UTI, GI infections Flashcards

1
Q

range of urinary tract infections

A

–Urethral syndrome –Cystitis –Pyelonephritis –Renal abscess –Sepsis syndrome (‘septicaemia’; ‘bloodstream infection’) –Renal calculi with infection

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2
Q

define bacteriuria

A

the presence of bacteria in urine

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3
Q

significant bacteriuri (define)

A

large numbers of one type of bacteria in tthe urine

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4
Q

define pyuria

A

the presence of pus cells in the urine

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5
Q

uropathogens

A

E. coli Enterococcus sp Staph saprophyticus Staph aureus Klebsiella sp Enterobacter sp Proteus sp Pseudomonas Candida/adenovirus

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6
Q

Bacterial factors for infection

A

Mostly derived from gut flora – enter urethra via perineum, and ascend to bladder •Multiply rapidly in urine •Large inoculum favours infection •Some bacteria have specific virulence factors e.g. fimbriae (sometimes called pili (sing. pilus)) •They have features that enhance resistance to host immunity

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7
Q

virulence factors in e. coli for UTs

A

•Uropathogenic E. coli clones •Cystitis and pyelonephritis strains distinct. •Virulence factors: adhesins, P & F , haemolysin, K-antigen, endotoxin/exotoxin. •Close regulation of gene expression

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8
Q

Host factors for infection

A

•Short urethra •Pregnancy •Sexual intercourse •UTI abnormality •Urine abnormality •Urinary catheter/instrumentation

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9
Q

CA-UTI extraluminal

A

early: by insertion Late: by capillary action

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10
Q

CA-UTI intraluminal

A

break in the seal

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11
Q

how many HAI are CA-UTI?

A

20%

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12
Q

how many HA-UTI relate to catheters?

A

65%

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13
Q

how much each CA-UTI costs>

A

1200GBP

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14
Q

Types of urinary catheters:

A

•Standard silicone bladder catheters •Condom-style catheters •Silver-impregnated catheters •Intermittent self-catheterisation •Suprapubic catheters

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15
Q

ways to obtain CSU specimen

A

•‘CSU’ – aseptically-removed urine from a long-standing catheter or bag? •‘CSU’ - a sample taken by brief catheterisation

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16
Q

Definition of CA-UTI

A

•An infection occurring in a person whose urinary tract is currently catheterised OR has been catheterised within the previous 48 h

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17
Q

clinical manifestations of UTI

A

•May be asymptomatic •Dysuria, frequency, urgency, polyuria, suprapubic pain & tenderness •Loin pain, fever & malaise, rigors •Haematuria •Babies – failure to thrive, convulsions •Elderly - confusion, fevers, urine ‘off’ •Renal colic if stones •Occasional incontinence

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18
Q

types of diagnostic specimens for urine

A

•MSU – mid-stream urine •CSU – catheter specimen of urine •‘Clean catch’ •Bag urine (infant) •SPA - supra-pubic aspirate •EMU – early morning urine (for TB) •Terminal – final part of urine stream (for schistosomiasis) •Others e.g. renal calculus or sample from ureter •NB Blood cultures if septicaemic

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19
Q

laboratory examination of urine criteria How many bacteria is significant? Is it normal for catheterised patients to have organisms in urine? Is it normal in suprapubic urine?

A

•Classically if > 10^5 bacteria per ml (one type only) then this is significant. In practice lower numbers likely significant in pure growth. •This cut-off is used as a few organisms normally come from the urethra and contaminate the urine. •Catheterised patient – catheter urine nearly always has organisms after a few days. •Suprapubic urine – should be sterile

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20
Q

Mangement of UTIS

A

•Non-specific •Specific: Trimethoprim, cephalosporins, nitrofurantoin, [amoxicillin], [ciprofloxacin] –Typically 3 or 5 days (7 d male, pregnant woman) •Severe (?pyelonephritis): IV co-amoxiclav +/- gentamicin OR cefuroxime –Typically 7-10 days •Prophylaxis – Trimethoprim, nitrofurantoin; cranberry juice? •Radiological imaging, IVU, Ultrasound, CT etc •Surgical correction of abnormalities

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21
Q

what abx can you use in pregnancy for uti?

A

cephalosporins, nitrofurantoin, [amoxicillin], cefuroxime

22
Q

management of UTI in hospital

A

•Don’t treat catheter colonisation only •Check for recent urine cultures and recent antibiotics to guide treatment •Non-compromised (no sens, not severe): best guess: oral co-amoxiclav; nitrofurantoin –Typically 5 days •Compromised/Severe: IV piperacillin-tazobactam (or meropenem if known MDR pathogens) +/- gentamicin; OR ciprofloxacin (+/- gent) if allergy –Typically ~7 days •Change catheter if present

23
Q

becteria resistance in UTIs

A

• In General Practice: ESBL- producing E.coli and other coliforms • Resistant to nearly all oral agents and often IV ones also • Even if patient has not been in hospital recently

24
Q

common communit acquired GI bacteria

A

●Campylobacter spp ●Salmonella spp – food poisoning & enteric fever species ●Shigella spp ●Escherichia coli - various types e.g. enteropathogenic, enteroinvasive; also E. coli O157 ●Vibrio cholerae [travellers] ●Toxin-producers: Clostridium perfringens, Cl. botulinum, Staphylococcus aureus ●Helicobacter pylori: Gastric infection

25
Q

Viruses and parasites (GI) in community

A

Rotabirus, norovirus, Giardia, Cryptosporidium, worms

26
Q

Hospital acquired GI infections

A

C Diff Norovirus

27
Q

GI organisms in immunocompromised

A

●Clostridium difficile, Norovirus PLUS any community-acquired organism ●CMV, Mycobacterium avium, Isospora etc

28
Q

GI infections specifically of concern in sickle cell pateints

A

SICKLE CELL PATIENTS ●Special concern about Salmonella – can be disseminated and cause osteomyelitis

29
Q

uk epidemiology of GI infections

A

□Campylobacter (87 cases per 100,000) □Salmonella (21 cases) □Cryptosporidium (9 cases) □Escherichia coli 0157 (2 cases

30
Q

Specific toxins & other virulence factors S aureaus C Botulinum V cholerae E coli Helicobacter pylori Shigela C diff

A

●Staph aureus toxin, Botulinum toxin in food (i.e. not strictly GI infections) ●Cholera toxin ●E. coli LT toxin (very similar to cholera toxin) & ST ●VTEC (i.e. vero-cytoxin producing E. coli) e.g. strain O157 – if severe, haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopaenic purpura (TTP) ●Helicobacter urease, cagA ●Shigella shiga toxin ●Clostridium difficile toxin A+B

31
Q

Clinical features of GI infection

A

●Diarrhoea! More than 3 in a day & sample takes shape of pot ●May be blood and/or pus in stool, or just watery ●Nausea & vomiting ●Fever & systemic illness uncommon – of concern ●Abdominal pain/cramps ●Often lasts only a day – self limiting ●Dehydration & Na+ & K+ depletion, esp. children (can lead to death) □?Travel history ?Antibiotic history ?Immunocompromised

32
Q

Amoeboids Distribution How humans get infected what can cysts survive and not?

A

□Worldwide distribution □Free-living environmental species e.g. Acanthamoeba, Naegleria □Human pathogens - ingestion of cysts contaminating food/water. E.g. Entamoeba histolytica □Only some strains of amoebae cause disease; non-pathogenic amoebae found in normal gut (e.g. Entamoeba coli; Iodamoeba) □Cysts survive water chlorination (e.g. tablets): destroyed at 50oC

33
Q

Entamoeba histolytica Distribution Diseases caused Diagnosis/ Ix Tx

A

□Asia, Africa, S America; faecal-oral spread - ingestion of cysts contaminating food/water. □Amoebic dysentery, flask-shaped ulcers in colon; Liver (& occasionally lung/other) abscess □Diagnose by examining a “hot stool” for amoebae; also serology (amoebic FAT). Metronidazole treatment for dysentery, abscesses; diloxanide follow up to kill residual cysts. □Non-pathogenic E. dispar

34
Q

clinical syndrome with amoebae infection

A

□Intestinal disease ●Asymptomatic ●Dysentery, toxic megacolon, amoeboma. Perianal ulceration □Extra-intestinal disease ●Liver abscess with or without peritonitis, empyema, pericarditis ●Lung & brain abscess

35
Q

TYPICAL PRESENTATION OF AMOEBA DISEASE

A

Presentation - Intestinal ●History days to weeks ●Diarrhoea +/- blood & mucus ●Abdo pain & tenderness ●Weight loss ●Fever (30-40%) □Extra-intestinal disease ●Depends on site: fevers, plus RUQ pain (liver), + abdo pain; cough, chest pain (lung) seizures (CNS)

36
Q

diagnosis and treatment of amoeba disease

A

□‘Hot stool’ sample! – microscopy for trophozoites x 3 □Stool for cysts □Colonic biopsy/histology □Aspiration of abscess □Amoebic serology (IFAT) □Metronidazole treatment of all acute infections □Diloxanide to kill gut cysts

37
Q

Classes of parasitic worms

A

Roundworms (Nematodes) □Adult and larval roundworms cylindrical & inhabit intestinal and extraintestinal sites. Flukes (Trematodes) □Adult flukes are leaf-shaped flatworms. The life-cycle includes a snail intermediate host. Tapeworms (Cestodes) □Adult tapeworms are elongated, segmented flatworms that inhabit the intestinal lumen. Larval forms inhabit extraintestinal tissues.

38
Q

species of roundworms

A

□Ascaris lumbricoides □Whipworm (Trichuris trichiura) □Hookworms (Necator, Ancylostoma) □Pin worm (thread worm) (Enterobius vermicularis) □Strongyloides stercoralis □Animal roundworms □[Non-GI: ‘Tissue nematodes’: Filiariasis, Dracunculiasis, Trichinosis]

39
Q

Ascaris lumbricoides epidemiology distribution

A

□1-1.5 bn infected □Distribution: mostly tropics, warm temperate if poor sanitation □Most asymptomatic □60,000 deaths/yr

40
Q

ascaris lumbricoides basic life cycle

A

●ingest ova directly or in water (faecal contamination), ●larvae penetrate gut, migrate through lungs ●larvae coughed up & swallowed, ●male & female adults in small bowel ●ova excreted in faeces. □Children most heavily infected □Faeces used for fertilising crops □80% of people in endemic areas □Eggs viable up to 6 yrs □One egg ingested=one worm □In UK mostly travellers/immigrants from endemic areas

41
Q

clinical features of ascaris lumbriocoides

A

□Asymptomatic □Pulmonary hypersensitivity response to migrating larvae – cough, fever, eosinophilia; CXR changes in some □Mild abdo discomfort, nausea, dyspepsia □Heavy worm burden e.g. 50-500 worms: (exacerbate) malnutrition; intestinal obstruction; perforation; cholangitis; secondary sepsis

42
Q

Diagnosis and Tx of ascariasis

A

Diagnosis □Stool examination □Larvae in sputum or gastric aspirate □Discovery at gut surgery or endoscopy Treatment: □Mebendazole □(Surgery

43
Q

Whipworm (trichuris trichiura) distribution epidemiology

A

Whipworm (Trichuris trichiura) □1 bn people infected (co-infection Ascaris) □Distribution: tropics - poverty □Most asymptomatic □Heavy infestation: Dysentery-type syndrome; rectal prolapse; Fe deficiency anaemia, growth retardation

44
Q

Whioworm - trichuris trichiura basic life cycle

A

●ingest ova directly or in water (faecal contamination); male & female adults in epithelium of caecum/colon; ova excreted in faeces

45
Q

Pin worm (thread worm) (enterobius vermicularis) epidemiology and basic life cycle

A

□Disease: Enterobiasis □0.5 bn? people infected, most children □Distribution: worldwide inc temperate zones □Most asymptomatic □Perianal itching; ?appendicitis □Basic life cycle: ●ingest ova directly on hands; larvae hatch, form adult in caecum; female adult migrates through anus, lays ova peri-anally; ova contaminate hands/nails

46
Q

hookworm (necator americanus, ancylostoma duodenle epidemiology clinical fetures

A

□Disease: Hookworm □1-1.5 bn people infected □Distribution: Tropical, subtropical zones □Most asymptomatic; Fe deficiency anaemia □Basic life cycle: ●Filariform larvae penetrate skin, migrate through lungs; larvae coughed up & swallowed, male & female adults in duodenum; ova excreted in faeces, larvae mature 1-2 days from rhabditiform to filariform. Clinical: □“Ground Itch” at site of penetration of skin □Transient pneumonitis □Diarrhoea, abdo discomfort in new host □Eosinophilia □Iron deficiency anaemia □Treatment: albendazole / mebendazole

47
Q

Strongyloides stercoralis

A

□30-300 m people infected □Distribution: Tropical, subtropical zones □Most asymptomatic; hyperinfection syndrome □Basic life cycle: ●Filariform larvae penetrate skin, migrate through lungs; larvae coughed up & swallowed; female adults in duodenum/jejunum; eggs through parthenogenesis, hatch into rhabditiform larvae in mucosa (into faeces) which then develop into filariform larvae [free-living male/female cycle] ●Some filariform larvae form in host - autoinfection Clinical: Acute: □Rash at site of penetration of skin □Transient pneumonitis □Diarrhoea & abdo pain, eosinophilia Chronic: Infection regulated by cell-mediate immunity □Asymptomatic (50% or perianal rashes, abdo pain, fluctuating eosinophilia)

48
Q

strongyloides in the compromised host

A

Steroids, lymphomas, leukaemias, HTLV-1, [HIV] Hyperinfection syndrome □Increased numbers in lung, gut Dissemination □Larvae also in CNS, kidneys, liver, etc □Often no eosinophilia □Gut ulceration, sepsis syndrome & meningitis, GI haemorrhage, pneumonitis □Diagnosis: ●Clinical awareness of residency in risk country at time of immunosuppression ●Larvae in stool, sputum ●Biopsies of tissue ●Antibody studies □Treatment: ivermectin / thiabendazole; reduce immunosuppression

49
Q

Trichinella spiralis

A

□Eat meat containing larval cysts □In stomach larvae released, in small intestine mucosa develop into adult worms □Adults produce larvae which enter host skeletal muscle □Form cyst, may calcify □Myositis, periorbital oedema, fever, eosinophilia □Possibly mebendazole

50
Q

FLukes

A

□Liver flukes: Clonorchis, Opisthorcis, (biliary tree; mainly Asia; snail-fish cycle, humans eat undercooked fish); Fasciola (sheep liver fluke: snail, watercress, gut lumen, peritoneum, liver) □Intestinal flukes: Fasciolopsis (pigs mainly - snail, watercress, gut lumen only) □Lung flukes: Paragonimus (snail, crustaceans, gut, peritoneum, lung)

51
Q

tapeworms (Cestodes)

A

□Pork Taenia solium □Beef T. saginata □Fish Diphyllobothrium □From dogs: Hydatid Echinococcus granulosus, E. multilocularis