiratory tract symptom, such as sputum production, wheezing, chest pain; (d) no alternative explanation for the symptoms.

Answer 10

One of the most common conditions encountered in clinical practice. Acute bronchitis is among the most common adult outpatient diagnoses. In the UK, respiratory tract infections account for 300 to 400 consultations per 1000 patients annually. The highest incidence is in the autumn and winter.

Answer 11

Most cases of acute bronchitis are viral infections. The most common viruses implicated in acute bronchitis are the same as those that cause URIs and include coronavirus, rhinovirus, respiratory syncytial virus, and adenovirus. May be Chlamydia pneumoniae and Mycoplasma pneumoniae in YOUNGER PTs Bordetella bronchiseptica if immunocompromised

Answer 12

STRONG Viral or atypical bacterial infection exposure WEAK Cigarette smoking Household pollution exposure

Answer 13

``` COMMON <30 day cough Productive cough No Hx chronic illness Exclusion of pneumonia, CHF, PND - ie NO RALES Low grade fever ``` UNCOMMON Wheezing Rhonchi

Answer 14

Clinical diagnosis Possible to do PFT CXR may rule out pneumonia if unclear CRP - order if considering ABx

Answer 15

Mild - no wheeze Observation Significant wheeze/cough SABA 1-2 puffs 4-6hrly Antitussive - dextromorphan 20mg orally or codeine phosphate 15-30mg Cough persisting beyond 4w Evaluate for other causes In patients with risk factors or other symptoms suspicious for GORD, an empirical trial with an H2 antagonist or proton-pump inhibitor may be warranted.

Answer 16

Nearly all patients with acute bronchitis recover within 6 weeks of their initial symptoms. Patients generally return to full function with no residual symptoms following acute bronchitis.

Answer 17

Chronic cough | Pneumonia (older pt)

Answer 18

Acute bronchitis Acute bronchitis can also present as wheezing that resembles asthma with minimal cough, or as a nocturnal cough only. While most patients with acute bronchitis will have a productive cough, patients in later phases of the illness may have a non-productive cough.

Answer 19

Urticaria (also called hives) are erythematous, blanching, oedematous, non-painful, pruritic lesions that typically last less than 24 hours and leave no residual markings upon resolution. Approximately 40% of episodes of urticaria have associated angio-oedema. Angio-oedema is swelling involving the deeper layers of the sub-dermis and can occur in both the acute and chronic setting. <6w = acute >6w = chronic

Answer 20

The life-time prevalence for acute urticaria is approximately 20% While the majority of these cases are acute and self-limiting events, roughly 30% of people will go on to experience prolonged symptoms. Acute urticaria is more common in children and adolescents than in adults, while chronic urticaria more typically affects adults. In chronic urticaria, women are affected more often than men (60% versus 40% of cases, respectively). Incidence of ACE inhibitor-related angio-oedema has been reported to be more common in black people compared with white people

Answer 21

``` TYPES: Acute Chronic Physical Angio-oedema Other ``` Many cases of acute urticaria and/or angio-oedema are allergic in nature and caused by an IgE-mediated reaction. The most common agents involved are drugs (e.g., penicillins, sulfonamides, muscle relaxants, diuretics, NSAIDs) and foods (e.g., milk, eggs, peanuts, tree nuts, finfish, shellfish). Insect bites or contact with other allergens can also lead to acute urticaria and/or angio-oedema. Non-IgE-mediated mechanisms can also be responsible and these cases tend to involve certain drugs (e.g., NSAIDs, opioids, vancomycin), radiocontrast dye, or acute viral infections (especially in children). The aetiology of chronic urticaria and/or angio-oedema is far more difficult to elucidate. Approximately 40% of cases are thought to be autoimmune in nature, while many cases are idiopathic. Unlike in acute urticaria, less than 10% of patients with chronic urticaria have an identifiable, exogenous cause of their disease. Individuals with physical urticaria do not experience lesions in the absence of triggers, whereas individuals with acute or chronic urticaria experience spontaneous and unpredictable lesions. Of note, strong emotional situations are often reported to be a significant exacerbating stimulus.

Answer 22

``` COMMON Erythematous oedematous lesions Pruritus Resolution within 24hrs Swelling of face/tongue/lips Blanching lesions ``` UNCOMMON Stridor

Answer 23

FBC with differential Complete metabolic panel Urinalysis - may show proteinuria, bacteriuria, or presence of white cells ESR - elevated C-reactive protein - elevated anti-IgE receptor antibody and related tests - elevated or normal antithyroid antibodies - Positive in Hashimoto thyroiditis antinuclear antibodies (ANA) - positive in many rheumatological diseases C4, C1 esterase inhibitor level + function - decreased in hereditary angio-oedema C1Q levels - normal levels in hereditary angio-oedema; low levels in acquired angio-oedema

Answer 24

STRONG FHx Exposure to drug trigger - (e.g., penicillins and cephalosporins), cardiovascular drugs (e.g., amiodarone, procainamide), immunotherapeutics and vaccines, cytostatic agents (e.g., bleomycin, cisplatin, fluorouracil), ACE inhibitors, calcium-channel blockers, and various drugs that can cause non-specific histamine release (e.g., NSAIDs, narcotics, succinylcholine, amfetamine, hydralazine, and radiographic contrast media). Exposure to food triggers - eggs, nuts, and shellfish are particularly common triggers. Recent viral infection Recent insect bites WEAK Female sex - women are affected more often than men (in a ratio of 2:1)

Answer 25

``` With airway involvement: Adrenaline + airway protection H1 antihistamine IV corticosteroids Trigger identification and avoidance ``` Hereditary angio-oedema with airway involvement: Airway protection C1 inhibitor / ecallantide / icatibant ``` Chronic: H1 antagonists H2 antagonists Systemic corticosteroids LT-receptor antagonists Alternative immunomodulating therapy - omazilumab / ciclosporin / azathrioprine / hydroxychloroquine / dapsone / colchicine / methotrexate ```

Answer 26

Excoriations Sedation (first gen antihistamines) Skin infection

Answer 27

The prognosis for patients with acute urticaria is excellent. The vast majority of patients with urticaria respond well to therapy with non-sedating antihistamines, and the condition is short-lived. Patients with chronic urticaria also generally do well, but their disease course is typically more prolonged. Most patients can be managed with antihistamines alone; only a small sub-set of patients require additional medicines for control of symptoms. Patients with physical urticaria or urticarial vasculitis tend to have a more severe clinical course. Patients with concurrent disorders, such as autoimmune thyroiditis, may be more difficult to treat successfully and require concurrent therapy for the associated condition. A prospective study published in 2004 found that duration of urticaria was longer in patients who had associated angio-oedema or had positive anti-IgE receptor antibody.[49] As a general rule, spontaneous resolution of chronic urticaria occurs in up to 50% of patients within 1 year. By 5 years, 80% of patients will experience resolution of symptoms. However, patients whose chronic urticaria has resolved can still experience recurrence several years later.

Answer 28

Urticaria + angio-oedema Rarely, a patient presents with angio-oedema in the absence of any associated urticaria. This unusual pattern should prompt additional evaluation for hereditary angio-oedema, acquired angio-oedema, or drug-related angio-oedema (e.g., ACE inhibitor related). For patients with urticaria, unusual features can include pain/burning rather than pruritus, lesions that last longer than 24 hours, or lesions that leave residual bruising or discoloration upon resolution. These features should raise the possibility of a different diagnosis, such as urticarial vasculitis.

Answer 29

Urticaria + angio-oedema Rarely, a patient presents with angio-oedema in the absence of any associated urticaria. This unusual pattern should prompt additional evaluation for hereditary angio-oedema, acquired angio-oedema, or drug-related angio-oedema (e.g., ACE inhibitor related). For patients with urticaria, unusual features can include pain/burning rather than pruritus, lesions that last longer than 24 hours, or lesions that leave residual bruising or discoloration upon resolution. These features should raise the possibility of a different diagnosis, such as urticarial vasculitis.

Answer 30

A systemic vasculitis, first described by Hulusi Behcet, a Turkish dermatologist, Behcet's syndrome is most commonly seen in Turkey, Israel, the Mediterranean basin, and eastern Asia (where Japan and South Korea report the most cases). It can cause skin and mucosal lesions, uveitis, major arterial and venous vessel disease, and GI and neurological manifestations. These can present in various combinations and sequences in patients over time.

Answer 31

Patients are most commonly from the Middle East, the Mediterranean region, and eastern Asia, with Japan and South Korea leading the list. Behcet's syndrome is rare in northern Europe and Africa. The prevalence in Turkey is 1 in 250 of the adult population. It can affect any age group, but it is rare before puberty and after the sixth decade. It is most commonly seen in patients in their second and third decades. M=F

Answer 32

Aetiology is not known. Family studies show a possible genetic predisposition. Increased inflammation and immunological mechanisms play a role, but it is not clear whether it is an auto-immune or auto-inflammatory disorder. Unlike other auto-immune diseases, Behcet's syndrome is not typically associated with auto-antibodies, Raynaud's disease, Sjogren's syndrome, thrombocytopenia, haemolytic anaemia, sun hypersensitivity, serosal involvement, or increased risk of other auto-immune diseases.

Answer 33

STRONG Age 20-40 FHx Genetic predisposition

Answer 34

COMMON Oral ulcers - these lesions are always in the moist mucosal surfaces inside the mouth and do not occur on the outer surfaces of the lips. Genital ulcers - Can be painful and scar, especially when on the scrotum. Tend to get infected, which interferes with the healing process. Penis is usually spared. Uveitis - Panuveitis subtype is the leading cause of morbidity. It is more common in males and also has a more severe course in males. Acne lesions on arms/legs Erythema nodosum - usually in lower extremities and tend to resolve in 1-2 weeks. Short duration of symptoms - symptoms in Behcet's syndrome tend to abate with time Superficial thrombophlebitis hypopyon stroke eye pain, blurry vision, photophobia, or photosensitivity memory loss headache, confusion, or fever haemoptysis, cough, shortness of breath, or chest pain eye redness or tearing impaired speech, balance, or movement cramping abdominal pain, diarrhoea, or GI ulceration

Answer 35

``` Pathergy testing - formation of pustule within 48 hours. 60% positive RF - neg ANA - neg ANCA - neg HLA-B51 - present ``` MRI - white matter changes commonly involving midbrain Colonoscopy - inflammation and aphthous-type ulcers, possibly vasculitis on biopsy Upper GI endoscopy - inflammation and aphthous-type ulcers, possibly vasculitis on biopsy High-resolution chest CT / CT angiography - haemorrhage, pulmonary aneurysm

Answer 36

Mucocutaneous ulcers 1st topical triamcinolone paste 2nd colchicine or oral corticosteroid or immunosuppressive therapy 3rd TNF-alpha inhibitor Eye involvement prednisolone plus azathioprine prednisolone plus immunosuppressant therapy Gastrointestinal involvement prednisolone plus immunosuppressant therapy CNS involvement and/or large-vessel disease prednisolone plus immunosuppressant therapy

Answer 37

Many patients go into remission with time. Most new manifestations present within the first 5 to 6 years after the onset of symptoms. Because patients are not likely to require lifelong treatment with immunosuppressants, long-term complications of treatment are a lesser concern. If symptoms are controlled and flares are minimal for 1 to 2 years, medication doses may be tapered down to allow observation on whether the severity of the syndrome has abated. CNS involvement occurs in 2 types: parenchymal and dural sinus thrombi. Dural sinus thrombi are easier to treat with immunosuppressants and have a better prognosis. Parenchymal involvement has a poor prognosis, is difficult to treat, and responds intermittently to treatment. Large-vessel disease also has a worse prognosis.

Answer 38

Blindness - More likely in males. Left untreated, eye involvement could progress to blindness within 5 years. increased risk of neoplasia with long-term immunosuppressant use Aneurysm formation

Answer 39

Behcet's syndrome

Answer 40

Behcet's syndrome

Answer 41

An acute, self-limiting inflammation of the upper respiratory tract mucosa that may involve any or all of the nose, throat, sinuses, and larynx. The condition is rarely characterised by a discrete set of specific symptoms, with the illness varying according to individual and causative pathogen. Occasionally, there is spread to the lower respiratory tract. Symptoms include sore throat, sneezing, blocked, and/or runny nose, headache, cough, malaise, and low-grade fever. The condition is associated with more than 200 virus subtypes. ◊ Most of the population experience at least one episode per year; these are usually self-limiting and resolve within a few days. ◊ Diagnosis is generally clinical, based on history and examination. Investigations may be required when symptoms worsen or do not resolve in the usual timeframe. ◊ Treatment includes reassurance that this is a self-limiting condition, rest, adequate fluid intake, and an analgesic/antipyretic for pain/fever. Antibiotics are not recommended. ◊ Decongestants and/or antihistamines may have a role in reducing nasal symptoms in adults; however, the evidence is limited, and these treatments are generally not recommended in young children. Antitussives may be used for cough; however, there is no evidence to support or refute their use, and opioids are not recommended for this indication in children and adolescents under 18 years of age. ◊ Complications include bacterial infections such as otitis media, sinusitis, or pneumonia.

Answer 42

``` Children = 6-8 Adults = 2-4 URTs = 11% GP practices ```

Answer 43

``` Rhinovirus = 50% Coronavirus = 15% Influenza = 10% ``` Pharyngitis is commonly due to adenoviruses, which can also cause lower respiratory tract infections. Common respiratory tract bacteria ( Streptococcus pneumoniae , Haemophilus influenzae , Moraxella catarrhalis) may be associated with the common cold

Answer 44

``` STRONG Exposures Young age Winter Day-care CS exposure ```

Answer 45

COMMON Acute onset 1-2 days Rhinitis (NB - Coloured secretions are often a sign of oxidation and do not necessarily indicate any complications to a viral illness bacterial superinfection.) Sneezing PN-drip Cough Fever (more likely in children, if >38 -> seek alternative diagnosis) Non-specific red pharynx Nasal oedema, erythema Pulse <100 + NO hypotension OTHER Malaise, myalgia, halitosis

Answer 46

None needed WCC may be raised Possible to do throat swab to assess for streptococcal infection Heterophile Ab testing if suspecting infectious mononucleosis Can rule out sinusitis

Answer 47

1st - reassurance + supportive care +/- antipyretic / analgesic ibuprofen: children: 5-10 mg/kg orally every 4-6 hours when required, maximum 30 mg/ kg/day; adults: 200-400 mg orally every 4-6 hours when required, maximum 2400 mg/day +/- decongestant ipratropium nasal: (0.06%) children 6-11 years of age: 2 sprays in each nostril three times daily when required; children ≥12 years of age and adults: 2 sprays in each nostril three to four times daily when required +/- antihistamine cetirizine/pseudoephedrine: children ≥12 years of age and adults: 5 mg/120 mg (1 tablet) orally (extended-release) twice daily when required +/- antitussive Honey has been shown to offer more relief of cough symptoms compared to no treatment, placebo, and diphenhydramine in children aged 1 to 18 years, but is not better than dextromethorphan.[

Answer 48

2 week max recovery

Answer 49

common cold

Answer 50

``` Otitis media Asthma, acute exacerbation Sinusitis Bronchospasm Pneumonia (CAP) COPD ```

Answer 51

Cytomegalovirus (CMV) is a ubiquitous beta-herpes virus that infects the majority of humans. Primary infection in individuals with normal immune function is usually asymptomatic. After primary infection, CMV establishes a state of lifelong latency in various host cells, with periodic sub-clinical re-activations that are controlled by a functioning immune system. When re-activation (or primary infection) occurs in patients with severely compromised immune function (transplant patients or patients with AIDS and CD4 count <50 cells/microlitre), uncontrolled CMV replication often ensues, which leads to the clinical manifestations characterised by fever, bone marrow suppression, and tissue-invasive disease. ◊ In people with normal immune systems, CMV infection is often asymptomatic or manifests as infectious mononucleosis-like syndrome (fever, lymphadenopathy, and atypical lymphocytosis). ◊ In immunocompromised people (patients with AIDS and transplant recipients), disease manifests with fever, bone marrow suppression, and tissue-invasive disease such as pneumonitis, hepatitis, colitis, nephritis, and retinitis. ◊ In the fetus, CMV infection may lead to cytomegalic inclusion disease, characterised by severe neurological abnormalities, intellectual disability, and hearing defects. ◊ Tests for diagnosis include: serology, pp65 antigenaemia test, histopathology, and nucleic acid amplification and detection systems, most commonly quantitative polymerase chain reaction-based assays. ◊ In immunocompetent people, infection is usually self-limiting; therefore, treatment is usually not indicated. ◊ In patients with compromised immune function, the treatment of choice is oral valgancicllovir or intravenous ganciclovir. Intravenous foscarnet and cidofovir are less preferred agents.

Answer 52

CMV is a ubiquitous virus that infects people regardless of age, sex, race, or socioeconomic and geographical backgrounds. CMV seroprevalence rate ranges from 60% to 100% depending on the population. Seroprevalence is generally higher in the developing countries compared with countries in the developed world, and is higher in urban compared with rural communities.

Answer 53

CMV is a member of the herpes virus family. It contains a genome of double-stranded linear DNA, an icosahedral viral capsid, and a viral envelope protein that includes the highly immunogenic glycoprotein B. The biological characteristic of all herpes viruses, including CMV, is the ability to establish latency after primary infection. Such a biological characteristic allows for periodic viral re-activations during the life of the human host. ``` Routes of transmission include person-to-person spread (kissing, intimate contact, sexual intercourse), vertical transmission (mother-to-child transmission resulting in congenital infection), blood transfusion, and organ or haematopoietic stem cell transplantation. ```

Answer 54

STRONG CMV D+/R- status (donor CMV seropositive, recipient seronegative) in solid organ transplant recipients CMV R+ (recipient seropositive) in transplant recipients Some immunosuppressive - High doses of corticosteroids, mycophenolate mofetil, anti-thymocyte globulin, anti-lymphocyte globulins, and alemtuzumab AIDs IBD ICU Newborn in CMV/infection in pregnancy

Answer 55

ASYMPTOMATIC IN PRIMARY INFECTION + immunocompetent If FEVER in transplant patient -> suspect CMV infection ``` Malaise Fever Diarrhoea N+V Visual floaters + blindness In the presence of CMV retinitis, fundoscopy will reveal areas of infarction, haemorrhage, peri-vascular sheathing, and retinal opacification ``` Newborn Sx = microcephaly, reduced tone, hearing loss, hepatosplenomegaly, petechiae or purpura

Answer 56

FBC - atypical lymphocytosis, anaemia, leukopenia or thrombocytopenia Serum CK - normal unless transplant with tissue invasive CMV AST + ALT - raised ALP - raised if herpatobiliary involvement Serology - raised CMV IgM (acute infection) raised CMV IgG (past infection) NEW TEST = pp65 antigenaemia NAAT possible

Answer 57

IMMUNOCOMPETENT = REASSURANCE TRANSPLANT RECIPIENT = IV GANCICLOVIR FOSCARNET IF DRUG RESISTANT May need CMV immunoglobulin if no response

Answer 58

The outcome of treatment for CMV disease is good, in general, with the possible exception of CMV retinitis, which could lead to irreversible blindness, both in transplant patients and in patients with AIDS In donor CMV-seropositive, recipient seronegative (CMV D+/R-) solid organ transplant recipients and haematopoietic stem cell transplant recipients with graft-versus-host disease recurrence of CMV replication is common, and repeated courses of antiviral therapy may be needed. In solid organ transplant recipients, some experts administer secondary prophylaxis in patients at high risk for recurrence (CMV D+/R-). There is increasing appreciation of the long-term deleterious outcomes of CMV infection and disease in transplant recipients, such as increased risk of chronic allograft failure (including accelerated vasculopathy after heart transplantation, obliterative bronchiolitis after lung transplantation, and tubulointerstitial fibrosis after kidney transplantation). The most common long-term clinical outcome of congenital CMV disease is hearing loss

Answer 59

ganciclovir- and valganciclovir-induced bone marrow suppression cidofovir- and foscarnet-induced renal toxicity foscarnet-induced electrolyte disturbances immune recovery uveitis congenital CMV infection resulting in intellectual disability, sensorineural deafness, visual impairment, and developmental abnormalities Blindness

Answer 60

CMV In a healthy, immunocompetent patient with no significant medical history, CMV infection may present with a mononucleosis-like syndrome that includes fever, body aches, and malaise. Enlarged cervical lymph nodes may be present. Laboratory examination reveals atypical lymphocytosis, normal renal function, and mildly elevated hepatic aminotransferases. Clinical symptoms usually resolve within 1 week, although some severe cases of end-organ disease have been described in immunocompetent patients. In patients with inflammatory bowel disease refractory to conventional treatment, CMV is implicated as a co-factor, because the virus has been demonstrated in colon biopsies. Some cases have responded to treatment with intravenous ganciclovir. In critically ill people who require admission to the intensive case unit for severe illness, such as sepsis, asymptomatic CMV re-activation may occur and may be associated with higher all-cause mortality. Congenital CMV infection presenting in a newborn can result in microsomal, intra-cranial calcification, hepatosplenomegaly, neurological abnormality (presenting as poor tone and motor function), petechiae or purpura, and hearing loss. Intellectual disability and sensorineural deafness are long-term complications.

Answer 61

CMV In a healthy, immunocompetent patient with no significant medical history, CMV infection may present with a mononucleosis-like syndrome that includes fever, body aches, and malaise. Enlarged cervical lymph nodes may be present. Laboratory examination reveals atypical lymphocytosis, normal renal function, and mildly elevated hepatic aminotransferases. Clinical symptoms usually resolve within 1 week, although some severe cases of end-organ disease have been described in immunocompetent patients. In patients with inflammatory bowel disease refractory to conventional treatment, CMV is implicated as a co-factor, because the virus has been demonstrated in colon biopsies. Some cases have responded to treatment with intravenous ganciclovir. In critically ill people who require admission to the intensive case unit for severe illness, such as sepsis, asymptomatic CMV re-activation may occur and may be associated with higher all-cause mortality. Congenital CMV infection presenting in a newborn can result in microsomal, intra-cranial calcification, hepatosplenomegaly, neurological abnormality (presenting as poor tone and motor function), petechiae or purpura, and hearing loss. Intellectual disability and sensorineural deafness are long-term complications.

Answer 62

Folliculitis is an inflammatory process involving any part of the hair follicle; it is most commonly secondary to infection. It is important to recognise non-infectious causes of folliculitis (e.g., eosinophilic folliculitis) as well as folliculitis primarily involving the scalp (e.g., folliculitis decalvans). The condition manifests clinically as erythematous papules or pustules around hair follicles. Depending on the aetiology and chronicity of the condition, histological examination reveals various populations of inflammatory cells around the pilosebaceous unit. Folliculitis commonly occurs in areas with terminal hair growth, such as the head and neck region, axillae, groin and buttocks; it also favours areas under occlusion. ◊ Causes include bacterial, fungal, viral, and parasitic microorganisms. ◊ Most commonly superficial and resulting from infection by Staphylococcus aureus; use of antibacterial soaps may suffice as treatment for uncomplicated folliculitis, which is self-limited. ◊ Deeper infection and inflammation of hair follicles from Staphylococcus aureus generally require systemic antibiotic therapy based on culture sensitivities. ◊ Other common infectious agents include gram-negative organisms, fungi, viruses, and parasites; can occur in acne patients undergoing long-term oral antibiotic therapy and may mimic an acne flare. ◊ Treatment is tailored to the underlying cause; hygienic measures, MRSA eradication, and symptomatic therapies are other important treatment modalities to consider.

Answer 63

Adults > children Herpes folliculitis occurs predominantly in the beard region in men, whereas Malassezia folliculitis has a slight female predominance. Hot-tub folliculitis occurs more commonly in young adults, as this population is more likely to use spa facilities. Among non-infectious causes of folliculitis, pseudofolliculitis barbae commonly affects men of African descent. The prevalence in this population is reported to be between 45% and 83% Eosinophilic pustular folliculitis tends to affect adults with an average age of 30, with a male to female ratio of 5:1.

Answer 64

The causative microorganisms include bacteria, fungi, viruses, or Demodex mite. The most common cause of superficial folliculitis is Staphylococcus aureus. Gram-negative species implicated include Klebsiella , Enterobacter, and Proteus . These organisms can be seen in acne vulgaris when long-term systemic antibiotic therapy is being given. Pseudomonas aeruginosa , a gram-negative bacteria, is seen in hot tub folliculitis. Fungal folliculitis is typically caused by infection with dermatophytes, Malassezia and Candida species. Herpes simplex , Varicella zoster, and Molluscum contagiosum viruses are commonly responsible for viral folliculitis. Demodex folliculitis is caused by the ectoparasite Demodex folliculorum . These mites are common inhabitants of the skin and pilosebaceous unit.

Answer 65

STRONG Trauma including shaving and extraction Topical corticosteroid preparations DM Immunosuppression Perspiration Systemic antibiotics Immersion in under chlorinated water (hot tub) Drug-induced folliculitis develops secondary to drugs such as corticosteroids, androgenic hormones, EGF-R inhibitors, halogenated drugs, lithium, isoniazid, and corticotrophin.

Answer 66

Flesh-coloured papules that have central umbilication are suggestive of folliculitis secondary to Molluscum contagiosum Papules on one side of the face in the submaxillary area - tinea barbae Small, uniform papules and pustules on the chest, back and shoulders that are highly suggestive of Malassezia folliculitis. Living in a warm climate or being immunocompromised favours this diagnosis. Erythematous papules and pustules against a background of diffuse erythema is suggestive of Demodex folliculitis Tinea capitis can present as alopecia with scaling of the scalp and brittle hair breaking off at the surface of the scalp Varicella zoster folliculitis primarily affects the hair follicles, but clinically presents as erythematous plaques with haemorrhagic crusts in a dermatomal distribution.

Answer 67

Clinical Gram stain - Grampo cocci staph A KOH preparation = dermatophyte Tzanck smear = herpes Direct fluorescent antibody assay = herpes + VCZ Diagnosis really unclear + recurrent Sx = can do a skin biopsy

Answer 68

Uncomplicated - benzoyl peroxide topical Recurrent, deep, MSSA » flucloxacillin: 250-500 mg orally four times daily for 10 days Should be taken at least 30 minutes before food. MRSA - » clindamycin: 150-300 mg orally four times daily for 10 days THEN vancomycin If MRSA carrier state = eradicae with: » mupirocin topical: (2% cream) apply to nasal vestibules twice daily for 10 -14 days -and- » chlorhexidine topical: (0.12% solution) apply all over body once daily for 5-7 days -and- » rifampicin: 600 mg orally once daily for 10-14 days If dermatophyte = use itraconazole or terbinafine HSV folliculitis = aciclovir

Answer 69

Most patients presenting with infectious folliculitis have excellent prognosis when the infectious agent is accurately identified and appropriately treated. While localised folliculitis progressing to systemic infection is rare in healthy individuals, this is an important consideration for immunocompromised patients. Superficial folliculitis due to infection with Staphylococcus aureus often recurs even after appropriate treatment due to high prevalence of carrier state for Staphylococcus aureus in the general population. For fungal folliculitis, topical therapy alone may be effective initially but recurrence rate is high, whereas systemic antifungal therapy is likely to reduce long-term recurrence. When left untreated, most cases of superficial, infectious folliculitis are self-limited. Deep folliculitis can progress to form abscesses, which not only causes significant discomfort but can also serve as a recurrent nidus for systemic infection. Deep folliculitis also carries a risk of scarring.

Answer 70

Sepsis | Scarring

Answer 71

folliculitis Folliculitis can affect any hair-bearing regions of the body; it is invariably characterised by localisation of skin lesions around a hair follicle. Careful and meticulous skin examination is thus helpful in the diagnosis. In Pseudomonas hot tub folliculitis, patients often present with oedematous papules on the flank 2 or 3 days after immersion in the spa water. In children with tinea capitis, presentation may include scaling of the scalp, brittle hair breaking off at the surface of the scalp, or sometimes an erythematous, boggy plaque known as kerion.

Answer 72

folliculitis

Answer 73

Infection of the colon caused by the bacteria Clostridium difficile. Characterised by inflammation of the colon and the formation of pseudomembranes. Occurs in patients whose normal bowel flora has been disrupted by recent antibiotic use. Also known as pseudomembranous colitis, CDI, or CDAD. This topic covers the diagnosis and management of adults only. This topic focuses on the diagnosis and management of C difficile infection in adults only. ◊ Patients usually present with diarrhoea, abdominal pain, and leukocytosis, and a history of recent antibiotic use. Other common symptoms include fever, abdominal tenderness, and distension. ◊ Testing should be limited to patients with unexplained, new-onset diarrhoea (defined as 3 or more unformed stools in 24 hours). Molecular testing alone or as part of a multistep algorithm is recommended depending on local institutional protocols. May be evidence of pseudomembranes on sigmoidoscopy or colonoscopy in some patients. ◊ Treatment is to discontinue the inciting antimicrobial agent and start therapy with oral vancomycin or fidaxomicin. Surgery may be required in fulminant disease. ◊ About 5% to 50% of treated patients have recurrence after discontinuation of therapy, but most respond to a second course of therapy. Faecal microbiota transplantation may be recommended in patients with multiple recurrences

Answer 74

White Female >65 Recurrence rates have been reported to vary from 5% to 50% Risk factors for recurrent infection include female sex, increasing age, chronic kidney disease, diagnosis in a nursing home, and recent use of corticosteroids or proton-pump inhibitors C difficile is responsible for 48% of health care-associated gastrointestinal infections in acute care hospitals across Europe.

Answer 75

Broad-spectrum antibiotics disrupt the normal bowel flora, the most common causative agents being ampicillin, cephalosporins, clindamycin, carbapenems, and fluoroquinolones. Clostridium difficile colonisation occurs after this disruption to bowel flora by ingestion of heat-resistant spores, which convert to vegetative forms in the colon Transmission in the healthcare setting is most likely to be the result of person-to-person spread through the faecal-oral route (e.g., via the hands of healthcare workers), high-risk fomites (e.g., inadequately cleaned bedpans or rectal thermometers), or direct exposure to a contaminated environment. Patients with colonisation who are asymptomatic may also contribute to the spread. The incubation period is generally 2 to 3 days. Clostridium difficile are gram-positive, anaerobic, spore-forming rods that produce toxins A and B.

Answer 76

STRONG ABx exposure - The most common antibiotics involved are ampicillin, cephalosporins, clindamycin, carbapenems, and fluoroquinolones, especially in the preceding 3 months ``` >age Recent hospitalisation PMHx PPI use IBD Solid organ transplants SCT CKD HIV infection ``` WEAK Immunosuppressives GI surgery

Answer 77

``` COMMON Diarrhoea NB absence of diarrhoea may be related to toxic megacolon or paralytic ileus. Abdominal pain Fever (low grade) Abdominal tenderness N+V Abdominal distension ``` SHOCK - systemic symptoms of shock including hypotension and tachycardia with severe abdominal pain and tenderness suggest fulminant colitis.

Answer 78

FBC - Inc WCC Faecal occult blood / stool guaiac - positive for occult blood Stool PCR - +ve Stool immunoassay - positive for A+B or glutamate dehydrogenase Abdo Xray - order if distension - air in bowel, colonic dilation

Answer 79

DISCONTINUE CAUSATIVE AGENTS INFECTION CONTROL MEASURES HYDRATION Initial episode: 1 » vancomycin: 125 mg orally four times daily for 10 days An oral formulation may need to be specially compounded in some countries. 2 » metronidazole: 500 mg orally three times daily for 10 days Fulminant, ie toxic megacolon = included normal human immunoglobulin

Answer 80

The expected response to treatment is rapid resolution of fever and diarrhoea within 4 to 6 days. The majority of patients respond to initial treatment. Recurrence rates vary depending on the presentation, immune function, severity of disease, and treatment type and duration. Recurrence rates have been reported to vary from 5% to 50%, although one study found at least one recurrence in 21% of health care-associated infections and 14% of community-associated infections

Answer 81

Ileus Perforation + peritonitis Toxic megacolon

Answer 82

clostridium difficile- associated disease Symptoms can range from isolated mild diarrhoea to copious watery diarrhoea with severe abdominal pain and high peripheral white blood cell count (WBC). Life-threatening colitis can develop, especially in older people. A sudden rise in WBC in a patient with diarrhoea and a history of recent antibiotic use may be an indicator of impending fulminant colitis.

Answer 83

MRSA is a type of Staphylococcus aureus that is resistant to most beta-lactam antibiotics, antistaphylococcal penicillins (e.g., methicillin, oxacillin), and cephalosporins. MRSA infections can include syndromes of bacteraemia, pneumonia, endocarditis, joint infections, and skin or soft-tissue infections. MRSA is an important cause of infection in both healthy people in the community and in patients in healthcare institutions. It is important to distinguish MRSA colonisation from infection. Healthcare-associated MRSA infections and community-associated MRSA infections exhibit important differences in antibiotic susceptibility. Community-associated MRSA most commonly results in skin and soft-tissue infections and therapy can often be with oral antibiotics. Healthcare-associated MRSA infections usually require treatment with intravenous antibiotics. Isolation of patients with MRSA, through contact precautions, may help to prevent spread of infection.

Answer 84

Prevalence of carriers of MRSA is estimated to be between 1% and 2% of the population. Factors associated with MRSA carriage include recent hospitalisation, recent outpatient visit, nursing-home exposure, chronic disease, illicit intravenous drug use, or contact with a person with known risk factors Children and younger adults (median age 22 years) are more commonly afflicted with community-associated MRSA, while hospital-associated MRSA is more common in older age groups (median age 64 years). Colonisation is believed to precede infection and is, therefore, considered a risk factor for invasive MRSA infection. The primary site of MRSA colonisation is the anterior nares, although non-nasal sites (e.g., throat, axilla, inguinal area, and peri-rectal area) can also be colonised.

Answer 85

Methicillin resistance is mediated by penicillin-binding protein 2a that is encoded by the mecA gene. MRSA is a gram-positive pathogen that can cause skin, soft tissue, joint, and lung infections, and bacteraemia. Skin and soft-tissue infections are most common, but in the US, Staphylococcus aureus is also a common cause of nosocomial pneumonia.

Answer 86

``` STRONG >50 <35 MSM IVDU Wound Indwelling device Hospitalisation within the last year Chronic illness requiring healthcare visits Crowded conditions Hx MRSA Exposure to MRSA person Nasal colonisation with MRSA Hx ABx use HIV infection ```

Answer 87

``` Erythematous skin lesions or bustles Irritation or pain at indwelling catheter site Endocarditis Sx Infection unresponsive to penicillins Hx of presumed spider bite Abscess Fever Fatigue SIRS MRSA pneumonia UTI Septic A ```

Answer 88

All dependent on the source ``` FBC Culture Echo CxR Arthrocentesis ```

Answer 89

If abscess - debridement -> incision and drainage IV ABx: vancomycin: 15 mg/kg intravenously every 12 hours, maximum 2000 mg/day or linezolid: 600 mg intravenously every 12 hours DECOLONISATION STRATEGIES: chlorhexidine topical: (2% to 4%) applied as a body wash from the neck down as a single application and mupirocin topical: (2%) apply to the anterior nares twice daily for 5-7 days

Answer 90

Generally patients with an infection caused by methicillin-sensitive Staphylococcus aureus have better outcomes than those infected with MRSA. Certain genetic factors contribute to poor outcomes, such as the presence of Panton-Valentine leukocidin genes, which are commonly associated with skin and soft-tissue infections, but have also been associated with necrotising pneumonia and invasive osteomyelitis.

Answer 91

``` Septic shock Vanc related nephrotoxicity Vac related red man syndrome Linezolid related serotonin syndrome Prolonged hospital admission Linezolid related thrombocytopenia and anaemia Vanc related ototoxicity ```

Answer 92

MRSA MRSA can present in older patients as complicated urinary tract infections with dysuria, a fever and flank pain, weakness, and confusion. Not uncommonly, these patients are in a hospital or other healthcare setting in which they have Foley catheters inserted. Urinalysis is typically consistent with urinary tract infection, and sensitivities on culture show MRSA. Bacteraemia may accompany this situation.

Answer 93

MRSA MRSA can present in older patients as complicated urinary tract infections with dysuria, a fever and flank pain, weakness, and confusion. Not uncommonly, these patients are in a hospital or other healthcare setting in which they have Foley catheters inserted. Urinalysis is typically consistent with urinary tract infection, and sensitivities on culture show MRSA. Bacteraemia may accompany this situation.

Answer 94

The major clinical manifestations of infection with herpes simplex virus (HSV) type 1 (HSV-1) or HSV type 2 (HSV-2) are oral, genital, and ocular ulcers. Less commonly, primary or recurrent HSV infections may also present at other sites with neurological, ocular, hepatic, or respiratory complications. The primary episode occurs during initial infection with HSV, in which the host lacks an antibody response. Herpes labialis (oral herpes) is infection of the mouth area and lips, most commonly with HSV-1. If symptomatic, fever, sore throat, and pharyngeal oedema may occur. Painful ulcers can appear a few days later on the pharyngeal and oral mucosa, and fever and mouth pain may last for several days. Recurrent infections can occur and typically recurrences are in the same site. Recurrences last from 6 to 48 hours; pain, burning, or tingling starts, and then vesicles form. Systemic manifestations do not typically occur and the lesions will crust and heal in about 10 days. Genital herpes is caused by infection with either HSV-1 or HSV-2. The first clinical episode of genital ulceration may represent either new acquisition of the virus or newly recognised disease with remote acquisition of the virus. Sexual contact passes infection to the patient. Women may have genital pain, discharge, and dysuria with ulcerative lesions on the vulva, perineum, buttocks, cervix, and vagina. During primary infection, women tend to have systemic symptoms including fever, neuralgia, and constipation, whereas men have a milder primary course. Men may have vesicles on the penis shaft or glans with urethritis. Proctitis may occur with discharge, rectal pain, tenesmus, constipation, impotence, and urinary retention after anorectal intercourse. About 90% have recurrent episodes within the first year, with recurrences becoming less frequent and severe over time. For both HSV-1 and HSV-2, asymptomatic shedding may occur in the absence of lesions; transmission of the virus may occur during asymptomatic shedding. HSV establishes latency in neuronal ganglia and periodically reactivates. Most reactivations are asymptomatic but can result in transmission of the virus. The classic clinical presentation of vesicles progressing to painful ulcers is unusual; atypical and mild symptoms are common, and most people have unrecognised disease. Symptoms of genital herpes range from asymptomatic to tingling and burning without lesions, to recurrent genital ulcerations. Symptoms of herpes labialis include tingling and burning followed by development of vesicular then ulcerative lesions involving the oropharynx and perioral mucosa. Aciclovir, famciclovir, and valaciclovir are effective at shortening the duration and severity of an outbreak. Daily suppressive therapy reduces recurrences by 80% and reduces transmission risk by approximately 50%. Glycoprotein G-based type-specific serology testing is used to diagnose infection with or without lesions and distinguish between type 1 and 2.

Answer 95

Worldwide, it is estimated that 67% of persons aged 0-49 years are infected with herpes simplex virus type 1 (HSV-1) 14-49 years, 47.8% are infected with HSV-1 and 11.9% are infected with HSV type 2 (HSV-2)

Answer 96

Herpes simplex virus type 1 (HSV-1) more commonly causes herpes labialis; however, it is also an increasing cause of initial episodes of genital herpes. HSV-1 is also associated with HSV encephalitis HSV type 2 (HSV-2) causes genital herpes. HSV-1 and HSV-2 are members of the Herpesviridae family and are related to varicella-zoster virus, cytomegalovirus, Epstein-Barr virus, and human herpesvirus-6, -7, and -8. HSV-1 and HSV-2 are large, enveloped, double-stranded DNA viruses. HSV can exist in both a latent and a lytic state. During latency, infectious virions are not produced. Latently infected cells persist for the life cycle of the host, causing chronic infection. Lytic infection is characterised by viral replication and transport of the virus to the skin, with infection of skin and mucosal surfaces.

Answer 97

STRONG HIV Immunosuppressives High risk sexual behaviour ``` WEAK Female Black Increased age Lack of condom use ```

Answer 98

``` COMMON Dysuria Lymphadenopathy Genital ulcer Oral ulcer Tingling sensation ``` UNCOMMON Fever [1st episode] Headache/aseptic meningitis [first episode only]

Answer 99

Viral culture - positive for HSV HSV PCR - positive copies Glycoprotein based serology - gG1 and gG2 - positive antibody to HSV-1 or HSV-2

Answer 100

Pneumonitis, hepatitis, or meningitis or encephalitis - IV aciclovir - aciclovir: 5-10 mg/kg intravenously every 8 hours for 10-21 days First or recurrent episode genital disease - aciclovir: 400 mg orally three times daily for 7-10 days; or 200 mg five times daily for 7-10 days Oral - topical or oral aciclovir

Answer 101

Genital herpes and oral herpes are chronic viral infections with a highly variable course. Some people may have frequent outbreaks of disease, whereas others will be completely asymptomatic.

Answer 102

``` Aciclovir resistence Oesophagitis Erythema multiform HSV keratitis Meningitis Neonatal HSV HSV1 encephalitis Acute retinal necrosis Herpetic whitlow or cutaneous infection Hepatitis Bells palsy ```

Answer 103

Acute respiratory tract infection typically caused by seasonal influenza A or B virus. The virus is transmitted by inhalation of infected respiratory secretions that have been aerosolised through coughing, sneezing, or talking. Characterised by upper and lower respiratory tract symptoms of rhinorrhoea, cough, fever, chills, headache, and myalgia. Typically presents in winter season. Can occur in local community outbreaks, epidemics, and, rarely, pandemics. Vaccination for prevention is available.

Answer 104

Overall, it is estimated to affect 20% of children and 5% of adults worldwide each year. There have been four influenza pandemics since 1918, with the most recent being the Influenza A (H1N1) 'swine flu' epidemic in April 2009. In 1957 and 1968, both pandemics were as a result of novel strains of both human and avian influenza. However, the pandemic of 2009 was as a result of a novel gene rearrangement of human, avian, and swine influenza. In 2017, a fast-mutating strain of influenza A (H3N2) was reported in Australia, which saw the highest number of cases since the 2009 pandemic.

Answer 105

Seasonal influenza virus is a member of the orthomyxovirus family. It has a segmented, single-stranded RNA genome that can be classified into influenza A, B, and C based on antigenic differences. Seasonal influenza virus types A and B are also divided into a number of subtypes. These subtypes are defined by the H and N antigens present on the virus. There are three antigenic subtypes of H antigen (H1, H2, and H3) and two antigenic subtypes of N antigen (N1 and N2), allowing for a number of different combinations. Antibodies to one subtype of H or N antigen do not react with another type of the H or N antigen. Influenza C is not associated with epidemics or pandemics and causes mild disease. Influenza A is responsible for frequent (usually annual) local outbreaks or larger epidemics of varying intensity every 2-3 years, or occasional pandemics. Influenza B causes outbreaks approximately every 4 years, with usually milder disease than influenza A.[9] Epidemics usually occur from late autumn to early spring.

Answer 106

``` STRONG AGE >65 AGE 6-59 months Chronic CV or respiratory conditions CKD Diabetes Haemoglobinopathy Immunocompromise Pregnancy Carers and household contacts of high-risk groups Healthcare workers ```

Answer 107

``` COMMON Winter Current influenza outbreak Unvaccinated Fever with cough Sore throat ``` UNCOMMON Cervical lymphadenopathy Dyspnoea

Answer 108

Clinical diagnosis - febrile respiratory illness during a known seasonal influenza outbreak Viral culture possible - detection of influenza virus or viral antigen OR Direct immunofluorescent antibody staining - detection of influenza virus CONSIDER CXR - Should be done to exclude either a primary viral or secondary bacterial pneumonia. Normal in uncomplicated cases; may show infiltrates consistent with pneumonia in complicated cases

Answer 109

Prophylaxis - oseltamivir or zanamivir ``` ACUTE 1. antipyretic / analgesic + Antiviral: oseltamivir: 75 mg orally twice daily zanamivir: 10 mg (two inhalations) twice daily ``` + ABx if BS-ABx With otitis media - otitis media may initially be treated with amoxicillin or co-amoxiclav

Answer 110

Uncomplicated seasonal influenza infection Seasonal influenza is usually a self-limiting acute respiratory illness that recurs each winter season as different strains emerge. Annual influenza vaccines are available to immunise against the 3 expected strains to pass through a community. If seasonal influenza is contracted, institution of antivirals within 36 to 48 hours of onset of symptoms will decrease days of illness by 1 to 2 days and reduce lower respiratory tract complications.

Answer 111

``` Bacterial / viral pneumonia Otitis media Rhabdomyolysis Encephalitis Transverse myelitis Aseptic meningitis GBS Toxic shock syndrome - Toxic shock syndrome, associated with Staphylococcus aureus infection and acute influenza, has been described after both influenza A and B infections in case reports Post-influenza encephalopathy ```

Answer 112

influenza Seasonal influenza may present rarely with an afebrile upper respiratory tract illness more typical of a common cold, or it may present predominantly with fever and myalgia, with few respiratory symptoms. Patients in high-risk populations (e.g., those with chronic cardiac or pulmonary conditions, diabetes mellitus, renal disease, haemoglobinopathy, immunosuppression, residence in chronic care facilities, age >50 years, or third trimester of pregnancy) may present with an established primary viral or secondary bacterial pneumonia. Characteristic features of primary viral pneumonia are persisting or worsening course of fever, with dyspnoea or other respiratory distress. Secondary bacterial pneumonia should be suspected if there is an initial improvement in symptoms followed by a relapse of fever with productive cough and shortness of breath. A chest x-ray confirms pulmonary infiltrates.

Answer 113

Genital herpes cannot be reliably differentiated on a clinical basis from other causes of genital ulcer disease. Proctitis or cervicitis can often result from a wide spectrum of manifestations involving the perineal, perianal, and rectal mucosa. Tingling and dysaesthesias may be prodromal symptoms of a recurrence. Herpes labialis classically presents with recurrent ulceration along vermillion border of lip but may also present with pharyngitis. Other manifestations include herpetic whitlow and herpes gladiatorum, which present with vesicular lesions and ulcerations on fingers or at sites of trauma, respectively. Immunocompromised patients may have more severe, prolonged ulceration of the genital or oral mucosa than immunocompetent patients. Other presentations of visceral or disseminated HSV infection, including hepatitis, pneumonitis, or central nervous system disease, may occur as primary or recurrent infections. These manifestations, as well as neonatal HSV, are discussed further in the Complications section.

Answer 114

Genital herpes cannot be reliably differentiated on a clinical basis from other causes of genital ulcer disease. Proctitis or cervicitis can often result from a wide spectrum of manifestations involving the perineal, perianal, and rectal mucosa. Tingling and dysaesthesias may be prodromal symptoms of a recurrence. Herpes labialis classically presents with recurrent ulceration along vermillion border of lip but may also present with pharyngitis. Other manifestations include herpetic whitlow and herpes gladiatorum, which present with vesicular lesions and ulcerations on fingers or at sites of trauma, respectively. Immunocompromised patients may have more severe, prolonged ulceration of the genital or oral mucosa than immunocompetent patients. Other presentations of visceral or disseminated HSV infection, including hepatitis, pneumonitis, or central nervous system disease, may occur as primary or recurrent infections. These manifestations, as well as neonatal HSV, are discussed further in the Complications section.

Answer 115

A zoonosis with worldwide distribution, which represents a significant public-health problem. The infection is caused by motile spirochetes from the genus Leptospira and is maintained in nature by chronic renal infection of carrier animals. Re-emerging as a result of increased international travel and climate changes elicited by global warming. Outbreaks have been associated with flooding and natural disasters. Associated with occupational exposure, water sports, and flooding. Higher rates have been reported in tropical areas during rainy season and temperate regions during late summer. Biphasic presentation. Can present with an extensive spectrum of clinical manifestations ranging from subclinical illness in approximately 90% of cases to renal and hepatic failure and pulmonary haemorrhage. Treatment includes antibiotics and supportive therapy.

Answer 116

More than 1 million cases occur worldwide each year. Estimated annual incidence rates range from 0.02 per 100,000 to 1.00 per 100,000 persons in temperate areas, and from 10 per 100,000 to 100 per 100,000 persons in tropical regions. Incidence rates are higher (100 per 100,000 persons) during outbreaks. Pathogenic and non-pathogenic strains chronically infect urine of carrier animals. The main risk factor for acquiring the infection is direct or indirect contact with urine of infected animals. Contact can occur secondary to occupational exposure or accidentally from contact with water. Direct transmission from animals to humans is common in occupations such as veterinarians, butchers, cattle and pig farmers, and rodent-control workers. Travellers and athletes participating in water sports represent a growing population at risk. Freshwater swimming, rafting, kayaking, canoeing, fishing, hunting, and trail biking are activities associated with leptospirosis infections, particularly after heavy rainfall or flooding. Men are usually affected more frequently than women.

Answer 117

Leptospira interrogans and L biflexa. Specificity of the various serovars within the species serogroups is conferred by lipopolysaccharide (LPS) O-antigens.

Answer 118

``` STRONG Contact with urine of infected animals Residence or travel to endemic area Recent flooding Involvement in water sports ```

Answer 119

``` COMMON Acute Sx: High remittent fever Headache Myalgia Conjunctival suffusion Muscle tenderness Chills/rigors Abdopain NV Diarrhoea Asthaenia / weakness Anorexia Photophobia Eye pain Neck stiffness (aseptic men) ``` ``` During Immune phase: Cough Dyspnoea Chest pain Haemoptysis Oliguria or polyuria Cardiac arrhtymias Lymphadenopathy Splenomegaly Hepatomegaly Jaundice Mental state changes [rare] - Can include confusion, hallucinations, aggressive behaviour, and delirium. Macropapular rash (non-pruritic) ```

Answer 120

FBC - high WBC count; low platelet count; anaemia Urinalysis - mild proteinuria; pyuria; haematuria; hyaline or granular casts DARKFIELD EXAM - presence of spirochetes Blood culture - positive after 1 week to 4 months (Leptospires can be isolated from blood during the first week to 10 days (acute/initial phase).) CSF culture ECG - arryhtmias PCR, ELISA, MAT tests possible CXR - small nodular densities and patchy alveolar infiltrates; air-space nodules LFTs - elevated aminotransferases or alkaline phosphatase Conjugated bilirubin - elevated direct bilirubin; markedly elevated conjugated bilirubin levels (≤1368 micromol/L (80 mg/dL)) U+E - elevated urea and creatinine; hypokalaemia

Answer 121

Prophylaxis: doxycycline: 200 mg orally once weekly starting 1-2 days prior to and during period of exposure Mild disease doxycycline: children >8 years of age: 2-4 mg/kg/day orally given in divided doses every 12 hours, maximum 200 mg/day; adults: 100 mg orally every 12 hours Severe disease = IV ABx ceftriaxone: children: 80-100 mg/kg/day intravenously given in divided doses every 12-24 hours, maximum 4000 mg/day; adults: 1-2 g intravenously every 12-24 hours Manage arrhythmia, AKI + hepatic involvement

Answer 122

In general, the prognosis in patients with mild disease is favourable; however, patients affected by severe disease have a poor prognosis. Prognosis varies according to various factors, such as patient's immunological status and age. Risk factors associated with a poor outcome include hypotension, oliguria, hyperkalaemia, and an abnormal chest auscultation; all present on initial evaluation.

Answer 123

Leptospirosis during pregnancy may lead to fetal death, spontaneous abortion, stillbirth, and congenital leptospirosis; a few cases have been reported. ``` Aseptic meningitis Chronic fatigue syndromes Neuropsychiatric manifestations Ophthalmic complications of leptospirosis include uveitis and iridocyclitis Pancreatitis ```

Answer 124

leptospirosis Aseptic meningitis is a common manifestation during the immune phase of the disease; its incidence is approximately 25%.[6][7] Symptoms invariably include headache, mental status changes, and fever. However, in a minority of patients, neurological involvement can present with a spectrum of unusual manifestations, such as coma, meningoencephalitis, transverse myelitis, hemiplegia, and Guillain-Barre syndrome.[1] Symptoms include restlessness, confusion, hallucinations, delirium, and psychotic behaviour. A small proportion of patients develop acute pancreatitis as a complication, which can be fatal.[8] A case of leptospirosis with clinical features of nephrotic syndrome with massive proteinuria has been reported.[9] Certain patient populations, such as the elderly and pregnant women, have a higher risk of developing severe disease as a result of leptospiral infection. During pregnancy, fetuses can acquire infection during the acute/initial phase through placental transmission, which can lead to fetal death.[10] Women are more likely to have a spontaneous abortion if leptospirosis occurs in the early months of pregnancy.[11] Fetuses are at risk of morbidity and mortality if the mother has high fever or marked haemodynamic disturbances.[12] Elderly patients may develop more aggressive disease. Patients in this age group who develop Weil's disease have a high mortality.[5] Patients with immunosuppressive status can manifest with cardiovascular complications such a complete heart block. This is a very rare presentation.[13]A case of leptospirosis complicated with bowel gangrene has also been reported.[14] It has also been documented that leptospirosis can present as co-infection with various malarial species. These patients can have severe manifestations such as hepatorenal dysfunction.[15]Co-infection with Leptospirosa species and dengue virus has been reported in tropical areas, which represents a diagnostic challenge in light of overlapping clinical manifestations.[16]

Answer 125

leptospirosis Aseptic meningitis is a common manifestation during the immune phase of the disease; its incidence is approximately 25%.[6][7] Symptoms invariably include headache, mental status changes, and fever. However, in a minority of patients, neurological involvement can present with a spectrum of unusual manifestations, such as coma, meningoencephalitis, transverse myelitis, hemiplegia, and Guillain-Barre syndrome.[1] Symptoms include restlessness, confusion, hallucinations, delirium, and psychotic behaviour. A small proportion of patients develop acute pancreatitis as a complication, which can be fatal.[8] A case of leptospirosis with clinical features of nephrotic syndrome with massive proteinuria has been reported.[9] Certain patient populations, such as the elderly and pregnant women, have a higher risk of developing severe disease as a result of leptospiral infection. During pregnancy, fetuses can acquire infection during the acute/initial phase through placental transmission, which can lead to fetal death.[10] Women are more likely to have a spontaneous abortion if leptospirosis occurs in the early months of pregnancy.[11] Fetuses are at risk of morbidity and mortality if the mother has high fever or marked haemodynamic disturbances.[12] Elderly patients may develop more aggressive disease. Patients in this age group who develop Weil's disease have a high mortality.[5] Patients with immunosuppressive status can manifest with cardiovascular complications such a complete heart block. This is a very rare presentation.[13]A case of leptospirosis complicated with bowel gangrene has also been reported.[14] It has also been documented that leptospirosis can present as co-infection with various malarial species. These patients can have severe manifestations such as hepatorenal dysfunction.[15]Co-infection with Leptospirosa species and dengue virus has been reported in tropical areas, which represents a diagnostic challenge in light of overlapping clinical manifestations.[16]

Answer 126

Lyme disease is a zoonotic infection caused by a spirochete of genus Borrelia, which is transmitted to humans by ticks. Zoonotic diseases are transmitted between vertebrate animals and humans. Animals serve as the primary reservoir of Borrelia. Ticks become infected by feeding on an infected animal. Most common initial manifestation is typical skin lesion known as erythema migrans. Later manifestations may include arthritis, or central nervous system or cardiac involvement. Erythema migrans develops at the site of tick bite usually within 1 to 2 weeks and is a pathognomic feature of Lyme disease. Constitutional symptoms such as fever, headache, myalgias, fatigue, and arthralgias may occur. Complications of Lyme disease may be neurological, cardiac, or musculoskeletal. Mainstay of treatment is antibiotic therapy. There is currently no vaccine; prevention is centred around reducing exposure to ticks.

Answer 127

Lyme disease can occur at any age, but two peak age groups have been identified: 10 to 19 years and 50 to 59 years. M=F Onset is usually between May and October, mostly related to increased outdoor activity compared with the rest of the year. In Europe, Lyme disease is most common in central European and Scandinavian countries, with an estimated incidence rate of up to 155 cases per 100,000 per year. A higher incidence rate of greater than 450 cases per 100,000 per year was reported from southern Sweden.

Answer 128

Lyme disease in Europe is caused by B afzelii, B garinii, and B burgdorferi sensu stricto B burgdorferi is inoculated into the skin by the feeding Ixodes tick, usually after the tick has fed for more than 48 hours.

Answer 129

STRONG Exposure to ticks Outdoor activities Tick bite duration

Answer 130

COMMON Erythema migrans Constitutional symptoms - Fever, headache, myalgias, fatigue, or arthralgias may occur after infection. ``` UNCOMMON Facial palsy Arthritis (usually knees) Regional lymphadenopathy Stiff neck (aseptic meningitis) AV block or myopericarditis Radiculoneuropathy Encephalomyelitis, peripheral neuropathy / encephalopathy ```

Answer 131

ELISA or IFA - +ve | Lyme-specific IgM or IgG - positive

Answer 132

Known tick bite - doxycycline 200mg oral Erythema migrans - doxycycline: children: 2 mg/kg orally twice daily; adults: 100 mg orally twice daily IV ABx if neurological involvement

Answer 133

If patients are diagnosed and treated properly with recommended antibiotic therapy, Lyme disease is usually curable. A small proportion of patients may report subjective symptoms for a month to several months without any evidence of ongoing infection. In untreated patients, most of the erythema migrans lesions improve spontaneously, but 5% to 10% of patients will have recurrent lesions. Up to 80% of patients develop a chronic joint problem ranging from arthralgia to arthritis, while 20% do not manifest any chronic sequelae. Of the patients with chronic sequelae, about 11% and 4% also develop neurological and cardiac involvement. Reinfection can occur in patients who have a repeat tick bite.

Answer 134

``` Acute neurological complications Cardiac complications Borrelial lymphocytoma - red earlobe Arthritis Post-Lyme disease syndrome ```

Answer 135

Lyme disease Early Lyme disease includes erythema migrans and early disseminated infection (multiple erythema migrans lesions, carditis, cranial nerve palsy [most commonly cranial nerve VII], aseptic meningitis, or acute radiculopathy). Erythema migrans (EM), which is the most common presentation, can be seen in 50% to 90% of patients with Lyme disease. It develops at the site of tick bite usually within 1 to 2 weeks and is a pathognomic feature of Lyme disease. It is a non-tender, non-pruritic annular expanding skin lesion that may be homogeneously erythematous or have central clearing (bull's eye) and is generally 5 cm or greater in diameter. Central clearing is less common in patients in endemic areas of the US (approximately 20%) compared with non-endemic areas of the US and Europe (approximately 80%).[1] It is typically accompanied by constitutional symptoms such as fever and arthralgias.[2][3][4] Untreated solitary EM lesions usually improve within a few days to a few weeks. Multiple lesions occur as the organism disseminates from the primary site of infection. In Europe, the primary site of skin infection generally shows a more indolent form of EM lesion, with less inflammation and slower progression.[2][3][4] Borrelial lymphocytoma, a rare cutaneous manifestation, presents as a solitary bluish-red swelling commonly on the ear lobe, near the nipple or in the scrotal area. It is seen in Europe and is usually caused by Borrelia garinii or B afzelii.[2][3][4] Musculoskeletal manifestations include arthralgia and arthritis. Arthritis typically presents with recurrent brief attacks of joint swelling in 1 or more joints, typically involving the knees. Neurological manifestations include facial (cranial nerve VII) and other cranial nerve palsies, aseptic meningitis, and radiculoneuropathy. The clinical manifestations of meningoradiculoneuritis (Bannwarth's syndrome) are the second most common presentation of early Lyme disease in Europe. Its clinical features include cranial nerve deficits (e.g., facial palsy), paresis, radicular pain and radiculitis, and lymphomonocytic meningitis with a relatively high concentration in the cerebrospinal fluid.[5] Cardiovascular complications include carditis with atrioventricular block (second- or third-degree) that resolves in days to weeks and, less commonly, myopericarditis. Late manifestations (>6 months after exposure) of Lyme disease include arthritis (chronic mono- or asymmetrical oligoarthritis), neurological involvement (encephalopathy, encephalomyelitis, peripheral neuropathy, and chronic progressive meningoencephalitis), and acrodermatitis chronica atrophicans (ACA). ACA is a chronic and slowly progressive skin condition with bluish-red atrophic skin lesions on sun-exposed surfaces of the extremities. It is seen in Europe and is caused by Borrelia afzelli.[2][3][4]

Answer 136

Lymphogranuloma venereum (LGV) is a STD caused by Chlamydia trachomatis genovars/serovars L1, L2, or L3 (collectively termed the 'LGV biovar'), which are endemic to the tropics, but now emerging in developed regions. Infection occurs through contact with mucous membranes or abrasions in the skin of the genital region. Primary manifestation of infection is painless penile or vulvar inflammation and ulceration at the site of inoculation; often not noticed by patient. Secondary stage typically occurs weeks after development of the primary lesion; presents as painful, unilateral, inguinal or femoral lymphadenopathy (often referred to as 'inguinal syndrome'). Proctocolitis has emerged as a more typical presentation in men who have sex with men (particularly those who are HIV-positive). Chronic inflammation can lead to scarring and fibrosis causing lymphoedema of the genitals, or formation of strictures and fistulae if anorectal involvement. Identification of Chlamydia trachomatis from the swab of a genital ulcer or aspiration of a bubo is definitive diagnosis. Doxycycline is the preferred first-line treatment; macrolides are an alternative treatment option (e.g., in pregnant or lactating women, or patients with allergies to tetracyclines). Large buboes may be aspirated, but incision and drainage or surgical excision of buboes may complicate healing.

Answer 137

The peak incidence is in the third and fourth decades of life, the ages when sexual activity is at its peak. Men are 6 times more likely to present acutely with inguinal lymphadenopathy than women, who tend to remain asymptomatic in the early stages of LGV infection. In women, the rectal mucosa can easily be auto-inoculated by vaginal secretions or lymphatic spread. Although it is unknown whether anal sex alone is a risk factor for women, both men who have sex with men (MSM) and women are more likely to develop late complications of proctocolitis with chronic ulcerations and rectal strictures.

Answer 138

Infection with Chlamydia trachomatis occurs through contact with mucous membranes or abrasions in the skin. Sexual transmission is the most common route, but extra-genital sites may be affected when inoculated by non-sexual contact, accidental laboratory inhalation or when transmitted by exposure to fomites.

Answer 139

``` STRONG Other STDs Risky sexual behaviour HIV seropositivity 20-40yos ``` WEAK Male

Answer 140

COMMON Inguinal lymphadenopathy Fever, malaise, arthralgias Lower abdominal or back pain ``` UNCOMMON Non-specific symptoms of Proctocolitis. Groove Sx of greenblatt Genital elephantiasis, saxophone penis, esthiomene - Late stages may occur several years after initial infection. These findings are a result of progressive lymphangitis, chronic oedema, and sclerosing fibrosis of the subcutaneous tissues Genital or anal ulcer NS-symptoms Erythema nodosum Anogenital sinus tracts, strictures or fistulae ```

Answer 141

NAAT Serum for complement fixation Swab via anoscopy for gram staining - anorectal Gram stain showing greater than 10 WBC/high-power field is suggestive of LGV

Answer 142

doxycycline: 100 mg orally twice daily for 7-21 days azithromycin: 1 g orally as a single dose; or 1 g orally once weekly for 3 weeks

Answer 143

Full recovery can be expected, especially when treatment is started early; however, re-infection or relapse may occur. When antibiotics are not started early, LGV can progress to late stages. Chronic genital oedema can result in scarring, fibrosis, and permanent disfiguration, which may require surgical reconstruction. In the late stages of anogenital LGV, proctectomy, perineal excision, and permanent colostomy may also be required for stricture or fistula formation. Healing in these cases can be prolonged and morbid. While the cervix may remain infected indefinitely in females, males are not likely to be infectious after the primary lesion has resolved.

Answer 144

``` Increased susceptibility to HIV + other STDs - due to ulcers Reactive arthritis Chronic lymphedema Stricture formation Fistulae or sinus tracts ```

Answer 145

lymphogranuloma venerium Extra-genital manifestations are rare, but LGV can present as pharyngitis, ulceration in the tongue or pharynx, or with cervical lymphadenopathy.[2][3][4] LGV has been detected by nucleic acid amplification tests in the pharynx and urethra of asymptomatic carriers.[5] Disseminated disease occurs as a result of bacteraemic spread producing conditions including arthritis, hepatitis, pericarditis, pneumonia, or meningoencephalitis.[6] Erythema nodosum is also occasionally associated.[7] Sequelae of chronic infection may result in fibrosis and formation of sinus tracts and strictures of the anogenital tract as abscesses rupture. In women this may progress to esthiomene (fibrotic genital elephantiasis) or fistulae involving the urethra, vagina, uterus, or rectum. In men, a physical finding known as saxophone penis or penoscrotal elephantiasis has also been described.[8] Late complications are rare and have been observed more frequently following proctocolitis.

Answer 146

lymphogranuloma venerium Extra-genital manifestations are rare, but LGV can present as pharyngitis, ulceration in the tongue or pharynx, or with cervical lymphadenopathy.[2][3][4] LGV has been detected by nucleic acid amplification tests in the pharynx and urethra of asymptomatic carriers.[5] Disseminated disease occurs as a result of bacteraemic spread producing conditions including arthritis, hepatitis, pericarditis, pneumonia, or meningoencephalitis.[6] Erythema nodosum is also occasionally associated.[7] Sequelae of chronic infection may result in fibrosis and formation of sinus tracts and strictures of the anogenital tract as abscesses rupture. In women this may progress to esthiomene (fibrotic genital elephantiasis) or fistulae involving the urethra, vagina, uterus, or rectum. In men, a physical finding known as saxophone penis or penoscrotal elephantiasis has also been described.[8] Late complications are rare and have been observed more frequently following proctocolitis.

Answer 147

Necrotising fasciitis is a life-threatening subcutaneous soft-tissue infection that may extend to the deep fascia, but not into the underlying muscle. The causal organisms may be aerobic, anaerobic, or mixed flora. Two main clinical forms exist. Type I necrotising fasciitis is a polymicrobial infection with an anaerobe such as Bacteroides or Peptostreptococcus and a facultative anaerobe such as an Enterobacteriaceae or non-group A streptococcus. Type II necrotising fasciitis is most commonly a monomicrobial infection with Streptococcus pyogenes (group A streptococci). A life-threatening subcutaneous soft-tissue infection that requires a high index of suspicion for diagnosis. Infection may be polymicrobial in aetiology (type I) due to mixed anaerobic/facultative anaerobic organisms, or due to a single organism (type II), most commonly Streptococcus pyogenes, also called group A streptococcus. Necrotising fasciitis should be suspected in any patient with a soft-tissue infection accompanied by prominent pain and/or anaesthesia over the infected area, or signs and symptoms of systemic toxicity. Signs that raise suspicion for necrotising fasciitis include the presence of hypotension and/or elevated creatinine, elevated creatine kinase, elevated C-reactive protein (>124 nanomol/L [13 mg/L]), elevated white blood cell count with marked left shift, and/or low serum bicarbonate. No laboratory or imaging studies, alone or in combination, are sufficiently sensitive and specific to definitively diagnose or rule out necrotising fasciitis. An urgent surgical consultation should be obtained as soon as the diagnosis is suspected. Treatment should not be delayed while awaiting microbiological and imaging investigations. Definitive treatment is surgical debridement, repeated as necessary. Antibiotic therapy is crucial, but is considered adjunctive to surgical management. Empiric antibiotics should cover major bacterial aetiological agents, and group A streptococcal toxin production that can accompany type II necrotising fasciitis.

Answer 148

Absolute data for the incidence and prevalence of necrotising fasciitis are lacking. Type I (due to mixed anaerobic-facultative anaerobic infections) is more common than type II necrotising fasciitis. Type II complicates about 7.5% of invasive group A streptococcal infections at an estimated rate of 3.6 cases per million population per year.

Answer 149

Type I necrotising fasciitis is a polymicrobial infection of subcutaneous tissue with an anaerobe (such as Bacteroides or Peptostreptococcus) plus a facultative anaerobe such as an Enterobacteriaceae (Escherichia coli, Enterobacter, Klebsiella, Proteus) or non-group A streptococcus with or without Staphylococcus aureus. Type II necrotising fasciitis is a monomicrobial infection of subcutaneous tissue most commonly caused by Streptococcus pyogenes (group A streptococci). Vibrio vulnificus, Aeromonas hydrophila, Panton-Valentine leukocidin (PVL)-positive Staphylococcus aureus, and MRSA can also cause it. Predisposing risk factors may include diabetes mellitus, peripheral vascular disease, immunocompromising conditions, chronic renal or hepatic insufficiency, chickenpox or herpes zoster, intravenous drug use, or certain medications (e.g., corticosteroids)

Answer 150

``` STRONG Inpatient contact (4 days later) Varicella zoster infection Cutaneous injury Non-traumatic skin lesions IVDU ``` WEAK Chronic illness Immunosuppression NSAIDs

Answer 151

COMMON Anaesthesia or severe pain over cellulitis Fever Palpitations, tachycardia, tachypnoea, hypotension and light-headedness NV ``` UNCOMMON Delerium Creptius Vesicles/bullae Grey discolouration of skin Oedema or induration Location of lesion ```

Answer 152

``` FBC + diff Hyponatraemia is a non-specific finding that may be seen in any systemic infection or circulatory collapse. Urea + creatinine - raised Serum CK - raised CRP - raised Serum lactate - elevated Blood and tissue cultures CT / MRI - oedema extending along fascial plane and/or soft tissue gas ``` A surgical consultation for inspection, exploration, and drainage of infected tissue should be obtained in every case of suspected necrotising fasciitis.

Answer 153

Surgical debridement + haemodynamic support Vancomycin + pip-taz for polymicrobial Vancomycin for staph BenPen + clindamycin for GAS For strep toxic shock - IVIG

Answer 154

Mortality from necrotising fasciitis properly treated with surgery plus antibiotics has been estimated at between 10% and 40%. Mortality is higher in patients who develop shock and end-organ damage, approaching 50% to 70%.

Answer 155

Mortality | Skin loss + scarring

Answer 156

necrotising fasciitisNecrotising fasciitis should be considered in a patient with cellulitis who also has systemic symptoms and signs such as hypotension, tachycardia, tachypnoea, nausea, vomiting, or delirium. The area of cellulitis may be either severely and constantly painful or, conversely, anaesthetic. Examination of the skin overlying the area of cellulitis may in some cases reveal underlying induration extending beyond the area of cellulitis, ecchymoses, vesicles, bullae, greyish discoloration, or oedema. Rapid extension of cellulitis despite the use of appropriate antibiotics should also raise suspicion for a necrotising process. About half of cases occur in the extremities, with the remainder concentrated in the perineum, trunk, and head and neck areas. Atypical presentations include necrotising fasciitis that occurs without an obvious overlying skin lesion (approximately 20% of cases), or that arise from a Bartholin gland or perianal abscess. Fournier's gangrene is a form of type I necrotising fasciitis that arises from the perineum.

Answer 157

Strongyloidiasis is an infection caused by the intestinal nematode Strongyloides stercoralis. Transmission occurs widely in tropical and subtropical areas, but also in countries with temperate climates. The primary mode of infection is through larvae penetrating the skin. Strongyloides larvae migrate from subcutaneous tissues into the venous circulation, then to the lungs. Larvae migrate up the airways, are swallowed, and establish chronic infection in the intestinal tract as adults. New larvae continue this cycle within the human host creating indefinite auto-infection; meaning that, without treatment, infection is lifelong. Should be considered in all migrants or residents from endemic areas regardless of time since immigration. Clinical clues include wheezing, abdominal distress, and eosinophilia. Stool ova and parasite tests are relatively insensitive for detection of strongyloides larvae but are currently the tests of choice. Treatment with ivermectin is recommended, regardless of resource setting. Rapid spread of infection can lead to hyperinfection syndrome and disseminated disease, both of which are associated with a high mortality rate in immunosuppressed patients. Empirical treatment should be considered when initiating corticosteroids in any high-risk patient due to risk of life-threatening hyperinfection.

Answer 158

Migrants and refugees from developing countries are at greatest risk with rates of 5% to 10% Estimates of global prevalence exceed 100 million The highest rates are in Southeast Asians. Initial human infection is via larvae living in infected soil penetrating the skin, typically the feet. Those with soil contact, such as subsistence farmers and agricultural workers, are at greater risk Therefore, men are at an approximately two- to threefold higher risk than women

Answer 159

Strongyloidiasis is caused by the intestinal nematode Strongyloides stercoralis. Humans become infected with S stercoralis after cutaneous contact with soil contaminated with human faeces. Person-to-person transmission is rare, but has been documented. Donor-derived cases in solid-organ transplant recipients have also been reported The incubation period is 14 to 30 days. The filariform larvae penetrate the skin and then travel through the venous systems to the lungs. The larvae exit into the alveoli and ascend the bronchial tree. The larvae are coughed up and typically subsequently swallowed. The swallowing is asymptomatic and is unknown by the person. The female adults establish chronic infection in the small intestine. Adult females shed eggs that hatch into non-infective rhabditiform larvae. These can be detected in the stool. At times, the larvae may mature into infective filariform larvae while still in the host. These infective larvae can penetrate the intestinal wall, migrating to the lungs and re-establishing infection in approximately 2 weeks.

Answer 160

STRONG Soil exposure Corticosteroids (hyper infection risk) HTLV infection WEAK Travellers Impaired immunity Solid organ transplant recipient

Answer 161

``` COMMON Abdo pain Altered bowel habit WL Fever (hyper infection) ``` ``` UNCOMMON Chronic cough Wheezing Pruritus / dermatitis Larva currens Urticaria Cutaneous larvae migrans (usually hookworm but can be seen with strongyloides) Sx of IBD (duodenitis) ```

Answer 162

Stool ova and parasites examination - strongyloides larvae seen on stool examination FBC - may or may not show eosinophilia Therapeutic trial of ivermectin - at follow-up at 6 months' post-treatment, eosinophilia will have resolved in successfully treated people

Answer 163

ivermectin: children <15 kg body weight: consult specialist for guidance on dose; children and adults ≥15 kg body weight: 0.2 mg/kg orally as a single dose for 1-2 days, may repeat in 2-4 weeks if necessary OR albendazole: children: consult specialist for guidance on dose; adults: 400 mg orally twice daily for 3-7 days

Answer 164

Once fully treated, strongyloides infection does not recur unless there is re-exposure to infected soil. Critical illness is more common when there are delays in diagnosis or in seeking health care. The mortality rate among patients who develop hyperinfection syndrome or disseminated strongyloidiasis may be as high as 90%

Answer 165

Loa loa encephalitis Incomplete eradification Hyperinfection

Answer 166

threadworm / strongyloides infection Chronic strongyloides infection may result in a misdiagnosis of somatisation disorder, psychogenic pruritus, irritable bowel disorder or asthma. People who have migrated from endemic areas who have chronic strongyloides infection and are started on corticosteroids may develop life-threatening hyperinfection. Hyperinfection may present with fever, cough, wheezing, and/or abdominal pain. Patients often rapidly become critically ill with bacteraemia and sepsis caused by an enteric organism, such as Escherichia coli or enterococcus. Strongyloides larvae may be detectable in stool or sputum specimens in patients with hyperinfection, and pulmonary infiltrates may be present on an chest x-ray. Eosinophilia may be absent. Absence of eosinophilia is a strong predictor of mortality from strongyloides hyperinfection.

Answer 167

threadworm / strongyloides infection Chronic strongyloides infection may result in a misdiagnosis of somatisation disorder, psychogenic pruritus, irritable bowel disorder or asthma. People who have migrated from endemic areas who have chronic strongyloides infection and are started on corticosteroids may develop life-threatening hyperinfection. Hyperinfection may present with fever, cough, wheezing, and/or abdominal pain. Patients often rapidly become critically ill with bacteraemia and sepsis caused by an enteric organism, such as Escherichia coli or enterococcus. Strongyloides larvae may be detectable in stool or sputum specimens in patients with hyperinfection, and pulmonary infiltrates may be present on an chest x-ray. Eosinophilia may be absent. Absence of eosinophilia is a strong predictor of mortality from strongyloides hyperinfection.

Answer 168

Typhoid infection is a faecal-oral transmissible disease caused by the bacterium Salmonella enterica, serotype S typhi. A similar clinical syndrome is caused by Salmonella enterica, serotype S paratyphi, and the terms 'enteric fever' and typhoid infection are used to describe both diseases. Unless otherwise stated, the information presented here will relate to both diseases (S typhi and S paratyphi) described by the term typhoid infection. Most typhoid infections occur in less-developed countries where sanitary conditions remain poor and water supplies are not treated. Humans are the only known reservoir, and transmission occurs through food and water contaminated by acutely ill or chronic carriers of the organism. Seen in developed countries mainly among travellers returning from endemic countries. Highest incidence is in the Indian subcontinent and among travellers returning from that area. Prolonged febrile illness with normal WBC count in returnees from an endemic area should increase suspicion. Definitive diagnosis is by blood culture. Presumptive antibiotic treatment in the traveller should depend upon the country of origin. The current vaccines available offer only moderate protection against Salmonella typhi and almost no protection against S paratyphi, which has become a more dominant pathogen. With the current vaccine efficacy and the increase in multidrug-resistant strains, cases are expected to continue to increase and become ever more challenging to treat.

Answer 169

21 million cases of typhoid annually worldwide 222,000 typhoid-related deaths

Answer 170

The main causative agent of typhoid infection is Salmonella enterica, serotype S typhi, which, in most regions, accounts for 60% to 80% of cases The other Salmonella enterica serovars are S paratyphi, species A, B, and C, which differ in their geographical distribution. S paratyphi A is a common pathogen in the Indian subcontinent, while S paratyphi B is found in Indonesia, Malaysia, the Mediterranean region, and South America, and S paratyphi C is found in Africa. All of these species are restricted human pathogens that, unlike many other salmonellae, do not infect poultry, reptiles, or mammalian livestock.

Answer 171

``` STRONG Overcrowded endemic areas Poor sanitation Poor hygiene Indian subcontinent / meico Longer duration of stay in endemic country ```

Answer 172

``` COMMON High fever - sometimes occurs in a step-wise fashion with 5 to 7 days of daily increments in maximal temperature of 0.5°C to 1°C, with the height of fever usually occurring in the afternoon. Dull frontal headache (80%) Abdominal pain Anorexia Apathetic-lethargic state Constipation (interestingly more common than diarrhoea) Cough Diarrhoea Prostration (flat lying) ``` ``` UNCOMMON Chills Hepatomegaly Pneumonia Relative Brady Rigors Rose spots Splenomegaly ```

Answer 173

FBC - WBC: low to normal; haemoglobin: mild anaemia; platelets: low to normal Transaminases - 2 to 3 times upper limit of norma Blood, stool + urine culture BM culture should be considered in patients who have already started antibiotic treatment = +ve

Answer 174

ceftriaxone: children: 75 mg/kg/day intravenously given in 1-2 divided doses for 7-14 days, maximum 2000 mg/day; adults: 2000 mg intravenously once daily for 7-14 days

Answer 175

With antibiotic treatment, prognosis is generally good.

Answer 176

``` Resistance Typhoid hepatitis Bowel perforation and GI bleed Neonatal sepsis Death Chronic biliary carriage Extra-Intestinal ```

Answer 177

typhoid fever

Answer 178

Subacute granulomatous thyroiditis is a self-limited inflammation of the thyroid gland. It is associated with a triphasic clinical course that lasts for a few weeks to many months, characterised by transient thyrotoxicosis, hypothyroidism, and then a return to normal thyroid function in >90% of patients. The initial thyrotoxic phase is associated with thyroid pain, high serum thyroid hormone levels with a low radioiodine uptake, elevated ESR, elevated CRP, and a systemic illness similar to influenza, with fever, myalgia, and malaise Inflammation of the thyroid characterised by a triphasic course of transient thyrotoxicosis, followed by hypothyroidism, followed by a return to euthyroidism. The thyrotoxic phase is due to thyroid follicular damage and release of preformed hormone and is characterised by low thyroid uptake on nuclear scan and elevated ESR or CRP. Thyroid pain and tenderness, which may be migratory and affect different areas of the gland at different times, is typical of the thyrotoxic phase. Thyroid is often enlarged, firm, and tender to palpation. Ultrasound of the thyroid shows areas of hypoechoic echotexture with decreased or normal vascular flow by Doppler. The condition is self-limited, and no specific therapy is generally necessary. Non-steroidal anti-inflammatory drugs and beta-blockers may be used for symptoms. Some patients with severe symptoms may also require corticosteroids, opioid analgesics, or potassium iodide or iopanoic acid to reduce the conversion of T4 to the more biologically active form of thyroid hormone, T3.

Answer 179

There does not seem to be any global difference in epidemiology. The overall age- and sex-adjusted annual incidence rate calculated for one state in the US was estimated to be 4.9 cases per 100,000. The female-to-male ratio was 3.5:1, with most cases occurring between the ages of 30 and 50 years. A seasonal variation has been noted in several studies in many countries, with the highest incidence in the summer and autumn in the northern hemisphere (July to December), which is typical for viral infections.

Answer 180

The aetiology is presumed to be viral. A seasonal variation has been noted in several studies in many countries, with the highest incidence in the summer and autumn (July to December), which is typical for viral infections. The disease tends to occur after an upper respiratory infection. Post-convalescent viral titres of many common viruses (influenza, adenovirus, mumps, coxsackie, echo, H1N1) are elevated and then decrease in patients after the diagnosis of subacute granulomatous thyroiditis.

Answer 181

STRONG Viral infection HLA-Bw35 and B35

Answer 182

``` COMMON Neck pain Tender, firm, enlarged thyroid Fever Paliptations Recent viral infection (<1month) Myalgia Malaise Tremor Heat intolerance ```

Answer 183

TSH - Undetectable level in most patients during the initial or thyrotoxic phase. Later, during the hypothyroid or recovery phases, the TSH level will be variable. T4 T3 and free. thyroxine ALL elevated T3:T4 ratio - ratio <15:1 Radioactive iodine uptake - very low uptake, typically <1% to 3% at 24 hours; the uptake is too low to allow imaging of the thyroid ESR + CRP - High Anti-TPO - normal or mild elevation

Answer 184

Analgesia or corticosteroids for pain BB or CCB. for tachycardia/anxiety/tremor propranolol: 20-40 mg orally (immediate-release) every 4-6 hours Severe thyrotoxicosis: potassium iodide: 250 mg orally three times daily and prednisolone: 40 mg orally once daily for 2-3 weeks then taper over 4-6 weeks Hypothyroid phase - can use levothyroxine (usually if TSH >15) levothyroxine: 75-125 micrograms orally once daily initially, adjust dose according to thyroid function tests During treatment, TSH and free thyroxine index should be checked every 4 to 6 weeks.

Answer 185

Thyroid storm | Long term hypothyroidism

Answer 186

In ≥90% of patients, there is a complete and spontaneous recovery and a return to normal thyroid function. However, the thyroid gland may exhibit irregular scarring between islands of residual functioning parenchyma. Up to 10% of patients may require permanent replacement with levothyroxine due to persistent hypothyroidism. During the acute episode of subacute granulomatous thyroiditis, the symptoms may be exacerbated, but once the patient is fully recovered, it is unlikely to recur. In one cohort, the recurrence of subacute granulomatous thyroiditis is 4% after the initial episode.[

Answer 187

thyroiditis Occasionally, the patient may present with little or no neck pain but with high ESR, a triphasic course of thyroid dysfunction, and a firm goitre. Only 40% to 50% of patients go through all 3 clinical phases of subacute granulomatous thyroiditis (thyrotoxicosis, hypothyroidism, and euthyroidism). Some patients have only the thyrotoxic phase or the hypothyroid phase but with typical thyroid pain and high ESR. Other patients do not have pain but present with fever of unknown origin.[6]

Answer 188

Viral hemorrhagic fevers (VHFs) are a diverse group of animal and human illnesses in which fever and hemorrhage are caused by a viral infection. VHFs may be caused by five distinct families of RNA viruses: the families Arenaviridae, Filoviridae, Bunyaviridae, Flaviviridae, and Rhabdoviridae. All types of VHF are characterized by fever and bleeding disorders and all can progress to high fever, shock and death in many cases. Some of the VHF agents cause relatively mild illnesses, such as the Scandinavian nephropathia epidemica (a hantavirus), while others, such as Ebola virus, can cause severe, life-threatening disease.

Answer 189

Epidemiology[edit] Cocoliztli in Mexico 1545 and 1576.[2][5][6][7][8] The Great Yellow Fever Epidemic of 1793 in Philadelphia, PA, US. Nearly 10% of the population of 50,000 succumbed to the disease. Mékambo in Gabon is the site of several outbreaks of Ebola virus disease. Orientale Province, Democratic Republic of the Congo villages of Durba and Watsa were the epicenter of the 1998–2000 outbreak of Marburg virus disease. Uíge Province in Angola was the site of another outbreak of Marburg virus disease in 2005, the largest one to date of this disease.[9] A VHF outbreak in the village of Mweka, Democratic Republic of the Congo (DRC) that started in August 2007, and that has killed 103 people (100 adults and three children), has been shown to be caused (at least partially) by Ebola virus. A viral hemorrhagic fever is a possible cause of the Plague of Athens during the Peloponnesian War.[10] A viral hemorrhagic fever is an alternate theory of the cause of the Black Death and the Plague of Justinian[11] The initial, and currently only, outbreak of Lujo virus in September–October 2008 left 4/5 patients dead.[12] The 2014 West Africa Ebola outbreak, which was the biggest outbreak in history

Answer 190

Five families of RNA viruses have been recognised as being able to cause hemorrhagic fevers. The family Arenaviridae include the viruses responsible for Lassa fever (Lassa virus), Lujo virus, Argentine (Junin virus), Bolivian (Machupo virus), Brazilian (Sabiá virus), Chapare hemorrhagic fever (Chapare virus), Venezuelan (Guanarito virus) and Whitewater Arroyo virus hemorrhagic fevers. The family Bunyaviridae include the causative agents of Hantavirus hemorrhagic fever with renal syndrome (HV-HFRS), the Crimean-Congo hemorrhagic fever (CCHF) virus from the genus Nairovirus, Garissa virus and Ilesha virus from the Orthobunyavirus and the Rift Valley fever (RVF) virus from the genus Phlebovirus. The family Filoviridae include Ebola virus and Marburg virus. The family Flaviviridae include dengue, yellow fever, and two viruses in the tick-borne encephalitis group that cause VHF: Omsk hemorrhagic fever virus and Kyasanur Forest disease virus. In September 2012 scientists writing in the journal PLOS Pathogens reported the isolation of a member of the Rhabdoviridae responsible for 2 fatal and 2 non-fatal cases of hemorrhagic fever in the Bas-Congo district of the Democratic Republic of Congo. The virus was named Bas-Congo virus.

Answer 191

``` Petechiae Flushing Bleeding Oedema Hypotension Shock Malaise Muscle pain Headache Vomiting Diarrhoea ```

Answer 192

``` FBC - reduced WCC + platelets LFTs - increased Increased PT + APTT Haematocrit elevated Urea + creatinine - High due to dehydration ```

Answer 193

Medical management of VHF patients may require intensive supportive care. Antiviral therapy with intravenous ribavirin may be useful in Bunyaviridae and Arenaviridae infections (specifically Lassa fever, RVF, CCHF, and HFRS due to Old World Hantavirus infection)

Answer 194

An abscess is a collection of pus that has built up within the tissue of the body.

Answer 195

Incision + drainage ABx Sometimes packing - However, evidence from emergency medicine literature reports that packing wounds after draining causes pain to the person and does not decrease the rate of recurrence, nor bring faster healing or fewer physician visits Primary closure - Closing an abscess immediately after draining it appears to speed healing without increasing the risk of recurrence. This may not apply to anorectal abscesses. While they heal faster, there may be a higher rate of recurrence than those left open Loop drainage More recently, several North American hospitals have opted for less-invasive loop drainage over standard drainage and wound packing. In one study of 143 pediatric outcomes, a failure rate of 1.4% was reported in the loop group versus 10.5% in the packing group (P

Answer 196

Local clotrimazole oropharyngeal: 10 mg orally (dissolved in the mouth) five times daily for 14 days Systemic: fluconazole: 200 mg orally on day one, followed by 100-200 mg once daily for at least 2 weeks

Answer 197

Hepatotoxicity from systemic azole Rx Oesophageal candidiasis Disseminated candidiasis

Answer 198

Hereditary angioedema (HAE) is a disorder that results in recurrent attacks of severe swelling. The swelling most commonly affects the arms, legs, face, intestinal tract, and airway. Itchiness does not typically occur. If the intestinal tract is affected abdominal pain and vomiting may occur. Swelling of the airway can result in its obstruction. Attacks, without preventive treatment, typically occur every couple of weeks and last for a few days.

Answer 199

The prevalence of HAE is relatively low – between 1 in every 10,000 to 1 in every 50,000 persons.

Answer 200

AD inheritance Type I and II are caused by a mutation in the SERPING1 gene that makes the C1 inhibitor protein while type III is often due to a mutation of the factor XII gene.

Answer 201

Symptoms generally begin around puberty but can occur earlier. These individuals have recurrent swelling in the extremities, genitals, face, lips, larynx or GI tract. Some patients describe a sensation of fullness but not pain or itching in the affected area except for those with abdominal swellings who often experience acute abdominal pain. Others experience an intense amount of pain, described as radiating from the bone outward along with intense itching just beneath the skin and intense heat, regardless of the area targeted. Instances of swelling around the throat or larynx can cause difficulties in breathing should the swelling obstruct airways. This has been known to cause a large number of fatalities in those afflicted with the disorder. Episodes that attack the gastrointestinal tract can cause a number of complications including dehydration from being unable to keep anything down (which, depending on length of the episode, can prove fatal). Symptoms from GI tract swelling including violent vomiting, intense pain from the midsection, dehydration, and intense exhaustion. Some suffered of HAE suffer from 'wandering' attacks. These attacks will center around an extremity. For example: Should the sufferer's hand swell up, it will go through the normal swelling cycle before 'transferring' to either the connection limb (In this case wrist to forearm) or move to the opposite hand. Sufferers with this symptom may find their episodes last longer, and may find their triggers more difficult to track.

Answer 202

Genetic studies Complement testing - LOW C1 INHIBITOR or POSITIVE C1 INHIBITOR ANTIGENIC PROTEIN Also: low C4,C3, normal CH50

Answer 203

ACEi CONTRAINDIACTED (lead to bradykinin accumulation which precipitates disease episodes) C1 inhibitor concentrates.

Answer 204

About 25% of those affected die in the first two decades of life, mainly due to lack of treatment.

Answer 205

Death due to laryngeal obstruction

Answer 206

Trigger ID and avoidance H1 receptor antagonists - cetirizine: 10 mg orally once daily diphenhydramine: 25-50 mg orally every 4-6 hours when required prednisolone: 0.5 to 1 mg/kg/day orally given in 1-2 divided doses for 5-7 days Roughly 15% of the histamine receptors in the skin are H2-receptors. On this basis, H2-receptor antagonists (e.g., ranitidine, cimetidine) have been used in the treatment of chronic urticaria. montelukast: 10 mg orally daily

Answer 207

Takayasu's arteritis Buergers disease Giant cell arteritis

Answer 208

Buergers disease Giant cell arteritis Polyarteritis nodosa

Answer 209

Polyarteritis nodosa | Wegeners granulomatosis

Answer 210

Wegeners granulomatosis | Rheumatoid vasculitis

Answer 211

Inflammatory, obliterative arteritis affecting aorta and branches Females> Males

Answer 212

Symptoms may include upper limb claudication Clinical findings include diminished or absent pulses ESR often affected during the acute phase

Answer 213

Segmental thrombotic occlusions of the small and medium sized lower limb vessels Commonest in young male smokers

Answer 214

Proximal pulses usually present, but pedal pulses are lost

Answer 215

An acuter hypercellular occlusive thrombus is often present | Tortuous corkscrew shaped collateral vessels may be seen on angiography

Answer 216

Systemic granulomatous arteritis that usually affects large and medium sized vessels Females > Males Temporal arteritis is commonest type

Answer 217

Granulomatous lesions may be seen on biopsy (although up to 50% are normal) ESR + CRP high Temporal artery US - may show wall thickening (halo sign), stenosis or occlusion

Answer 218

Jaw claud Loss of vision - There is partial or complete loss of vision (painless) in one or both eyes in up to 20% of patients, which can progress to total blindness. Other vision symptoms may include amaurosis fugax and diplopia. Absent temporal pulse Tenderness, thickening, and nodularity of the frontal or parietal branches of the superficial temporal arteries may be present. A prominent or enlarged temporal artery is highly predictive of a positive temporal artery biopsy (likelihood ratio of 4.3) Possible bruit

Answer 219

Systemic necrotising vasculitis affecting small and medium sized muscular arteries Most common in populations with high prevalence of hepatitis B Renal disease is seen in 70% cases

Answer 220

Angiography may show saccular or fusiform aneurysms and arterial stenoses

Answer 221

Immunosupression is the main treatment for vasculitides.

Answer 222

Predominantly affects small and medium sized arteries Systemic necrotising granulomatous vasculitis Cutaneous vascular lesions may be seen (ulceration, nodules and purpura)

Answer 223

Loads but U+LRT involvement = the most prominent In the upper respiratory tract, these can include otorrhoea, pain or a muffled sensation in the ears, sinus pain, nasal discharge and crusting, epistaxis, hoarseness, stridor, oral and nasal ulcers, mucosal bleeding and inflammation, nasal septal perforation, saddle nose deformity, sinus tenderness, and tympanic perforation. In the lower respiratory tract, these can include SOB, cough, haemoptysis, chest pain, dyspnoea, focal dullness to percussion, crackles, rhonchi, focal reduction of air entry on auscultation.

Answer 224

c-ANCA +ve | Sinus imaging may show mucosal thickening and air fluid levels

Answer 225

Systemic lupus erythematosus (SLE) is a chronic multi-system disorder that most commonly affects women during their reproductive years. It is characterised by the presence of antinuclear antibodies. In addition to constitutional symptoms, it most frequently involves the skin and joints, although serositis, nephritis, haematological cytopenias, and neurological manifestations may occur during the course of the disease. Earlier diagnosis and better management have resulted in a lower prevalence of life-threatening disease. Generalised disorder that can affect any system. Symptoms and signs may accumulate over time. The diagnosis is made using criteria recommended by the American College of Rheumatology. Treatments for mild to moderate serositis or arthritis include hydroxychloroquine, non-steroidal anti-inflammatory drugs, or corticosteroids. Treatments for more severe disease may include cyclophosphamide, mycophenolate, or tacrolimus plus corticosteroids.

Answer 226

Common to all studies is that the disease occurs most frequently between the ages of 15 and 45 years, when it is 12 times more common in females than in males In those aged >45 years, the female-to-male ratio is 2:1 In one study, there was a racial gradient of 21 per 100,000 in white people, 47 per 100,000 in people of Asian descent, and 112 per 100,000 in those of African descent The disease is both much more common and severe in those of African and Asian descent than in white populations in Europe and the US

Answer 227

ANA DsDNA Smith antigen

Answer 228

``` STRONG Female 15-45 African / asian descent Drugs ``` WEAK Sun FHx Tobacco

Answer 229

``` "SOAP BRAIN MD": Any person having 4 or more of the 11 criteria is considered to have SLE. S = serositis O = oral ulcers A = arthritis P = photosensitivity B = blood disorder R = renal disease A = ANA positive I = immunological disorder N = neurological disease M = malar rash D = discoid rash ```

Answer 230

FBC - anaemia, leukopenia, thrombocytopenia; rarely pancytopenia APTT - may be prolonged in patients with antiphospholipid antibodies Urea + creatinine - elevated urea and creatinine if renal involvement ESR + CRP - H ANA + DsDNA + Smith antigen - positive Urinalysis - ANA DsDNA Smith antigen CxR - pleural effusion, infiltrates, cardiomegaly

Answer 231

hydroxychloroquine: 200-400 mg orally once daily - Now the cornerstone of treatment as it reduces disease flares and other constitutional symptoms. NSAIDs Corticosteroids - prednisolone: 5-40 mg orally once daily Lifestyle changes include dietary advice, smoking cessation, sun protection, and exercise. Alternative Rx: methotrexate: consult specialist for guidance on dose and folinic acid: consult specialist for guidance on dose

Answer 232

An updated meta-analysis on overall and cause-specific mortality in SLE suggested that patients with SLE have higher rates of death from all causes, regardless of sex, ethnicity, renal disease, cardiovascular disease, or infection. However, the risk of death due to malignancy is not increased

Answer 233

``` Complications table COMPLICATION TIMEFRAME LIKELIHOOD  anaemia long term high  leukopenia long term high  thrombocytopenia long term high  corticosteroid-related cataracts long term medium  corticosteroid-related osteoporosis long term medium  corticosteroid-related diabetes mellitus long term medium  amenorrhoea secondary to cyclophosphamide long term medium  male infertility secondary to cyclophosphamide and/or disease long term medium  pericarditis long term medium  myocarditis long term medium  endocarditis long term medium  pleuritis long term medium  pleural effusion long term medium  malignancy secondary to cyclophosphamide or azathioprine long term low  corticosteroid-related avascular necrosis long term low  haemolytic anaemia long term low  progressive multifocal leukoencephalopathy (PML) long term low  Raynaud's phenomenon variable high  infection due to immunosuppression variable medium  non-steroidal anti-inflammatory drug (NSAID)-related renal failure variable medium  NSAID-related gastritis variable medium  fetal loss variable medium  depression variable medium  pulmonary hypertension variable medium  diffuse interstitial lung disease variable medium  fracture risk variable medium  septic arthritis due to immunosuppression variable low  haematuria secondary to cyclophosphamide variable low  chronic active hepatitis variable low  lupus peritonitis variable low  pancreatitis secondary to disease or azathioprine variable low  arterial thrombosis variable low  venous thrombosis variable low  tendon rupture variable low  valvular heart disease variable low  transverse myelitis variable low  pulmonary haemorrhage ```

Answer 234

systemic lupus erythematosus Most patients present with symptoms of fatigue, typical rash and/or musculoskeletal symptoms. Other symptoms and signs at presentation may include headaches or lymphadenopathy (cervical or axillary). Patients may present with pleuro- or pericarditis. Uncommon presentations include severe serositis or organ manifestations such as nephritis, possibly following triggers such as sun exposure or infection.

Answer 235

systemic lupus erythematosus Most patients present with symptoms of fatigue, typical rash and/or musculoskeletal symptoms. Other symptoms and signs at presentation may include headaches or lymphadenopathy (cervical or axillary). Patients may present with pleuro- or pericarditis. Uncommon presentations include severe serositis or organ manifestations such as nephritis, possibly following triggers such as sun exposure or infection.

Answer 236

Artificial tears Ophthalmic ciclosporin drops Cholinergics - pilocarpine: 5 mg orally three times daily Specticle eye shields/humidifiers Salivary substitutes for improving lubrication and hydration of oral tissues are used alone as first-line therapy.

Answer 237

Explanation of symptoms to the patient is important, including reassurance that lifespan is generally not shortened.

Answer 238

Gram +ve suspected - vancomycin: 30 mg/kg/day intravenously given in divided doses every 12 hours The affected joint or joints should be aspirated to dryness as often as is necessary. G-ve suspected: ceftriaxone: 2 g intravenously every 24 hours IN GENERAL IV 2 weeks then 4 weeks oral Always seek microbiological input

Answer 239

Delayed or inadequate treatment can lead to irreversible joint destruction and subsequent disability. There is also an estimated case fatality rate of 11% A survey in the UK revealed that certain factors might be associated with a poor prognosis including older age, pre-existing joint disease, and the presence of a joint prosthesis

Answer 240

Allergic reaction to ABx Osteomyelitis Joint destruction

Answer 241

Septic arthritis

Answer 242

Septic arthritis

Answer 243

Prion diseases (or transmissible spongiform encephalopathies) are a group of uniformly fatal neurodegenerative diseases characterised by progressive dementia and motor dysfunction. These diseases occur in spontaneous, genetic, and acquired forms. Patients commonly present with behavioural or personality changes, myoclonus, visual disturbances, movement problems, and/or incoordination. Survival from first symptom is typically <1 year in sporadic and acquired cases. Group of rare, uniformly fatal neurodegenerative diseases. In humans they occur in 3 forms: sporadic (85% to 90% of cases), genetic (10% to 15%), and acquired (<1%). Prions or proteinaceous infectious particles are the misshaped proteins responsible for causing transmissible spongiform encephalopathies, or prion diseases. Present as very rapidly progressive dementias. Symptoms may vary, but include behavioural/psychiatric changes, memory impairment, visual disturbances, myoclonus, ataxia, language and hearing problems, and movement dysfunction. Misdiagnosis is common, as Creutzfeldt-Jakob disease (CJD) can present similarly to other neurological conditions. Pathology currently is the only definitive way to diagnose prion disease, although biopsy and even autopsy may yield false-negative results. Pre-mortem diagnostic tools that may be helpful include MRI, EEG, and CSF findings, as well as blood tests to rule out other conditions. Brain MRI, particularly diffusion-weighted imaging, has very high sensitivity and specificity for CJD, as does the real-time quaking-induced conversion (RT-QuIC) test on CSF. Currently, there is no cure for prion disease, and treatment consists of management of symptoms and palliative care. Survival for most sporadic prion patients is generally about 1 year or less, whereas survival of genetic prion disease varies greatly from a few months to several years depending on the mutation.

Answer 244

1 to 2 per million per year Median age of onset is mid to late 60 Approximately 85% to 90% of prion disease cases are sporadic, 10% to 15% are familial, and <1% are acquired

Answer 245

Sporadic Creutzfeldt-Jakob disease (sCJD) This is believed to occur spontaneously. This disease process begins when endogenous prion proteins, consisting of mostly alpha-helical and a small portion of beta-pleated sheet structure, spontaneously change shape into predominantly beta-pleated structures, called proteinaceous infectious particles or prions. It is not yet known how the prion forms from the prion protein. The working model is that once a prion forms, it becomes a template so that when prion proteins (primarily alpha-helical structured) come in contact with it, they are also transformed into the beta-pleated structure, the prion. Genetic prion diseases These are caused by a mutation in the gene encoding the endogenous prion protein (PRNP) located on chromosome 20 Acquired prion diseases These include iatrogenic CJD (iCJD), variant CJD (vCJD), and the nearly extinct kuru. iCJD is categorised by the transmission of prions from one person to another through medical procedures. Prions are in highest concentrations in the brain (the eyes are directly connected to the brain through the optic nerve). Although not contagious in the traditional sense, prions can be directly transferred through invasive medical procedures such as cadaver-derived corneal transplants, dura mater grafts, and pituitary hormone replacement, as well as any other neurosurgery involving prion-contaminated surgical instruments vCJD occurs primarily from the transmission of prion disease in bovines to people through ingestion of prion-contaminated beef, with evidence that PrPSc is absorbed through the GI tract, enters the reticuloendothelial system and bloodstream, and eventually makes its way to the brain through the nervous system

Answer 246

``` STRONG Genetic predisposition Prion contaminated surgical instruments Transfusion Consumption of UK beef from 1980-1996 ``` WEAK Consumption of US beef American deer, moose, and elk Use of human growth hormone

Answer 247

``` COMMON Aphasia Gait ataxia Myoclonus Parkinsonism Psychiatric changes Visual changes ``` UNCOMMON Insomnia Painful sensory symptoms Movement disorder

Answer 248

Brain MRI - often demonstrates hyperintensity in the cerebral cortex (cortical ribboning), basal ganglia (caudate and putamen), and thalamus on diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) sequences, and hypointensity (restricted diffusion) on attenuated diffusion coefficient map (ADC) sequences

Answer 249

Supportive BDZ Antipsychotics SSRIs

Answer 250

There is no cure for prion disease due to its neurodegenerative nature. Pharmaceutical treatment is targeted for symptom management and palliative care.

Answer 251

``` Aspiration pneumonia DVT PE Constipation SBO LBO Pressure ulcer UTI ```

Answer 252

prion disease Some clinicians call Creutzfeldt-Jakob disease (CJD) the great imitator, as it can present like many other neurological/psychiatric conditions, depending where in the brain the prions are accumulating and causing neuronal dysfunction. Although typically of subacute onset (symptoms developing over days to weeks), sporadic CJD (sCJD) sometimes presents acutely, similar to a stroke.[15] Two variations of sCJD, the Heidenhain and Brownell-Oppenheimer variants, may also occur. In the Heidenhain variant of sCJD, patients present early on with predominantly visual symptoms, generally in the absence of other symptoms.[16][17] The Brownell-Oppenheimer variant is a cerebellar variant with first symptoms of profound ataxia.[18] The occurrence of a rapidly progressive dementia with motor signs (e.g., parkinsonism, incoordination, and myoclonus) and behavioural changes all progressing over several weeks, with generally normal CSF findings (mildly elevated protein is common) and a brain diffusion-weighted imaging MRI showing hyperintensity of the cortical gyri and basal ganglia is virtually pathognomonic for sCJD.

Answer 253

Osteomyelitis is an inflammatory condition of bone caused by an infecting organism, most commonly Staphylococcus aureus. It usually involves a single bone but may rarely affect multiple sites. Severity can be staged depending on the aetiology of the infection, its pathogenesis, extent of bone involvement, duration, and host factors particular to the individual patient. Broadly, bone infection is either haematogenous (originating from bacteraemia) or contiguous focus (originating from a focus of infection adjacent to the area of osteomyelitis). Despite these different causes all forms of acute osteomyelitis may evolve and become chronic, sharing a final common pathophysiology, with a compromised soft-tissue envelope surrounding dead, infected, and reactive new bone. Suspect osteomyelitis in those with a history of open fracture, recent orthopaedic surgery, or a discharging sinus; in the immunocompromised patient; or in the unwell child. Plain radiographs provide a good initial imaging modality for screening acute and chronic osteomyelitis. Magnetic resonance imaging and computed tomography (CT) may be used to determine diagnosis and treatment decisions. In some cases positron emission tomography/CT or single-photon emission computed tomography/CT may have a role. Diagnosis must be confirmed using deep microbiological samples via radiological guided biopsy or open surgery. In chronic osteomyelitis, surgery to remove the dead bone is the primary treatment modality. Antibiotics alone cannot achieve a cure. Giving empirical antibiotics without microbiological sampling should be avoided, with the exception of patients who are septic and unwell. Even then, blood cultures should be taken before antibiotics are given. Only cultures from deep sites are reliable. There is no value in surface or sinus swabs.

Answer 254

21.8 cases per 100,000 person-years

Answer 255

Osteomyelitis may be caused from haematogenous spread, direct inoculation of micro-organisms into bone, or from a contiguous focus of infection. A trivial skin infection may be the source of bacteraemia, or it may have emerged as the result of a more serious infection such as acute or subacute bacterial endocarditis. Intravenous drug misuse has been linked to haematogenous osteomyelitis involving the long bones or vertebrae. The commonest organism causing osteomyelitis remains Staphylococcus aureus, which is responsible for one third of all acute osteomyelitis and up to half of all vertebral osteomyelitis. The next most common organisms implicated in acute osteomyelitis are streptococci, Enterobacteriaceae, and anaerobic bacteria. Different groups of patients are more susceptible to different organisms. Common micro-organisms in acute haematogenous osteomyelitis Infants: S aureus Group B streptococci Aerobic gram-negative bacilli Children up to 4 years: S aureus Streptococcus pyogenes Haemophilus influenzae (in those not immunised) Kingella kingae (increased incidence in children under 4 years) Older children and adults: S aureus Older adults: Gram-negative bacilli Patients with intravascular devices: S aureus Candida species Patients who misuse intravenous drugs: S aureus Pseudomonas aeruginosa Patients with sickle cell disease; patients from developing countries: S aureus Salmonella species In endemic areas, Brucella, Burkholderia pseudomallei (melioidosis), and dimorphic fungal infections should be considered.

Answer 256

``` STRONG Penetrating injuries Surgical decontamination IVDU DM Periodontitis ```

Answer 257

``` COMMON NS pain at site of infection Malaise + fatigue Local inflammation, erythema, swelling Low grade fever Wound drainage Scars Previous flaps Reduced ROM Reduced sensation in diabetic foot ulcer ``` ``` UNCOMMON UTI Torticollis - May be suggestive of vertebral osteomyelitis; occurs secondary to soft-tissue infection of the neck. Limb deformity Tenderness to percussion ```

Answer 258

WCC ESR CRO Plain xray - acute disease: osteopenia appears 6-7 days after infection onset, and evidence of bone destruction, cortical breaches, and periosteal reaction follow quickly; involucrum and sequestra can sometimes be seen, with further diffuse osteopenia developing later secondary to disuse of the affected limb; chronic disease: intramedullary scalloping, cavities, and cloacae may be seen, with a ‘fallen leaf’ sign noted when a piece of endosteal sequestrum has detached and fallen into the medullary canal MRI - may show high signal on T2 images or fat suppression sequences

Answer 259

In general, patients with acute osteomyelitis require intravenous antibiotics for 2 to 4 weeks. Alternatively, intravenous antibiotics may be given for 2 weeks followed by an additional 2 to 4 weeks of oral antibiotics. Supportive Consideration of surgical Rx Chronic osteomyelitis will need surgery

Answer 260

Management of osteomyelitis in dedicated units, with close multidisciplinary working, is associated with high success rates and high patient-satisfaction scores. The prognosis from early intervention is usually better, particularly in the context of implant-related infection. Delay in treating these patients is likely to worsen long-term outcomes. The functional outcome for osteomyelitis of the lower extremity depends on the status of the foot and knee. Most patients with acute osteomyelitis recover with no long-term complications if osteomyelitis is diagnosed promptly and treated adequately.

Answer 261

``` Drug reactions Flap failure Amputation Growth disturbance Joint stiffness Recurrence Fracture Neurological impairment if abscess or bony collapse - degenerative disc disease Intravascular catheter related infections ```

Answer 262

osteomyelitis Symptoms of osteomyelitis vary with the duration of the disease and may have a gradual onset over several days. A patient with acute osteomyelitis typically presents as acutely unwell, with bone pain in the region affected along with tenderness, warmth, and swelling. Pain may occur with or without movement. This classic presentation does not occur in all cases. Some sites, such as the vertebrae or pelvis, may present a diagnostic challenge with a systemically unwell patient displaying signs of sepsis but without clear localising signs. Chronic osteomyelitis generally has a longer duration of symptoms. The pain may be less severe, with minimal fever and fewer constitutional symptoms. There is often a history of a discharging sinus or signs of old healed sinuses, soft-tissue abscesses, or scars from previous surgery or injury. Patients may have lived with discharging sinuses for years, having previously been told that there is nothing that can be done for their problem. Chronic osteomyelitis may produce long-term ill health with weight loss, malaise, fatigue, or depressed mood. Acute systemic upset is less common but pyrexia, sweating attacks, and anorexia are associated with flare-ups of the disease.

Answer 263

osteomyelitis Symptoms of osteomyelitis vary with the duration of the disease and may have a gradual onset over several days. A patient with acute osteomyelitis typically presents as acutely unwell, with bone pain in the region affected along with tenderness, warmth, and swelling. Pain may occur with or without movement. This classic presentation does not occur in all cases. Some sites, such as the vertebrae or pelvis, may present a diagnostic challenge with a systemically unwell patient displaying signs of sepsis but without clear localising signs. Chronic osteomyelitis generally has a longer duration of symptoms. The pain may be less severe, with minimal fever and fewer constitutional symptoms. There is often a history of a discharging sinus or signs of old healed sinuses, soft-tissue abscesses, or scars from previous surgery or injury. Patients may have lived with discharging sinuses for years, having previously been told that there is nothing that can be done for their problem. Chronic osteomyelitis may produce long-term ill health with weight loss, malaise, fatigue, or depressed mood. Acute systemic upset is less common but pyrexia, sweating attacks, and anorexia are associated with flare-ups of the disease.

Answer 264

osteomyelitis Symptoms of osteomyelitis vary with the duration of the disease and may have a gradual onset over several days. A patient with acute osteomyelitis typically presents as acutely unwell, with bone pain in the region affected along with tenderness, warmth, and swelling. Pain may occur with or without movement. This classic presentation does not occur in all cases. Some sites, such as the vertebrae or pelvis, may present a diagnostic challenge with a systemically unwell patient displaying signs of sepsis but without clear localising signs. Chronic osteomyelitis generally has a longer duration of symptoms. The pain may be less severe, with minimal fever and fewer constitutional symptoms. There is often a history of a discharging sinus or signs of old healed sinuses, soft-tissue abscesses, or scars from previous surgery or injury. Patients may have lived with discharging sinuses for years, having previously been told that there is nothing that can be done for their problem. Chronic osteomyelitis may produce long-term ill health with weight loss, malaise, fatigue, or depressed mood. Acute systemic upset is less common but pyrexia, sweating attacks, and anorexia are associated with flare-ups of the disease.

Answer 265

Empirical ABx - piperacillin/tazobactam: 4.5 g intravenously every 6 hours If high risk for MRSA include: vancomycin: 1 g intravenously every 12 hours The use of empirical granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF) in patients with febrile neutropenia is typically not recommended. I saw it given tho.

Answer 266

Approximately 20% to 30% of patients with febrile neutropenia present with complications that require in-hospital management. Approximately 80% of patients admitted with their first episode of febrile neutropenia will be hospitalised for anywhere from 1 to 10 days (40% <5 days, 42% 5 to 10 days), with a median hospital stay of 11.21 days. The length of hospital stay appears to increase with repeated episodes

Answer 267

ABx induced fungal overgrowth Mortality ABx induced CDIF ABx induced MDR

Answer 268

Febrile neutropenia is defined as single oral temperature measurement of >38.3°C (>101°F) or a temperature of ≥38.0°C (≥100.4°F) sustained over 1 hour, with an absolute neutrophil count (ANC) of <500 cells/microlitre, or an ANC that is expected to decrease to <500 cells/microlitre over the next 48 hours. Febrile neutropenia is the most common life-threatening complication of cancer therapy; its treatment is often an oncological emergency. Empirical antibiotic therapy upon presentation has dramatically improved outcomes and decreased mortality from febrile neutropenia. A causative organism is only identified one third of the time, and therefore antibiotics are aimed at treating a broad spectrum of expected pathogens. Due to an inability to mount an inflammatory response, many patients with febrile neutropenia do not demonstrate localising signs or symptoms other than fever. Some patients may even be afebrile. Prophylactic antibiotics and growth factor support at the onset of neutropenia have only been shown to benefit a small subgroup of high-risk cancer patients receiving chemotherapy. Emerging resistance is limiting the role of prophylactic antibiotics.

Answer 269

Patients with febrile neutropenia often present without localising signs or symptoms due to an inability to mount an inflammatory response. Careful attention should be paid to all skin surfaces, skin folds, bodily orifices, sinuses, prior surgical or biopsy sites, and intravenous sites as possible sources of infection. Patients may occasionally be afebrile, especially if they are receiving corticosteroids.

Answer 270

Malaria is a parasitic infection caused by protozoa of the genus Plasmodium. Five species are known to infect humans; Plasmodium falciparum is the most life-threatening. It is naturally transmitted to humans through a bite by an infected female Anopheles mosquito but may potentially be transmitted by blood transfusion or organ transplantation. It is widely distributed throughout tropical and subtropical regions, and the main burden of disease falls on these areas. Travellers account for the majority of disease in Western countries. In Western countries, almost all malaria occurs in travellers; therefore, the diagnosis may be missed if a history of travel is not elicited. Patients typically present with non-specific symptoms such as fever, chills, sweats, headache, and myalgia. Examination of a Giemsa-stained blood film remains the diagnostic test of choice. Once the diagnosis of malaria is confirmed, treatment should be started urgently, as a delay may be associated with disease progression and complications. Management should be undertaken in conjunction with an infectious diseases specialist.

Answer 271

There were an estimated 219 million malaria cases worldwide (in 87 countries) in 2017, resulting in an estimated 435,000 deaths. Approximately 92% of all malaria cases and 93% of all malaria deaths occurred in the African region, and the majority of deaths were due to Plasmodium falciparum infection. Pregnant women and children aged under 5 years remain the most susceptible to disease in endemic areas.

Answer 272

Malaria is caused by protozoa from the genus Plasmodium and is transmitted to humans through a bite from one of 40 species of female Anopheles mosquitoes. Five Plasmodium species cause human disease: Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, Plasmodium malariae, and Plasmodium knowlesi. The majority of infections are caused by P falciparum and P vivax, and P falciparum is responsible for the most severe disease.

Answer 273

COMMON Fever - swinging in nature. Characteristic paroxysms of chills and rigors followed by fever and sweats may be described. Usually associated tachycardia. Patterns of fever are rarely diagnostic at presentation but may develop over time: fevers occurring at regular intervals of 48 to 72 hours may be associated with Plasmodium vivax, Plasmodium ovale, or Plasmodium malariae infections. In most patients there is no specific fever pattern. ``` Headache Weakness Myalgia Arthralgia Anorexia Diarrhoea ``` UNCOMMON ``` Seizures - falciparum NV Abdo pain Pallor Hepatosplenomegaly Jaundice Altered level of consciousness Hypotension Anuria/oliguria - falc Influenza like symptoms may occur as the only Sx in children ```

Answer 274

Thick blood smear - detection of parasitaemia Thin smear - detection of type of parasite Rapid diagnostic tests - detection of parasite antigen or enzymes FBC - may show thrombocytopenia, anaemia, variable white cell count Clotting - PT may be prolonged U+E - usually normal or mildly impaired; renal failure may be present in severe infection LFTs - may show elevated bilirubin or elevated aminotransferases Blood glucose - hypoglycaemia or hyperglycaemia Urinalysis - may show trace to moderate protein; urobilinogen and conjugated bilirubin may be present ABG - may demonstrate metabolic acidosis or lactic acidosis in severe disease

Answer 275

1. Chloroquine or hydroxychloroquine 2. IV Artesunate (1st line if severe) Primaquine can be used in low transmission areas

Answer 276

There were approximately 435,000 deaths from malaria globally in 2017. Children were the most vulnerable group, accounting for 61% of all malaria deaths worldwide. Most deaths occurred in the African region (93%). The majority of deaths were due to Plasmodium falciparum infection. Approximately 90% of travellers who acquire malaria will not become symptomatic until they return home.

Answer 277

``` COMPLICATION AKI Hypoglycaemia Metabolic acidosis Severe anaemia DIC Blackwater fever (Intravascular haemolysis resulting in haemoglobinuria) Septicaemia Seizures ARDS ```

Answer 278

malaria The symptoms of malaria are non-specific, and their severity depends in part on the infecting species and host immunity. Adults who live in endemic areas may develop only minimal symptoms, due to immunoglobulin G antibody and cell-mediated immunity, and to physiological tolerance of parasitaemia. However, individuals without pre-existing immunity, pregnant women, children, older adults, and those with comorbidities (e.g., HIV infection) are more at risk of severe malaria with Plasmodium falciparum. Pregnant women are also at risk of miscarriage, anaemia, and hyperparasitaemia. Complications of severe malaria include cerebral involvement, which may present as reduced consciousness level, diffuse disturbance of cerebral function, or seizures. Other complications include metabolic acidosis leading to respiratory distress, renal impairment, jaundice, severe anaemia, hypoglycaemia, disseminated intravascular coagulation, and shock. It is important to consider concurrent bacterial sepsis if there is shock or there are focal symptoms or signs. Lymphadenopathy (usually an important negative finding) has been reported in a case report. While non-falciparum infections are usually uncomplicated, there have been rare reports of severe disease.

Answer 279

malaria The symptoms of malaria are non-specific, and their severity depends in part on the infecting species and host immunity. Adults who live in endemic areas may develop only minimal symptoms, due to immunoglobulin G antibody and cell-mediated immunity, and to physiological tolerance of parasitaemia. However, individuals without pre-existing immunity, pregnant women, children, older adults, and those with comorbidities (e.g., HIV infection) are more at risk of severe malaria with Plasmodium falciparum. Pregnant women are also at risk of miscarriage, anaemia, and hyperparasitaemia. Complications of severe malaria include cerebral involvement, which may present as reduced consciousness level, diffuse disturbance of cerebral function, or seizures. Other complications include metabolic acidosis leading to respiratory distress, renal impairment, jaundice, severe anaemia, hypoglycaemia, disseminated intravascular coagulation, and shock. It is important to consider concurrent bacterial sepsis if there is shock or there are focal symptoms or signs. Lymphadenopathy (usually an important negative finding) has been reported in a case report. While non-falciparum infections are usually uncomplicated, there have been rare reports of severe disease.

Answer 280

``` STRONG Endemic area Inadequate prophylaxis Settled grants Low host immunity Pregnancy Age < 5 Older age ``` WEAK Iron administration in children

Answer 281

In most regions, a first-line antiretroviral therapy regimen will generally consist of 2 nucleoside reverse transcriptase inhibitors (NRTIs) in combination with a third agent (usually an integrase strand transfer inhibitor [INSTI] if available, or a non-nucleoside reverse transcriptase inhibitor [NNRTI] or boosted protease inhibitor [PI]). Supportive - counselling + prophylaxis + vaccinations + micronutrient supplementation + comorbidity management

Answer 282

Most patients on ART achieve virological suppression within 3 to 6 months. Viral rebound rates have decreased over the years, and the risk decreases with increasing duration of viral suppression. A UK-based cohort study of over 16,000 HIV-positive persons found that a substantial proportion of patients on ART will not experience viral rebound over their lifetime (approximately 1% of men who have sex with men aged 45 years and older experienced viral rebound per year)

Answer 283

``` Acute seroconversion Rapid progression AIDS HIV associated hypotestosterone ART associated CVD HIV associated thrombotic events HIV associated cancer, liver disease, neurodysfunction, DM Hearing impairment HIV opportunistic infections ```

Infection Flashcards

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