Microbiology

19 - 30yo commonest is Neisseria gonnorhoea, the arthritis occurs after an asymptomatic period. Take a sexual history in a young person with a single inflammed joint!

Red/pink

• Do not retain crystal violet as outer membrane prevents it getting in
• Retain safranin (red)

• Have 2 membranes:
• 1. cytoplasmic membrane
• ------ thin peptidoglycan layer
• ----- periplasmic space
• 2. outer membrane containing LPS and porins
•       LPS includes lipid A, a core polysaccharide and the O Ag

• more antibody resistant (impenetrable wall)
• pathogenesis may be associated with cell envelope especially LPS (endotoxin) layer- LPS --> cytokines --> inflammation
• don't sporulate (except Coxiella burnetii)

Purple

Retain crystal violet after washing

• salmonella typhi (G-)
• salmonella paratyphi

Incubation: 21d or less

Clinical: stepwise temperature increase, malaria has been excluded, abdo symptoms, relative bradycardia (expect heart rate to increase by 15bpm for each degress above 37ish so tachycardia expected if pyrexial. 80 - 90 therefore = bradycardia).

"Rose Spots"= 2 - 3mm pale pink spots, mainly on torso

"pea soup" diarrhoea or constipation.

Investigations: blood and stool cultures diagnostic. EXCLUDE MALARIA.

Sequelae: GI perforation, bleeding

gram negative

Transmission: faecal-oral

• Enteric Fever.

Incubation: 2 - 6 weeks

Clinical: flu-like prodrome (2 weeks), icteric hepatitis (2 weeks - 3 months). May be asymptomatic in <5yo

Transmission: faecal-oral (sometimes sexual, especially in MSM)

Outcome: moratlity ~1-%, increased in >40yo, CLD, HepB or C or EtOH

• Investigations:
• 1. hepatitic biochemistry (high AST/ALT, BR, mildly high ALP)
• 2. IgM anti-HAV using EIA

Management: symptom control, rest, hydration, outpatient care. May give Ig or HAV vaccine to contacts.

ALT and AST 500 - 10,000 IU/L in first few weeks

BR 30 - 100 umol/L, conj and unconj and bilirubinuria

ALP <300IU/L

PT 1 - 5 seconds prolonged. (>5s suggests impending hepatic failure)

Transmission: global majority acquired vertically. Efficient sexual transmission.

• Clinical: asymptomatic in children and immunosuppressed. ~30% icteric, can --> fulminant hepatitis, cirrhosis, and hepatocellular cancer.
• 1% get fulminant hepatitis - decompensated liver disease, 50% mortality.

10% get chronic HBV (antigen + for >6mo), typically asymptomatic until cirrhosis and decompensated liver disease - ascites, jaundice, varices, confusion, cachexia, death.

10% with cirrhosis --> Ca (enlagring liver, weight loss, death).

• Investigations:
• 1. hepatitic biochemistry when acute (high AST/ALT, BR, mildly high ALP) OR mildly high AST/ALT when chronic
• 2. Worsening LFT and PT if cirrhosis or Ca
• 3. Serology - sAg proves infection. e and c are also useful and DNA is the most sensitive assay. NB. some mutations give HBeAg negative active infection (pre-core mutations).

Management: symptom control, fluids, rest. Lamivudine, adeofovir, inteferon. Liver transplant (if cirrhosis/Ca).

sAb = antibodies against the surface - positive with any exposure, incluidng infection and vaccination

eAb = antibodies against the core - positive in anyone who has had replicating virus in them - infected, chronic, carrier, and had previously but now cleared.

sAg = surface antigen - positive if currently have virus or recently vaccinated

eAg = core antigen - positive if currently replicating virus in the system - infected and infectious

HBV-DNA = DNA of the virus, positive if currently replicating virus in the system - infected and infectious

RNA virus, only occurs as co-infection with HBV

Transmission: sexual, IVDU. Acquired with acute HBV or as superinfection during chronis HBV. (May get two acute bouts of virus.)

Incubation: 3 - 7 weeks

• Clinical: 10x more likely to be fulminant, 80% fatal.
• When + acute HBV: severe icteric hepatitis (--> chronic in 80%). More rapid progression to cirrhosis and Ca.

Investigations: serum anti-HDV (antigen and RNA tests also possible)

Management: no effective antivirals. HBV vaccination and protective behaviour.

Transmission: IVDU, vertical (esp is HIV coinfection), some sexual (esp if HIV)

Incubation: 150 days

Clinical: ~20% are icteric, mainly asymptomatic. Fulminant rare unless HAV superinfection. 80% --> chronic HCV. ~20% develop cirrhosis 20 years later. 5% develop Ca 20 - 30 years later. Cirrhosis more likely and more rapid with HIV, HBV or EtOH.

Investigations: Ab assays (may be negative for first 9 months). ELISA for screening, RIBA for confirmation. PCR.

Management: no vaccine. Education and prevention. Vaccinate for HAV and HBV. pegylated inteferon injections + 6 - 12mo of ribavirin is curative for 50% (expensive).

• gram negative
• obligate intracellular cocci

• 3 human biovars:
• -- Ab, B, Ba, C = trachoma in the eyes
• -- D - K = STI cervicitis, urethritis, PID, neonatal pneumonia and conjunctivitis
• -- L1 - L3 = LGV

• discharge
• post-coital bleeding
• dysuria (especially in men)
• mucopurulent discharge in men
• pelvic pain
• cobble-stone appearance of cervix
• 50% women and 80% men aysmptomatic
• 2 week incubation

• salpingitis, PID
• infertility
• subsequent ectopic pregnancy
• perihepatitis (if ascends into abdomen)
• epididymitis
• conjunctivitis (neonatorum)
• Reiter's disease

ascending chlamydia enters the abdomenal cavity and causes perihepatitis??

• urine antigen detection
• vaginal swab culture
• NAAT?

• doxycycline
• contact tracing

• Chlamydia trachomatis
• L1, L2, L2a or L3
• infects lymphatics then monocytes
• commoner in MSM
• commoner in HIV infection
• primary stage: painless ulcer
• secondary: buboes and lymphangitis
• tertiary: fibrosis and long-term oedema

• painless genital ulcer 3 - 12 days after infection
• self-resolving, often goes unnoticed
• 10% get Erythema Nodosum

• 10 - 30 days after primary stage
• unilateral buboes - inflammed LN in groin
• lymphangitis, e.g. dorsal penis (cord-like)
• proctitis or proctocolitis
• cervicitis, perimetritis, salpingitis
• fever, malaise, anorexia

• painful enlarged inguinal LN
• inflammation --> thin skin, fixation
• progress to: necrosis, flutuant/suppurative LN, abscess, fistula, stricture, sinus tract, fibrosis obstructing lymphatics, chronic oedema

• anorectal pain
• tenesmus
• rectal discharge

• anorectal pain
• tenesmus
• rectal discharge
• diarrhoea
• abdominal cramps

• Plasmodium: falciparum (deadliest), vivax, ovale, malariae
• Protazoan

• Falciparum has most cases in UK and increasing.
• Malaria is 22% of the cases of fever in the returning traveller in the UK

Endemic Areas: subsaharan African (incl Ghana, Nigeria, Kenya), India, Southeast Asia, Central America and the northern part of South America

• Clinical: fevers and rigors (acute phase response), flu-like syndrome, cough, diarrhoea, jaundice
• NB. not typically rash or lymphadenopathy

Clinical differentials may include: flu, URTI, gastroenteritis, hepatitis

• Investigations:
• - blood film: thick blood film shows plasmodium, thin film shows subtype. 3 may be needed 24 h apart. Not diagnostic if patient is on semi-immunosuppressant levels of antimalarials.
• see "ring form" of RBC containing small parasite that has an eosinophilic nucleus, basophillic cytoplasm and a vacuole in the middle. Classify parasitaemia as % of the RBC on the film containing parasites.

increasing prevalence

Endemic Areas:

• lyssa virus
• an enveloped ssRNA with negative sense
• family: rhabdoviridae

Transmitted by bats, monkeys, cattle

Pathology: travels up peripheral nerves, incubation depends on distance to travel

Early: malaise, headache, fever (early encephalitis)

Mid: acute pain, violent movements, slight or partial paralysis, mania, depression, hydrophobia, hypersalivation, paranoia, hallucinations. Sometimes inflammation of spinal cord → transverse myelitis.

Late: mania, lethargy, confusion, coma, renal failure

Ix: hx, examine animal which bit, Negri inclusion bodies (eosinophilic, sharp outlines in cytoplasm of neurons, they are proteins produced by the virus)

• Management:
•       1. Thoroughly wash wound (reduces number of viral particles) - iodine or alcohol, or flush mucus membranes with water
•       2. If no pre-exposure vaccine: Human Rabies Immunoglobulin (1 dose) <20U/kg - around bite as much as possible, the rest as deep IM in
• distant site
•      3. rabies vaccine (4 doses over 14 days) PEP within 10 days can be up to 100% effective.

BUT rabies is usually fatal (respiratory insufficiency) once neuro symptoms begin.

Enzyme-linked immunosorbent assay

• 1. Sample Ag applied to surface
• 2. Ab-enzyme complex to this Ag applied
• 3. Enzyme's substrate is added

Reaction  colour change

• flagellated protazoan
• invades superficial epithelium of urogenital tract

• offensive, frothy, greeny-grey discharge
• dyspareunia
• dysuria
• vaginits
• vulvitis
• strawberry cervix (punctate erythema)
• (asymptomatic in males)

metronidazole

• gram negative diplococcus
• infects mucosal surface of genito-urinary tract, rectum and pharynx
• typically asymptomatic

• Bartholin's abscess
• salpingitis +/- irreversible tubal damage

• dysuria
• frequency
• mucopurulent discharge 3 - 5d after exposure
• urethritis
• meatal oedema
• (females usually symptomatic)

• <1% cases
• pyrexia
• vasculitic rash
• polyarthritis
• managed with antibiotics (culture for sensitivity)

• mixed anaerobic flora
• may include Gardnerella vaginalis, Mycoplasma hominis
• creamy grey discharge
• fishy odour
• no itching
• risk of preterm delivery and late miscarriage if present in pregnancy