Herpes B

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Classification according to ICD-10
B00.4 + Herpes simiae virus encephalitis and encephalomyelitis
ICD-10 online (WHO version 2019)

Herpes B (also herpes simiae infection , monkey herpes ) is a serious infectious disease in humans with the herpes virus simiae , which is transmitted to humans by certain monkey species of the Cercopithecidae family . Herpes B is therefore one of the zoonoses . Its clinical picture resembles rapid herpes simplex encephalitis and, if left untreated, is fatal in about 80% of cases. The disease was first observed and characterized by Albert Sabin in 1932 . He named the disease after the surname of William Bartlet Brebner, who died of severe encephalitis .

Pathogen and transmission

The causative agent of herpes B is the herpes virus simiae (CeHV-1), a simplex virus from the genus simplex virus that is very similar to the human herpes simplex viruses . It is particularly detectable in rhesus monkeys and other Asian species of the genus Macaca as a natural reservoir and is transferred to humans through bites (saliva), scratches or objects contaminated with feces, urine or vesicle contents; transmission from person to person has been described in individual cases. Animal keepers in zoos and scientific institutions as well as laboratory staff who work with cell cultures from infected monkey species are considered at risk . There is also a risk of transmission to tourists and local people in areas with free-range monkeys (free animal enclosures, Hindu temple districts). The virus is not very virulent for the monkey species and only causes mild symptoms similar to herpes labialis .

illness

The virus first multiplies in epithelial cells at the entry point and arrives in the central nervous system via axonal transport along sensitive nerves. After 3 to 5 days, typical herpes sores can appear at the entry point and lymphangitis can be detected in the lymph nodes of the corresponding lymphatic drainage area . After another 3 to 7 days, the first symptoms of myelitis and encephalitis appear , which progress rapidly. In contrast to herpes simplex encephalitis, herpes B encephalitis has widespread foci of hemorrhagic necrosis throughout the brain. In addition, internal organs in the sense of pneumonia or hepatitis can rarely occur due to the spread of the virus . Death occurs after a few days through the destruction of certain areas of the brain that are responsible for vital functions (breathing).

Diagnosis

The detection of antibodies against CeHV-1 is possible, but often false positive due to the cross-reactivity with HSV-1 and HSV-2. Differentiation appears to be possible when using the glycoprotein D of CeHV-1 and the HSV glycoproteins G1 and G2, but is not yet available for routine diagnostics. Direct detection of the pathogen can also be carried out from the contents of the vesicles and liquor (in the case of viraemia also blood serum). Detection by means of polymerase chain reaction (PCR) is not established in diagnostic laboratories in Germany, Austria and Switzerland or is not approved for diagnostics in humans, although protocols are available for this. A PCR method for the detection of CeHV-1 in monkeys is currently available at the German Primate Center . The virus can be detected by replication in cell culture, but may only be carried out under protection level 3 .

therapy

A CeHV-1 infection in humans can with a high-dose, intravenous administration of acyclovir to be treated; treatment for a longer period than a comparable HSV infection is recommended. In vitro, 5-ethyldeoxyuridine and penciclovir inhibit CeHV-1 better than aciclovir, so that they represent an alternative for acyclovir resistance that is not uncommon. A hyperimmunoglobulin preparation is not available. Treatment in animals does not make sense because it neither removes the virus from the animal nor prevents reactivation.

Prevention

A vaccine is not available, so prevention is limited to avoiding transmission. The examination of monkeys in animal facilities for the herpes virus simiae and the observance of the hygiene and safety guidelines when handling monkeys are of great importance here.

Reporting requirement

In Germany, Austria and Switzerland there is no obligation to report infections in humans.

literature

  • G. Darai, M. Handermann, E. Hinz, H.-G. Sunday: Lexicon of Infectious Diseases in Humans . 2nd edition, Berlin, Heidelberg 2003 pp. 41ff ISBN 3-540-44168-9

Individual evidence

  1. ^ AB Sabin, AM Wright: Acute ascending myelitis following a monkey bite, with the isolation of a virus capable of reproducing the disease . J. Exp. Med. (1934) 59: pp. 115-136 ( pdf )
  2. ↑ JD Pimentel: Herpes B virus - "B" is for Brebner: Dr. William Bartlet Brebner (1903-1932) . CMAJ (2008) 178 (6) [1]
  3. ↑ A. Fujima, Y. Ochiai et al .: Discrimination of antibody to herpes B virus from antibody to herpes simplex virus types 1 and 2 in human and macaque sera . J. Clin. Microbiol. (2008) 46 (1): pp. 56–61 PMID 17989200 , PMC 2224259 (free full text)
  4. ↑ M. Hirano et al .: One-step PCR to distinguish B virus from related primate alphaherpesviruses. Clin. Diagn. Lab. Immunol. (2002) 9 (3): pp. 716-719 PMID 11986284
  5. ↑ F. Focher et al .: Sensitivity of monkey B virus (Cercopithecine herpesvirus 1) to antiviral drugs: role of thymidine kinase in antiviral activities of substrate analogs and acyclonucleosides . Antimicrob Agents Chemother . (2007) 51 (6): pp. 2028-2034 PMID 17438061
  6. ↑ T. Reme et al. (2009): Recommendations for post-exposure prophylaxis after potential exposure to herpes B virus in Germany. J. Occup. Med. Toxicol. 4, 29.