NCASM November Case Study 
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 NCASM November Case Study

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www.asmusa.org/branch/brcano/Case_Studies.html

NCASM November Case Study

Northern California Branch, American Society for Microbiology

This case was put together with help from Michele Kiger, Case Manager at St.
Helena Hospital, and Dr. Ann Warford, Standford University Medical Center,
faithful NCASM member.

Hepatitis C already infects three times more people than does AIDS. It is
responsible for more than one-third of all liver transplants. And by the turn
of the century, it will kill far more people than AIDS each year.   Message of
C. Everett Koop, Former U.S. Surgeon General

The Case:

The patient was a 45 year old well developed and well nourished male from a
local rural county who was admitted to the hospital with bleeding esophageal
varices. His medical history revealed a problems with {*filter*} a decade before
being admitted, but had been rehabilitated. He smoked ? pack a day. The
patient was found to be infected with hepatitis C pervious to the admission.

Operative and non-operative methods were employed to counteract the bleeding
varices but the patient continued to bleed out because his liver was failing
to produce clotting factors. In an effort to counteract the bleeding he was
transfused with 24 units of packed cells, 15 units of fresh frozen plasma and
one unit of platelet phoresis. By the end of his admission, his SGPT (ALT) was
416 (indicating severe liver inflammation) with his BUN increasing to 49 and
creatinine to 1.2 (kidney failure). He was found to have Candida albicans in
the {*filter*}, urine and sputa late in the admission. A recheck of his hepatitis
panel showed antibodies to hepatitis A and C.

After a months admission, the patient died of liver failure secondary to
cirrhosis and to bleeding esophageal varices. The cirrhosis was felt to be the
result of {*filter*}ism and hepatitis C and A.

Over 4? Million Americans are believed to be infected with hepatitis C, 202
Million worldwide

Hepatitis C virus (HCV) is an enveloped, single-stranded RNA virus,
approximately 50 nm in diameter, that has been classified as a separate genus
in the Flaviviridae family. It was discovered in 1989. The 5' end of the
genome codes for core and envelope proteins, followed by nonstructural
proteins, which extend to the 3' end. The ability of HCV to undergo rapid
mutation in a hypervariable region(s) of the genome coding for envelope
protein allows it to escape immune surveillance by the host; thus, most
persons infected with HCV develop chronic infection. Symptoms are typically
flu like initially. Fatigue is the most common symptom. Other symptoms include
mild fever, muscle and joint aches, nausea, vomiting, loss of appetite, vague
abdominal pain, and sometimes diarrhea, although symptoms can come and go.

Typically, the most common test for HCV is the Enzyme Immunoassay for
detection of antibodies to HCV. Recombinant Immunoblot Assay (RIBA) is used as
a supplemental test for antibody identification and is much more specific for
HCV antibodies. New generations of antibody identification continue to become
more specific and sensitive. Qualitative and quantitative (viral load) testing
for HCV RNA is available by PCR. Quantitative testing for HCV RNA is sensitive
down to 100 copies per ml of {*filter*} for those labs that are experienced with
the assay. HCV nucleic acid sequencing is available to those with hepatitis C.
Reports suggest that patient prognosis and course of disease may be genotype
dependent. For example, HCV type 1b infections may be associated with more
severe liver damage and higher HCV viral loads, with a poor response to
interferon therapy. Type 2 and 3 infections may be associated with lower viral
loads and a more favorable response to therapy. Some believe that a general
screening for all common viral hepatitis should be done, rather than specific
ones (RIBA) since multiple viruses may be infecting the patient. Most labs can
test for hepatitis A, B and C. Hepatitis A and C together appear to be a
deadly combination.

Many studies have demonstrated a high prevalence of anti-HCV among {*filter*}ic
patients with liver disease. HCV antibody is seven times higher among
{*filter*}ics than in the population at large (10 percent vs. 1.4 percent), but
is even higher in those with liver disease (30 percent). Most of those with
liver disease have detectable HCV RNA which may also be present in some HCV
antibody negative patients. HCV antibody positive (RIBA+) patients are likely
to have HCV RNA detected, which is indicative of active viral infection,
usually associated with some degree of necroinflammatory changes, with or
without fibrosis, regardless of SGPT (ALT) levels. There are 3 courses
hepatitis C takes in chronic patients. Most commonly, the liver enzymes stay
high as long as the disease is active. In others, liver enzymes drop and stay
low after the initial acute phase, even though the disease continues to be
active. Still others have liver enzymes and viral load go up and down
independently of each other.

Studies have shown that HCV is constantly mutating, not only in-vivo, but out
in the world. A European researcher has found 6 quasi-species, each
correlating with a different part of the world. This hyper-mutability seems to
be one of the virus means of dealing with hum{*filter*}and/or cellular immune
attacks. Obviously, this makes it very difficult for researchers to find a
reliable cure/prevention method although most agree that the virus needs to be
hit hard and at multiple points in its replication cycle.

HCV is believed to have originated in Laos, and spread by wars - the oldest
patients are veterans in their 70's who got transfusions in WWII. The Korean
and Vietnam wars spread the virus back to Europe and the United States. It is
believed that the event that spread the virus the most was the World Health
Organization's mass inoculation programs in the 50's and 60's when needles
were re-used. 20 percent of the population of Egypt is viremic positive from
the WHO program.

Almost any exposure to {*filter*}, {*filter*} products or fluids containing {*filter*} are
suspect in transferring HCV. Typical exposure is through {*filter*} transfusions
prior to 1990 ({*filter*} units were checked for HCV after 1990), I.V. drug use,
tattooing or body piercing, or any activity where {*filter*} is transferred such as
unbandaged cuts or sharing a toothbrush. Saliva and {*filter*} milk do not appear
to be significant means of transferring the virus. Laboratorians are in a
particular high risk category from exposure to HCV from {*filter*} spills. A
renewed commitment to personal protective equipment by laboratorians is in
order for those working with body fluids, especially serum and plasma.

More on Hepatitis C:  Cartoon of Hep C viral genome, good general site, Hep C
personal risk assessment

Seen anything interesting in the lab lately?   Submit case studies to Chuck
Regeski.

This webpage was designed and authored by Northern California ASM, which is
fully
responsible for its contents. Please send comments or corrections to Chuck
Regeski.
This page was originally created August 1997.  This page was last updated on
10/30/98.

As always do not substitute what you read in a post w/competent professional
medical advice which encompasses your unique medical condition



Tue, 10 Jul 2001 03:00:00 GMT
 
 [ 1 post ] 

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