A familial cluster of pneumonia

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person-to-person transmission: a study
of a family cluster Jasper Fuk-Woo
Chan
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 Articles
Lancet 2020; 395: 514–23
Published Online
January 24, 2020
https://doi.org/10.1016/
S0140-6736(20)30154-9
See Comment pages 469 and
470
*Contributed equally
State Key Laboratory of
Emerging Infectious Diseases,
Carol Yu Centre for Infection,
Department of Microbiology,
Li Ka Shing Faculty of Medicine,
The University of Hong Kong,
Pokfulam, Hong Kong Special
Administrative Region, China
(J F-W Chan MD, S Yuan PhD,
K-H Kok PhD, K K-W To MD,
H Chu PhD, C C-Y Yip PhD,
R W-S Poon PhD, H-W Tsoi MPhil,
K-H Chan PhD,
V K-M Poon MPhil,
W-M Chan PhD, J D Ip MSc,
J-P Cai BSc, V C-C Cheng MD,
Prof H Chen PhD); and
Department of Clinical
Microbiology and Infection
Control (J F-W Chan, K K-W To,
J Yang MD, F Xing MD,
J Liu BNurs, S K-F Lo MPhil,
Prof H Chen, Prof K-Y Yuen MD)
and Department of Medicine
(C K-M Hui, MD), The University
of Hong Kong-Shenzhen
Hospital, Shenzhen,
Guangdong Province, China
Correspondence to:
Prof Kwok-Yung Yuen,
Department of Clinical
Microbiology and Infection
Control, The University of
Hong Kong-Shenzhen
Hospital, Shenzhen,
Guangdong Province 518009,
China
kyyuen@hku.hk
514
A familial cluster of pneumonia associated with the 2019
novel coronavirus indicating person-to-person transmission:
a study of a family cluster
Jasper Fuk-Woo Chan*, Shuofeng Yuan*, Kin-Hang Kok*, Kelvin Kai-Wang To*, Hin Chu*, Jin Yang, Fanfan Xing, Jieling Liu, Cyril Chik-Yan Yip,
Rosana Wing-Shan Poon, Hoi-Wah Tsoi, Simon Kam-Fai Lo, Kwok-Hung Chan, Vincent Kwok-Man Poon, Wan-Mui Chan, Jonathan Daniel Ip,
Jian-Piao Cai, Vincent Chi-Chung Cheng, Honglin Chen, Christopher Kim-Ming Hui, Kwok-Yung Yuen
Summary
Background An ongoing outbreak of pneumonia associated with a novel coronavirus was reported in Wuhan city,
Hubei province, China. Affected patients were geographically linked with a local wet market as a potential source. No
data on person-to-person or nosocomial transmission have been published to date.
Methods In this study, we report the epidemiological, clinical, laboratory, radiological, and microbiological findings of
five patients in a family cluster who presented with unexplained pneumonia after returning to Shenzhen, Guangdong
province, China, after a visit to Wuhan, and an additional family member who did not travel to Wuhan. Phylogenetic
analysis of genetic sequences from these patients were done.
Findings From Jan 10, 2020, we enrolled a family of six patients who travelled to Wuhan from Shenzhen between
Dec 29, 2019 and Jan 4, 2020. Of six family members who travelled to Wuhan, five were identified as infected with
the novel coronavirus. Additionally, one family member, who did not travel to Wuhan, became infected with the
virus after several days of contact with four of the family members. None of the family members had contacts with
Wuhan markets or animals, although two had visited a Wuhan hospital. Five family members (aged 36–66 years)
presented with fever, upper or lower respiratory tract symptoms, or diarrhoea, or a combination of these 3–6 days
after exposure. They presented to our hospital (The University of Hong Kong-Shenzhen Hospital, Shenzhen)
6–10 days after symptom onset. They and one asymptomatic child (aged 10 years) had radiological ground-glass lung
opacities. Older patients (aged >60 years) had more systemic symptoms, extensive radiological ground-glass lung
changes, lymphopenia, thrombocytopenia, and increased C-reactive protein and lactate dehydrogenase levels. The
nasopharyngeal or throat swabs of these six patients were negative for known respiratory microbes by point-of-care
multiplex RT-PCR, but five patients (four adults and the child) were RT-PCR positive for genes encoding the internal
RNA-dependent RNA polymerase and surface Spike protein of this novel coronavirus, which were confirmed by
Sanger sequencing. Phylogenetic analysis of these five patients’ RT-PCR amplicons and two full genomes by next-
generation sequencing showed that this is a novel coronavirus, which is closest to the bat severe acute respiatory
syndrome (SARS)-related coronaviruses found in Chinese horseshoe bats.
Interpretation Our findings are consistent with person-to-person transmission of this novel coronavirus in hospital
and family settings, and the reports of infected travellers in other geographical regions.
Funding The Shaw Foundation Hong Kong, Michael Seak-Kan Tong, Respiratory Viral Research Foundation Limited,
Hui Ming, Hui Hoy and Chow Sin Lan Charity Fund Limited, Marina Man-Wai Lee, the Hong Kong Hainan
Commercial Association South China Microbiology Research Fund, Sanming Project of Medicine (Shenzhen), and
High Level-Hospital Program (Guangdong Health Commission).
Copyright © 2020 Elsevier Ltd. All rights reserved.
Introduction geographically linked to the Huanan seafood wholesale
The Health Commission of Hubei province, China, first market, which was subsequently reported by journalists
announced a cluster of unexplained cases of pneumonia to be selling freshly slaughtered game animals.3 To
on Dec 31, 2019.1 27 patients were initially reported, date, no evidence of person-to-person transmission or
which was subsequently revised to 41 on Jan 11, 2020, affected health-care workers has been published in the
with seven severe cases and one death.2 Some patients scientific literature. The Chinese health authority said
were reported to have radiographic ground-glass lung that the patients initially tested negatively for common
changes; normal or lower than average white blood respiratory viruses and bacteria, but later tested positive
cell lymphocyte, and platelet counts; hypoxaemia; and for a novel coronavirus.2 The virus was soon isolated
deranged liver and renal function. Most were said to be and its genome sequenced by a number of Chinese
www.thelancet.com Vol 395 February 15, 2020

Research in context
Evidence before this study
We searched PubMed on Jan 13, 2020, with no starting date
limitations, using the terms “family”, “pneumonia”, “Wuhan”,
“coronavirus”, and “novel” for articles in English. Our search
did not reveal any reports of novel coronavirus pneumonia in
Wuhan before 2020. We only noted family clusters of
pneumonia due to the novel severe acute respiratory syndrome
(SARS) coronavirus in 2003, and Middle East respiratory
syndrome coronavirus in 2012.
Added value of this study
The epidemiological, clinical, laboratory, radiological, and
microbiological findings of unexplained pneumonia in a
Shenzhen family cluster connected to a Wuhan hospital were
presented. The diagnostic tests from relevant clinical samples
scientists.4 The virus was tentatively named by WHO as
the 2019 novel coronavirus (2019-nCoV). Here, we report
the epidemiological, clinical, radiological, laboratory, and
genomic findings of a family cluster of five patients in
Shenzhen who had a history of travel to Wuhan, and one
other family member who has not travelled to Wuhan.
Methods
Cases
On Jan 10, 2020, we initially enrolled two patients who
initially presented to The University of Hong Kong-
Shenzhen Hospital (Shenzhen, Guangdong province,
China) with fever, respiratory symptoms, and pulmonary
infiltrates on chest radiographs. Subsequently, between
Jan 11, and Jan 15, 2020, five other members of this family
also pre­sented to our hospital for the assessment of their
health conditions.
We recorded and analysed the history, physical
findings, and haematological, biochemical, radiological,
and microbiological investigation results. All laboratory
procedures for clinical samples have been previously
reported.5 Briefly, nasopharyngeal and throat swabs and
stool and urine samples were taken and put into viral
transport media. Plasma was separated from EDTA
bottles and serum were separated from clotted blood
bottles.
This study was approved by the Institutional Review
Board of The University of Hong Kong-Shenzhen
Hospital (number [2015]90). We obtained written consent
from the patients.
Respiratory and diarrhoeal pathogen detection
Respiratory samples of the patients were tested for
influenza A and B viruses and respiratory syncytial virus
using the Xpert Xpress Flu/RSV assay (GeneXpert
System, Cepheid, Sunnyvale, CA, USA) according to the
manufacturer’s instructions.6 To detect the presence of
18 respiratory virus targets and four bacteria (including
adenovirus, coronaviruses [HCoV-229E, HCoV-Nl63,
www.thelancet.com Vol 395 February 15, 2020
Articles
confirmed the presence of a novel coronavirus in five of
six patients with radiological changes of viral pneumonia.
The phylogenetic analysis of this novel coronavirus suggested
its linkage to a possible animal source.
Implications of all the available evidence
Although this novel coronavirus might have first originated
from animals and now jumped into humans, the possibility of
person-to-person transmission could not be excluded, as seen
in this family cluster with no known history of exposure to
markets or animals, and rapid intercity spread might be
possible by air travel. Vigilant epidemiological control in the
community and health-care facilities is important to prevent
another SARS-like epidemic.
HCoV-Oc43, HCoV-HKU1, and MERS-CoV], human
metapneumovirus, respiratory syncytial virus, human
rhinovirus or entero­ virus, influenza A viruses [H1,
H1-2009 and H3], influenza B virus, parainfluenza viruses
[types 1–4], Bordetella pertussis, Bordetella parapertussis,
Chlamydophila pneumoniae, and Mycoplasma pneumoniae),
samples were tested using BioFire FilmArray Respiratory
Panel 2 plus (bioMérieux, Marcy l’Etoile, France) according
to the manufacturer’s instructions.7 The two faecal sam­
ples were taken from the patients who had diarrhoea as
part of their symptoms, and the samples were tested by
BioFire FilmArray Gastrointestinal panel (bioMérieux) for
22 diarrhoeal pathogens.
Reverse transcription, in-house conventional RT-PCR
and sequencing
Reverse transcription was done using the SuperScript IV
reverse transcriptase (Invitrogen, Carlsbad, USA) as prev­
iously described.8 The reaction mixture (10 μL) contained
5·5 μL of RNA, 2 μL of 5 × SuperScript IV buffer, 0·5 μL of
100 mM dithiothreitol, 0·5 μL of 10 mM deoxynucleotide
triphosphate (dNTP) mixture, 0·5 μL of 50 μM random
hexamers, 0·5 μL of SuperScript IV reverse transcriptase
(200 U/μL), and 0·5 μl of RNase-free water. The mixtures
were incubated at 23°C for 10 min, followed by 50°C for
10 min and 80°C for 10 min. The PCR mixture (25 μL)
contained 1 μL of cDNA, 2·5 μL of 10X PCR buffer II, 2 μL
of 25 mM MgCl2, 0·5 μL of 10 mM dNTP mix, 2·5 μL of
each 10 μM forward and reverse primer, 0·125 μL of
AmpliTaq Gold Polymerase (Applied Biosystems, Foster
City, USA; 5 U/μL), and nuclease-free water.
The first set of primers was the forward pri­ m­
er (5ʹ-CAAGTGGGGTAAGGCTAGACTTT-3ʹ) and the
reverse primer (5ʹ-ACTTAGGATAATCCCAACCCAT-3ʹ)
targeting 344 bp of RNA-dependent RNA poly­
merase (RdRp) gene of all severe acute respiratory
syndrome (SARS)-related coro­naviruses. The second set
of primers was designed after our first 2019-nCoV
genome sequence by Nanopore sequencing from
515
 Articles

A Shenzhen Wuhan Shenzhen

December, January, 2020
2019
(RT-PCR and CT positive)
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Patient 1 (mother)

Fever, cough, and Attended Attended Attended HKU-SZH for persistent symptoms
generalised weakness clinic 1 clinic 2
(RT-PCR and CT positive)
Patient 2 (father) 26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Fever and Cough and Attended Attended HKU-SZH for persistent symptoms
generalised weakness attended clinic 1 clinic 2

(CT positive)
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Patient 3 (daugther)

Fever and diarrhoea Pleuritic chest pain Attended HKU-SZH for investigation
(RT-PCR and CT positive)
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Patient 4 (son-in-law)

Fever and diarrhoea Cough and runny nose Attended HKU-SZH for investigation
(RT-PCR and CT positive)
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Patient 5 (grandson)

Attended HKU-SZH for investigation

Patient 6
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
(grand daugther)

Attended HKU-SZH for investigation

Shenzhen
(RT-PCR and CT positive)
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Patient 7 (mother of patient 4)

Backpain and Fever and dry cough Attended HKU-SZH for

generalised weakness investigation

B Wuhan
December, 2019 January, 2020
Relative 1
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
(son of relative 2)

Fever, cough, and dyspnoea

Figure 1: Chronology of
symptom onset of the Relative 2
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
(cousin of patient 3)
Shenzhen family cluster and
their contacts in Wuhan
Dates filled in red are the dates Fever and Cough Attended clinic
on which patients 1–6 had generalised weakness
close contacts with their Relative 3
26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
relatives (relatives 1–5). (mother of relative 2)
Dates filled in yellow are the
dates on which patients 3–6 Fever, cough, and Hospitalised
stayed with patient 7. generalised weakness
The boxes with an internal red
cross are the dates on which Relative 4 (sister of relative 3) 26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
patients 1 and 3 or relatives 1,
2, and 3 had stayed overnight
Fever, cough, and Hospitalised
(white boxes) at or had visited
generalised weakness
(blue boxes) the hospital in
Relative 5
which relative 1 was admitted 26 27 28 29 30 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
(sister-in-law of patient 1)
for febrile pneumonia.
The information of relatives
1–5 was provided by patient 3. Fever, cough, and Hospitalised
No virological data were generalised weakness
available.

516 www.thelancet.com Vol 395 February 15, 2020

 Articles

Patient 1 Patient 2 Patient 3 Patient 4 Patient 5 Patient 7

Relationship Mother of patient 3 Father of patient 3 Daughter of Son-in-law of Grandson of Mother of patient 4
patients 1 and 2 patients 1 and 2 patients 1 and 2 in Shenzhen
Age (years) 65 66 37 36 10 63
Sex Female Male Female Male Male Female
Occupation Retired Retired Office worker Architect Student Retired
Chronic medical illness Hypertension; Hypertension None Chronic sinusitis None Diabetes
benign intracranial
tumour treated by
gamma knife
Interval between symptom onset and arrival at Wuhan 5 (hospital 6 4 (hospital 3 NA NA
(days) exposure) exposure)
Interval between admission to hospital and symptom onset 7 6 9 10 NA 7
(days)
Presenting symptoms and signs ·· ·· ·· ·· ·· ··
Fever + + + + – +
Cough + (dry) + (dry) – + (productive) – + (dry)
Generalised weakness + + – – – +
Nasal congestion – – + – – –
Rhinorrhoea – – – + – –
Sneezing – – – + – –
Sore throat – – + – – –
Pleuritic chest pain – – + – – –
Diarrhoea – – + (3 days, + (4 days, – –
5–6 times per day) 7–8 times per day)
Body temperature (°C) 39·0 39·0 36·2 36·5 36·5 39·0
Oximetry saturation (%) 94% 96% NA NA NA NA
Haemoglobin (g/dL); (male normal range 13·3–17·1; 13·1 15·6 15·0 15·2 14·6 13·0
female normal range 11·5–14·8)
White blood cell count (× 10⁹ cells per L); (normal range 4·8 4·2 5·6 11·4 (↑) 6·5 4·3
3·9–9·9)
Neutrophil count (× 10⁹ cells per L); (normal range 2·0–7·4) 4·0 3·2 3·1 8·1 (↑) 3·2 2·7
Lymphocyte count (× 10⁹ cells per L); (normal range 1·1–3·6) 0·6 (↓) 0·7 (↓) 2·2 2·7 2·8 1·2
Platelet count (× 10⁹ cells per L); (normal range 162–341) 157 (↓) 118 (↓) 224 196 197 205
Prothrombin time (s); (normal range 11·0–14·5) 12·6 12·5 13·0 13·0 13·1 12·9
International normalised ratio 1·0 1·0 1·0 1·0 1·0 1·0
Activated partial thromboplastin time (s); 45·4 (↑) 45·3 (↑) 36·0 31·4 34·0 35·8
(normal range 26·0–40·0)
D-dimer (µg/mL); (normal range 0·0–0·5) 0·6 (↑) 0·3 NA NA NA 0·6 (↑)
Fibrinogen (g/dL); (normal range 2·0–4·0) 6·2 (↑) 5·1 (↑) 3·8 3·8 2·9 4·5 (↑)
C-reactive protein (mg/L); (normal range 0·0–5·0) 55·6 (↑) 34·2 (↑) 0·5 4·9 0·2 44·9 (↑)
Albumin (g/L); (normal range 35·0–52·0) 39·4 38·5 50·4 48·1 49·1 41·2
Bilirubin (µmol/L); (normal range 0·0–21·0) 6·9 5·9 9·3 8·9 3·6 10·4
Alkaline phosphatase (U/L); (normal range 35–105) 68 56 56 48 211 (↑) 66
Alanine aminotransferase (U/L); (normal range 0·0–33·0) 14·2 13·9 25·9 20·2 23·9 17·3
Aspartate aminotransferase (U/L); (normal range 0·0–32·0) 20·5 23·3 27·4 18·1 28·2 27·6
Urea (mmol/L); (normal range 2·8–8·1) 3·5 5·7 3·1 5·2 5·6 4·9
Creatinine (µmol/L); (normal range 44–80) 53 93 (↑) 67 87 (↑) 51 55
Sodium (mmol/L); (normal range 136–145) 136 133 (↓) 142 141 141 139
Potassium (mmol/L); (normal range 3·5–5·1) 3·2 (↓) 3·7 3·7 3·7 3·9 3·8
Creatine kinase (U/L); (normal range 0–170) 42 109 50 137 78 143
Lactate dehydrogenase (U/L); (normal range 135–214) 286 (↑) 232 (↑) 192 176 194 252 (↑)
Amylase (U/L); (normal range 28–100) NA NA 70 61 61 NA
NA=not available. +=positive. –=negative. ↑=above normal range. ↓=below normal range.

Table 1: Summary of clinical features and laboratory results of the family cluster infected with 2019 novel coronavirus, at presentation

www.thelancet.com Vol 395 February 15, 2020 517

 Articles
the positive clinical samples: the forward primer
(5ʹ-CCTACTAAATTAAATGATCTCTGCTTTACT-3ʹ) and
the reverse primer (5ʹ-CAAGCTATAACGCAGCCTGTA-3ʹ)
targeting the 158 bp of Spike (S) gene of this novel
coronavirus. These sets were used for PCR using an
automated thermocycler (Applied Biosystems) with a
hot start at 95°C for 10 min, followed by 50 cycles of
94°C for 1 min, 55°C for 1 min, and 72°C for 1 min, and
a final extension at 72°C for 10 min. The PCR products
were detected by agarose gel electrophoresis. The PCR
products with correct target size were purified using
QIAquick Gel Extraction Kit (Qiagen). Both strands of
PCR products were sequenced with an ABI 3500xl Dx
Genetic Analyzer (Applied Biosystems) using the PCR
primers. During the set up of the assays, we initialy
used SARS-CoV cDNA as a positive control for RdRp
assay and gene-synthesised fragment for Spike assay.
Thereafter, diluted samples from positive patients were
used as the positive control for both assays. All positive
results were confirmed by Sanger sequencing.
In-house one-step real-time RT-PCR assay
See Online for appendix A total of 140 µL of respiratory, urine, stool, serum, or
plasma samples from each patient was subjected to
RNA extraction into 50 µL elutes using QIAamp Viral
RNA Mini Kit (Qiagen, Hilden, Germany). Forward
(5ʹ-CCTACTAAATTAAATGATCTCTGCTTTACT-3ʹ)
For BioProject see https://www. and reverse (5ʹ-CAAGCTATAACGCAGCCTGTA-3ʹ) pri­
ncbi.nlm.nih.gov/bioproject/ mers targeting the S gene of this novel coronavirus
were used for the assay. Real-time RT-PCR assay was
done using QuantiNova SYBR Green RT-PCR Kit
(Qiagen) in a LightCycler 480 Real-Time PCR System
(Roche, Basel, Switzerland), as previously described.9
Each 20 μL reaction mixture contained 10 μL of
A B
C D
Figure 2: Representative images of the thoracic CT scans showing multifocal ground-glass changes in the
lungs of patient 1 (A), patient 2 (B), patient 3 (C), and patient 5 (D)
518
2 × QuantiNova SYBR Green RT-PCR Master Mix,
0·2 μL of QN SYBR Green RT-Mix, 1 μM of each 10 μM
forward and reverse primers, and 5 μL of RNA and
nuclease-free water. Reactions were incubated at 50°C
for 10 min and 95°C for 2 min, followed by 45 cycles at
95°C for 5 s and 60°C for 30 s, and then subjected to
melting curve analysis (95°C for 5 s, 65°C for 1 min,
followed by a gradual increase in temperature to 97°C
with continuous recording of fluorescence).
Whole-genome sequencing and genome analysis by
bioinformatics
Whole-genome sequencing was done using Oxford Nano­
pore MinION device (Oxford Nanopore Technologies,
Oxford, UK) supplemented by Sanger sequencing. RNA
was extracted from host cell-depleted nasopharyngeal and
sputum samples using a QIAamp Viral RNA Mini Kit, as
described previously.10–12 Whole-genome amplification of
the coronavirus was done using a sequence-independent
single-primer amplification ap­proach, as described pre­
viously.13 Bioinformatics analyses were done using an in-
house pipeline. Details on the library preparation and
bioinformatics analysis are described in the appendix
(pp 1–2). The con­ sensus sequence of HKU-SZ-002a
(accession number MN938384) and HKU-SZ-005b
(accession number MN975262) have been deposited
into GenBank. Raw reads, after excluding human reads,
have been deposited into BioProject (accession number
PRJNA601630).
Phylogenetic tree construction
Phylogenetic trees were constructed using MEGA X
software using the RT-PCR amplicons of partial RdRp and
S gene regions of the strains detected in this study and
other related coro­naviruses.14 The trees of the amplicons
were constructed using maximum likelihood methods
with bootstrap values calculated from 1000 trees, with
human coro­navirus 229E as outgroup. The phylogenetic
tree of the full-length genome was constructed by use of
the neighbour-joining method using the Tamura-Nei
model with a gamma distribution. The bootstrap values
were calculated from 1000 trees and values only greater
than 70 were displayed.
Role of the funding source
The funders of the study had no role in study design, data
collection, data analysis, data interpretation, or writing of
the report. The corresponding author had full access to all
the data in the study and had final responsibility for the
decision to submit for publication.
Results
The family cluster of six patients (patients 1–6) flew from
Shenzhen to Wuhan on Dec 29, 2019, and flew back to
Shenzhen on Jan 4, 2020 (figure 1). This travel period
overlapped with the time period after the announcement
of the first case of Wuhan pneumonia (symptom onset
www.thelancet.com Vol 395 February 15, 2020
 Articles

on Dec 12, 2019) according to the Chinese health

Patient 1 Patient 2 Patient 3 Patient 4 Patient 5 Patient 7
authority.2 They had no history of contact with animals,
visits to markets including the Huanan seafood whole­sale Interval between sample 7 6 9 10 NA 7
collection and symptom onset
market in Wuhan, or eating game meat in restaurants. (days)
The family stayed in the same hotel throughout their Conventional RT-PCR ·· ·· ·· ·· ·· ··
travel. Patients 1 and 2 stayed in one room and patients 3–6 Nasopharyngeal swab ·· ·· ·· ·· ·· ··
stayed in another room. After patient 4 developed fever RdRp + + ND + ND +
and diarrhoea on Jan 1, 2020, patients 5 and 6 stayed in Spike + + ND + + +
the same room as patients 1 and 2, and patient 3 stayed
Throat swab ·· ·· ·· ·· ·· ··
with patient 4. Patients 1–6 had met with their relatives
RdRp NA NA ND ND ND +
(relatives 2–5: one female cousin and three aunts of
Spike NA NA ND + + +
patient 3) every day during their stay in Wuhan for meals.
Serum ·· ·· ·· ·· ·· ··
Relative 4 made frequent visits to the wet market but not
RdRp ND ND NA NA NA NA
the Huanan seafood wholesale market, which had been
Spike ND + NA NA NA NA
implicated by the health authority to be the epidemic
Plasma ·· ·· ·· ·· ·· ··
centre. Relatives 2–5 have developed fever, cough, and
RdRp NA NA ND ND ND NA
weak­ness since Jan 4, 2020. Patients 1 and 3 had visited
Spike NA NA ND ND ND NA
relative 1, aged 1 year, and the son of relative 2, on
Urine ·· ·· ·· ·· ·· ··
Dec 29, 2019, in a Wuhan hospital, who had been treated
RdRp ND ND ND ND ND NA
in hospital for febrile pneumonia (relative 2 accompanied
relative 1 in the hospital over­ night; relative 1 later Spike ND ND ND ND ND NA

recovered and was discharged home on Dec 31, 2019). Stool ·· ·· ·· ·· ·· ··

Patient 3, but not patient 1, had worn a surgical mask RdRp NA NA ND ND ND NA
during the hospital visit. The incubation period was Spike NA NA ND ND ND NA
estimated to be between 3 and 6 days. Patients 1–4 were Real-time RT-PCR (spike gene) ·· ·· ·· ·· ·· ··
symptomatic, and they only presented to our hospital Nasopharyngeal swab + (Ct 31) + (Ct 27) ND + (Ct 31) ND + (Ct 27)
(The University of Hong Kong-Shenzhen Hospital, Throat swab NA NA ND ND + (Ct 40) + (Ct 33)
Shenzhen) 6–10 days after symptom onset. For the two Sputum NA NA NA NA + (Ct 27) + (Ct 25)
asymptomatic children (patients 5 and 6), patient 5 had Serum ND + (Ct 40) NA NA ND NA
ground-glass lung opacities identified by CT scan. Unlike Plasma NA NA ND ND ND ND
patient 5, who was aged 10 years and non-compliant to Urine ND ND ND ND ND NA
parental guidance, patient 6, who was aged 7 years and Stool NA NA ND ND ND ND
reported by her mother to wear a surgical mask for most FilmArray RP2 plus ND ND ND ND ND ND
of the time during the period in Wuhan, was not found to (nasopharyngeal swab only)
be infected by virological or radiological investigations. Xpert Xpress Flu/RSV ND ND ND ND ND ND
(nasopharyngeal swab only)
The blood tests and CT scan of patient 6 were normal.
FilmArray GI panel (faecal NA NA ND ND NA NA
After they returned to Shenzhen on Jan 4, 2020, sample only)
patients 3–6 stayed in the same household of patient 7
Ct values for real-time RT-PCR presented in parentheses. Ct=cycle threshold. NA=not available. +=positive. ND=not
(mother of patient 4) until Jan 11, 2020. Patient 7, who detected. RdRp=RNA-dependent RNA polymerase. RP2=respiratory panel 2. Flu=influenza. RSV=respiratory syncytial
did not go to Wuhan or visit Shenzhen markets in the virus. GI=gastrointestinal.
preceding 14 days, developed back pain and generalised
Table 2: Microbiological findings from clinical specimens collected from the family cluter infected with
weakness and attended the outpatient clinic at another
2019 novel coronavirus, at presentation
local hospital on Jan 8, 2020. She was given cefaclor for
3 days with no improvement. She developed fever and
dry cough and attended the same outpatient clinic and congestion, and rhinorrhoea. Patient 3 also had pleuritic
was treated with intravenous cefazolin (two doses) on chest pain. Except for patient 4, all six had normal or lower
Jan 12, 2020. She was admitted to our hospital on than average total white blood cell counts. The three older
Jan 15, 2020, due to persistent symptoms. patients (patients 1, 2, and 7) all had substantially increased
Of the six patients with pulmonary infiltrates C-reactive protein, fibrinogen, and lactate dehydrogenase
(patients 1–5 and patient 7) on CT scans, three were male levels. Patients 1 and 2 also had lymphopenia, mild
and three were female, with ages ranging 10–66 years thrombocytopenia, and extended activated thromboplastin
(table 1). Four had chronic comorbidities and five had time. All six patients showed multifocal patchy ground-
history of fever. The three older patients (aged >60 years: glass opacities, especially around the peripheral parts
patients 1, 2, and 7) had dry cough and generalised of the lungs on CT scans, which were compatible with
weakness. Patient 4 had productive cough. Patients 3 and changes seen in viral pneumonia (figure 2). No other
4 were younger adults and had diarrhoea and upper clinical or radiological changes of lung congestion,
respiratory tract symptoms including sore throat, nasal fibrosis, or cancer to explain these ground-glass lung

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changes, or any concomitant radiological changes of All respiratory samples were negative on two point-of-
dense consoli­dation, pleural effu­sion, lymphadenopathy, care multiplex PCR systems for 18 respiratory viral and
or pneu­momediastinum were seen. four bacterial targets. The two faecal samples from
patients 3 and 4 who had preceding diarrhoea were nega­
tive on a multiplex PCR assay for common diarrhoeal
A viruses, bacteria, and parasites (table 2). The respiratory
0·1 97 Bat SL-CoV ZC45 2018 samples of patients 1, 2, 4, 5, and 7 were positive for both
Bat SL-CoV ZXC21 2018
2019-nCoV HKU-SZ-001 2020
RdRp and S genes by conventional RT-PCR, and for the
2019-nCoV HKU-SZ-002a 2020 S gene by real-time RT-PCR, which were confirmed by
100
2019-nCoV HKU-SZ-004 2020 Sanger sequencing of all amplicons (appendix pp 3–5).
2019-nCoV HKU-SZ-005b 2020 2019-nCoV
98 Although the respiratory samples of patient 3 were
2019-nCoV HKU-SZ-007a 2020
2019-nCoV HKU-SZ-007b 2020 negative for both RdRp and S gene (collected 9 days after
2019-nCoV HKU-SZ-007c 2020 symptom onset), she was still regarded as an infected
Human SARS-CoV GZ02 2003 case because she was strongly epidemiologically linked
Human SARS-CoV BJ01 2003
to the Wuhan hospital exposure and radiologically
Human SARS-CoV Tor2 2003
Human SARS-CoV HKU-39849 2003
lineage B showing multifocal ground-glass lung opacities. Only the
98 Paguma SARS CoV HC/SZ/61/03 2003 serum sample of patient 2 was positive and all other
Bat SL-CoV RsSHC014 2013 patients' serum, urine, and faecal samples were negative
Bat SL-CoV Rs4255 2016
Bat SL-CoV Rs3367 2013
for this novel coronavirus. Phylogenetic analysis of the
Bat SL-CoV Rs4231 2016 PCR products showed that the amplicon sequences of
97
Bat CoV YN2018D 2018 both RdRp and S genes from these five patients were
72 Bat CoV YN2018C 2018 novel (figure 3) and different from other known human
Bat SL-CoV Rs672 2006
or animal coronaviruses, including the SARS and bat
Bat SARS-related CoV BM48-31 2009
Bat CoV HKU9-1 2006 lineage D
SARS-related coronaviruses.
Bat CoV HKU4-1 2006 Two complete virus genomes (HKU-SZ-002a and HKU-
Bat CoV HKU5-1 2006 lineage C SZ-005b) were sequenced using Nanopore technology and
99 Human MERS-CoV 2012
showed a novel coronavirus that is most closely related to
Human CoV HKU1 2004
99 Human CoV OC43 2003
lineage A those of the bat SARS-like coronavirus bat-SL-CoVZXC21
Human CoV 229E 2000 (NCBI accession number MG772934) and bat-SL-CoVZC45
(NCBI accession number MG772933). Their genome
B
2019-nCoV HKU-SZ-007a 2020
organisation is typical of a lineage B betacoronavirus. The
0·2
2019-nCoV HKU-SZ-007b 2020 size of the virus genomes from patient 2 (HKU-SZ-002a)
2019-nCoV HKU-SZ-005b 2020 and patient 5 (HKU-SZ-005b) are around 29·8 kilobases
2019-nCoV HKU-SZ-005 2020
91
2019-nCoV HKU-SZ-004 2020
with GC content of 38% (appendix p 6). HKU-SZ-002a and
2019-nCoV HKU-SZ-002b 2020 2019-nCoV HKU-SZ-005b differ from each other by only two bases.
2019-nCoV HKU-SZ-002a 2020 One of them is a non-synonymous mutation at amino acid
2019-nCoV HKU-SZ-001 2020
position 336 of non-structural protein 4 (Ser336 for HKU-
2019-nCoV HKU-SZ-007c 2020
Bat SL-CoV ZXC21 2018
SZ-002a; Leu336 for HKU-SZ-005b; figure 4). Although
Bat SL-CoV ZC45 2018 amino acid sequence of the N-terminal domain of Spike
99 Bat CoV YN2018C 2018 subunit 1 of this novel coronavirus is approximately 66%
lineage B
Bat SL-CoV Rs4255 2016 identical to those of the SARS-related coronaviruses, and
97 Bat SL-CoV Rs672 2006
87 Bat CoV YN2018D 2018 the core domain of the receptor binding domain of this
Human SARS-CoV GZ02 2003 novel coronavirus has about 68% amino acid identity with
Human SARS-CoV Tor2 2003 those of the SARS-related coronavirus, the protein sequence
Human SARS-CoV HKU-39849 2003
97 Human SARS-CoV BJ01 2003
of the external subdomain region of receptor binding
Paguma SARS CoV HC/SZ/61/03 2003
domain of Spike subunit 1 has only 39% identity, which
100
Bat SL-CoV Rs3367 2013 might affect the choice of human receptor and therefore the
Bat SL-CoV RsSHC014 2013 biological behaviour of this virus (figure 4).
99 Bat SL-CoV Rs4231 2016 All six patients were admitted to hospital under isolation,
Bat SARS-related CoV BM48-31 2009 supportive care, and remained stable as of Jan 20, 2020.
Bat CoV HKU5-1 2006
Human MERS-CoV 2012 lineage C
Bat CoV HKU4-1 2006 Discussion
Human CoV HKU1 2004 We report here a familial cluster of unexplained pneu­
lineage A
Human CoV OC43 2003 monia due to 2019-nCoV. Six of seven family members
Bat CoV HKU9-1 2006 lineage D
Human CoV 229E 2000
had radiological changes of viral pneumonia, among
whom five (patients 1, 2, 4, 5, and 7) tested positive for
(Figure 3 continues on next page) 2019-nCoV by RT-PCR. Five patients (patients 1, 2, 3, 4,

520 www.thelancet.com Vol 395 February 15, 2020

 Articles

and 7) had associated symptoms at the time of

C
presentation. Complete genome sequences of the two
Human SARS-CoV Tor2 2003
strains from patients 2 and 5 showed almost complete 0·20
SARS coronavirus HKU-39849 2003
nucleotide identity with each other, and were closest to the Human SARS-CoV BJ01 2003
bat SARS-related coronaviruses reported in 2018. Several 78
Human SARS-CoV GZ02 2003
possible scenarios of transmission exist. The first and Paguma SARS CoV HC/SZ/61/03 2003

most likely scenario is that one virologically documented Bat SL-CoV Rs4231 2016
100
73 Bat SL-CoV RsSHC014 2013
patient with pneumonia (patient 1) acquired the infection 100 Bat SL-CoV Rs3367 2013
from a Wuhan hospital while visiting their relative Bat CoV YN2018C 2018
(relative 1) and then patients 1–5 transmitted the virus to Bat CoV YN2018D 2018
96 100 lineage B
patient 7 on returning to Shenzhen. The second scenario 100 Bat SL-CoV Rs4255 2016
is that patients 1–5 have directly acquired the infection 91 Bat SL-CoV Rs672 2006
Bat SL-CoV ZC45 2018
from relatives 2–5 and transmitted it to patient 7 on 100
100
Bat SL-CoV ZXC21 2018
returning to Shenzhen. But this scenario is less 100 HKU SZ 002a 2020
likely because patients 1–5 developed symptoms before 100 HKU SZ 005b 2020
2019-nCoV

relatives 2–5. The third scenario is that patients 1–5
acquired the infection from an unknown common source
in Wuhan and transmitted it to patient 7 when back in
Shenzhen. For the patients’ relatives (relatives 2–5), they
could have acquired the infection from the hospital or the
community, although no virological confirmation was
possible and they had no animal contacts, game food, or
visits to the Huanan sea­food wholesale market. Notably,
patient 1 or patient 3 who had visited Wuhan hospital
might have been infectious before symptom onset because
patient 5 was shedding virus without symp­toms. These
findings suggested that person-to-person transmission
and intercity spread of 2019-nCoV by air travel are possible,
supporting reports of infected Chinese travellers from
Wuhan being detected in other geographical regions.
Many of the epidemiological, clinical, laboratory, and
radiological features of this novel coronavirus pneumonia
were similar to those of SARS patients in 2003.8,15,16 The
incubation period of the Wuhan pneumonia appeared
similar to that of SARS. The attack rate is rather high,
up to 83% if we included the five patients (patients 1, 2,
3, 4, and 5) with unexplained ground-glass radiological
changes of the lungs on CT scan as the case definition in
this family outbreak after visiting Wuhan. A rather
unexpected finding from the lung CT scan of patient 5,
which was done on the insistence by the nervous parents,
also showed ground-glass pneumonic changes. Patient 5
was later confirmed virologically to have an asymp­
tomatic infection. Although asymptomatic patients with
SARS were uncommon, they were documented in our
retrospective study in the minor 2004 SARS outbreak
after reopening of the wildlife market in Guangzhou.17
Notably, patients 3 and 4 were afebrile at presentation to
our hospital. These cryptic cases of walking pneumonia
might serve as a possible source to propagate the
outbreak. Further studies on the epidemiological signifi­
cance of these asymptomatic cases are warranted.
The symptoms of this novel pneumonia were also non-
specific. The three oldest patients in this family with
comorbidities had more severe systemic symptoms of
generalised weakness and dry cough. As expected, they
might have decreased total white blood cell, lymphocyte, or
Bat SARS-related CoV BM48-31 2009
100 Human CoV OC43 2003
lineage A
91
Human CoV HKU1 2004
Bat CoV HKU9-1 2006 lineage D
Human MERS-CoV 2012
Bat CoV HKU5-1 2006 lineage C
100
88 Bat CoV HKU4-1 2006
Human CoV 229E 2000
Figure 3: Phylogenetic trees of genetic sequences
(A) Amplicon fragments of RNA-dependent RNA polymerase of patients 1, 2, 4, 5, and 7. (B) Amplicon fragments
of Spike gene of patients 1, 2, 4, 5, and 7. (C) The full genome sequences of strains from patients 2 and 5. Red text
indicates the coronavirus (CoV) strains detected in the patients in the present study. 2019-nCoV is 2019 novel
coronavirus. HKU-SZ-001 refers to the strain detected in the nasopharyngeal swab of patient 1; HKU-SZ-002a
refers to strain detected in the nasopharyngeal swab of patient 2; HKU-SZ-002b refers to strain detected in the
serum sample of patient 2; HKU-SZ-004 refers to the strain detected in the nasopharyngeal swab of patient 4;
HKU-SZ-005 refers to the strain detected in the throat swab of patient 5; HKU-SZ-005b refers to the strain detected
in the sputum sample of patient 5; HKU-SZ-007a refers to the strain detected in the nasopharyngeal swab of
patient 7; HKU-SZ-007b refers to the strain detected in the throat swab of patient 7; and HKU-SZ-007c refers to the
strain detected in the sputum sample of patient 7 (appendix p 6). The NCBI GenBank accession numbers of the
genome sequences are MN938384 (HKU-SZ-002a), MN975262 (HKU-SZ-005b), MG772934 (Bat SL-CoV ZXC21),
MG772933 (Bat SL-CoV ZC45), AY274119 (hSARS-CoV Tor2), AY278491 (SARS coronavirus HKU-39849),
AY278488 (hSARS-CoV BJ01), AY390556 (hSARS-CoV GZ02), AY515512 (Paguma SARS CoV HC/SZ/61/03),
KY417146 (Bat SL-CoV Rs4231), KC881005 (Bat SL-CoV RsSHC014), KC881006 (Bat SL-CoV Rs3367), MK211377
(Bat CoV YN2018C), MK211378 (Bat CoV YN2018D), KY417149 (Bat SL-CoV Rs4255), FJ588686
(Bat SL-CoV Rs672), NC014470 (Bat SARS-related CoV BM48-31), EF065513 (Bat CoV HKU9-1), AY391777
(hCoV OC43), NC006577 (hCoV HKU1), NC019843 (hMERS CoV), NC009020 (Bat CoV HKU5-1), NC009019
(Bat CoV HKU4-1), and NC002645 (hCoV 229E).
platelet counts, with also extended activated thrombo­
plastin time and increased C-reactive protein level. The
multifocal ground-glass changes on lung CT scan were
typical of viral pneumonia. Their lung involvement was
also more diffuse and extensive than those of the younger
patients, whose blood test results were largely normal.
Patient 4, who had a history of chronic sinusitis, might
have a bacterial superinfection because he had a productive
cough instead of a dry cough. He also had a high white
blood cell count, although the bacterial test was negative.
Interestingly, the two younger adults (patients 3 and 4)
initially had diarrhoea, which was also reported in
10·6% (15 of 142) of our SARS patients at presentation;18
however, the subsequent faecal samples of patients 3 and
4 that were collected 9–10 days after symptom onset were
negative for the virus after the diarrhoea had long
subsided. Up to 30% of patients with Middle East
respiratory syndrome coronavirus (MERS-CoV) also have

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 Articles

consistent with the observations in patients with MERS

2019-nCoV (human)
11 3a E 6 7a 9b who had higher viral loads in lower respiratory tract
NSP 1 2 3 4 5 6 7 8 9 10 12 13 14 15 16
samples than in upper respiratory tract samples.23 Thus,
5'- S M 8 N -3'
repeat testing of upper respiratory tract samples or
3b 7b
PL
pro
3CL pro
RdRP Hel testing of lower respiratory tract samples are warranted in
ExoN
clinically suspected cases with an initially negative result
DMV formation primase EndoU
2'-O-MT in nasopharyngeal or throat swab. Unlike our patients in
the 2003 SARS outbreak,22 we found no evidence of viral
shedding in urine and faeces in these six patients.
HKU-SZ-002a/HKU-SZ-005b However, improved systematic serial collection and testing
S1 S2 of an increased number of such samples is warranted.
RBD
SP NTD ESD FP HR1 HR2 TM Coronaviruses are enveloped, positive-sense, single-
S1 (70%) S2 (99%) stranded RNA viruses, capable of rapid mutation and
NTD (66%) RBD (68%) FP(100%) HR1 (96%) HR2 (95%) recombination. They are classified into alphacoro­
ESD (39%) naviruses and betacoronaviruses, which both have their
SP NTD ESD FP HR1 HR2 TM gene source from bats and are mainly found in mam­
bat-SL-CoV-ZC45 mals such as bats, rodents, civets, and humans; and
gammacoronaviruses and deltacoronaviruses, which
Genome Position (nucleotide) Gene Amino acid
both have their gene source from birds and are mainly
HKU-SZ-002a 9529 (TCA) NSP4 Ser336
HKU-SZ-005b 9577 (TTA) NSP4 Leu336
found in birds.24–26 Phylogenetic analysis of the PCR
amplicon fragments from five of our six patients and the
HKU-SZ-002a 15575 (TTA) NSP12 Leu723
HKU-SZ-005b 15623 (CTA) NSP12 Leu723
complete virus genome of 29·8 kilobases from patients 2
and 5 showed that the virus is a novel betacoronavirus
Figure 4: Genome organisation of 2019-nCoV and the amino acid identities of different subunits and domains belonging to the lineage B or subgenus sarbecovirus,
of the Spike between human 2019-nCoV strains (HKU-SZ-002a and HKU-SZ-005b) and bat-SL-CoV-ZC45 which also includes the human SARS coronavirus. The
2ʹ-O-MT=2ʹ-O-ribose methyltransferase. 3CLpro=3C-like protease. DMV=double-membrane vesicles. E=envelope. genome of our virus strains are phylo­genetically closest
EndoU=endoribonuclease. ESD=external subdomain. ExoN=exonuclease. FP=fusion peptide. Hel=helicase.
to the bat SARS-related coronaviruses first found in
HR1=heptad repeat 1. HR2=heptad repeat 2. M=membrane. N=nucleocapsid. NSP=non-structural protein.
NTD=N-terminal domain. ORF=open reading frame. PLpro=papain-like protease. RBD=receptor binding domain. the Chinese horseshoe bats, Rhinolophus sinicus, captured
S=spike. S1=subunit 1. S2=subunit 2. SP=signal peptide. TM=transmembrane domain. in Zhoushan, Zhejiang province, China, between 2015
and 2017.27 Notably, the first SARS-related coronavirus
diarrhoea.19 Sub­genomic RNA indicating viral replication was also discovered in the R sinicus found in Hong
was seen in faecal samples of patients with MERS.20 Kong, and central and south China in 2005.28,29 The full
Moreover, MERS-CoV was shown to survive in simulated virus genome had about an 89% nucleotide identity
fed gastrointestinal juice and the ability to infect with bat-SL-CoVZC45, which makes it a new species.
intestinal organoid models.20 Diarrhoea and gastro­ Moreover, the Spike protein of our virus has an 84%
intestinal involvement are well known in coronavirus nucleotide identity with the bat-SL-CoVZC45 coronavirus
infections of animals and humans.21 and an 78% nucleotide identity with the human SARS
On microbiological testing, we did not find any evidence coronavirus. Although substantial genetic differences
of other known respiratory viral or bacterial infections, but exist between this and other beta­ coronaviruses, cross
specific RT-PCR assays for two widely separated genome reactions in RT-PCR or antibody assays for SARS or other
targets—the highly conserved RdRp and the highly variable betacoronaviruses are possible if the primers and anti­
S genes—were positive for this novel 2019-nCoV. Two genic epitopes are not carefully chosen, as previously
complete genome sequences of this novel coronavirus reported.30 Further studies on the optimal diagnostic tests
were recovered from the naso­pharyngeal swab of patient 2 are warranted.
and the sputum sample of patient 5 with an earlier cycle In summary, an outbreak of novel coronavirus is
threshold value indicating a higher viral load. Patient 2 had ongoing at Wuhan in the winter of 2019–20. Similar to
more underlying comorbidities and clinical features and the 2003 SARS outbreak in Guangzhou, Wuhan is also a
radiological findings of more severe disease than the other rapidly flourishing capital city of the Hubei province and
patients included here. Moreover, the serum sample of the traffic hub of central China. Moreover, both outbreaks
patient 2 was also positive for 2019-nCoV, which might were initially connected to wet markets where game
indicate some virus spillover from the more severely animals and meat were sold. In the case of SARS, person-
infected lung into the systemic circulation, as previously to-person transmission was efficient and super-spreading
reported in patients with SARS.22 Sputum samples were events had led to major outbreaks in hotels and hospitals.
available for testing from patients 5 and 7. The cycle Learning from the SARS outbreak, which started as
threshold values of the sputum samples were 8–13 cycles animal-to-human transmission during the first phase of
earlier than those of throat swabs, indicating higher viral the epidemic, all game meat trades should be optimally
loads detected in the lower respiratory tract. This finding is regulated to terminate this portal of transmission. But as

522 www.thelancet.com Vol 395 February 15, 2020


shown in this study, it is still crucial to isolate patients
and trace and quarantine contacts as early as possible
because asymptomatic infection appears possible (as
shown in one of our patients), educate the public on both
food and personal hygiene, and alert health-care workers
on compliance to infection control to prevent super-
spreading events. Unlike the 2003 SARS outbreak, the
improved surveillance network and laboratory capability
of China was able to recognise this outbreak within a few
weeks and announced the virus genome sequences that
would allow the development of rapid diagnostic tests
and efficient epidemiological control. Our study showed
that person-to-person transmission in family homes or
hospital, and intercity spread of this novel coronavirus
are possible, and therefore vigilant control measures are
warranted at this early stage of the epidemic.
Contributors
JF-WC and K-YY had roles in the study design, clinical management,
patient recruitment, data collection, data analysis, data interpretation,
literature search, and writing of the manuscript. SY, K-HK, KK-WT,
HChu, CC-YY, RW-SP, H-WT, SK-FL, K-HC, VK-MP, W-MC, JDI, J-PC,
VC-CC, and HChe had roles in the experiments, data collection, data
analysis, and data interpretation. JY, CK-MH, FX, and JL had roles in
recruitment, data collection, and clinical management. All authors
reviewed and approved the final version of the manuscript.
Declaration of interests
We declare no competing interests.
Acknowledgments
This study was partly supported by the Shaw Foundation Hong Kong;
Michael Seak-Kan Tong; Respiratory Viral Research Foundation;
Hui Ming, Hui Hoy and Chow Sin Lan Charity Fund Limited;
Marina Man-Wai Lee; the Hong Kong Hainan Commercial Association
South China Microbiology Research Fund; Sanming Project of Medicine
in Shenzhen, China (SZSM201911014 and SZSM201612096); and the
High Level-Hospital Program, Health Commission of Guangdong
Province, China.
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Another random document with
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by posing as an amateur Morning Post. Why shouldn’t Billy get
married if he wants? And she was a deuce of a nice girl, too!”
“But—the murder—!” Thoyne stammered.
“Murder? What murder? We are talking about a marriage, not a
murder.”
“The murder of Sir Philip Clevedon,” Thoyne replied rather angrily.
“You must have heard of it.”
“Not a word,” Jimmy responded. “I’ve been abroad, and only
returned to England two days ago. Sir Philip Clevedon—why, that’s
—then Billy is Sir William and doesn’t know it.”
“We must tell Mr. Holt,” Kitty broke in, and Thoyne nodded his
agreement.
And thus it was that they came to me with their story. I listened to
them in silence and then put a few questions.
“Had Clevedon arranged that you should be his best man?” I asked
Trevor.
“Not at all,” he said, “nothing of the sort. I met him quite by accident
on Midlington station, and—”
“What date was that?”
“It was February 23rd.”
“Are you sure of that?”
“Yes, it was February 23rd right enough, because that was the day I
had to be in London. It had been fixed up with the lawyer chaps,
Finns and Tregarty, who did all my uncle’s business. I went down
from Blankester by a train that stops five minutes at Midlington—
beastly hole it is, too! Looking out, I saw Billy on the platform. We
were at school together, you know, and then in France—good pals.
He pulled me out of a damned mess once—a good story that, which
I’ll tell you some day. He’s one of the very best, is Billy. I shouted
out to him, ‘Billy, Billy,’ and he came up. ‘Good egg, Jimmy,’ he said,
‘I was getting a bit fed up with my own company.’ There was a
vacant corner seat, and he took it and we travelled to London
together.”
“What time would that be?” I interrupted.
“Let’s see; it was the 11.23 at Midlington, and 4.7 in London. We put
up at the Terminus Hotel, both of us, had dinner there, and went to
see Jimson’s Joy Ride at the Lyric. Then we trotted round to one or
two places we know of and got back to the Terminus at 1 a.m., and
so to bed, as What’s-his-name would say.”
“If we could make absolutely sure of the date—” I began.
“The date is right enough,” Jimmy Trevor replied. “You don’t come
into a little wad of fifteen thousand pounds every day, and that date
is in red letters in my almanac. But ask the lawyers—they’ll have it
down—or try the Terminus Hotel. Our names will be in the register.”
“Well,” I returned, “you went to see Jimson’s Joy Ride, then to bed.
Next morning—?”
“‘I’ve got to go to Jersey!’ Billy said to me, ‘to get married. The
young lady is there, waiting for me—suppose you come with me and
be best man.’ I had four weeks or so empty and plenty of money, so
I said ‘Right ho!’ The lawyers had come down with some coin and
didn’t want me for a bit until they’d straightened things some more.
And then Billy got a telegram, ‘Lost my luggage; bring some clothes
—Elsie.’ So off he went to a large shop and interviewed the
manageress. ‘I want some clothes for a young lady,’ he said, ‘all
sorts of clothes: nightdresses, stockings, whatever young ladies
usually wear; plenty of them, and some frocks—and you see that
young lady over there with the red hair?’ The manageress cast her
optics round. ‘Yes, I see her,’ she said, ‘but you’d better not let her
hear you describe her hair as red.’ Old Billy was a bit put out.
‘Sorry,’ he said, ‘but she is about the build. What’ll fit her will fit the
other.’ It was all easily arranged—anything is easy to arrange, you
know, when you have the money to pay for it, and Billy seemed to
have plenty. He came out of the shop carrying a brand new suit-
case containing about eighty pounds’ worth of female garments.
When he told me about it I said he was a silly Juggins; that what the
telegram had meant was that he was to go to her flat and tell her
maid to pack another box; which is what she told him when we got to
Jersey. ‘We’ll do both,’ Billy said, and we went to the flat and got
another lot of feminine mysteries. So we got to Jersey, and I saw
him tied up and then went on to St. Malo. That’s how I never heard
anything of Sir Philip Clevedon, and I bet Billy’s heard nothing,
either.”
“And who is the—the girl?” Kitty demanded, quite naturally a little
angry when she recollected the suspense and misery she had
endured through her brother’s unexplained absence.
“She’s Elsie MacFarren,” Jimmy replied.
I knew her quite well. Miss Elsie MacFarren was a youthful
American actress who had come across with a boisterous Yankee
comedy, entitled Chick Tottle’s Turnout. The play itself had been a
failure, but Elsie had been a success, and had remained here to
earn one of the big salaries the British theatre-loving public willingly
pays to those who take its fancy. She was not only pretty, but clever;
and invitations to return to America—invitations heavily larded with
dollars—were cabled to her at short intervals. But she stayed here
proof against all temptations.
“And now,” I added briskly, “the next thing is to wire Sir William
Clevedon to return immediately. He must come back. His presence
here will dispel a lot of suspicion, and the story of his romance will
counteract some ugly rumours. We will meet them in London.”
When I told Pepster the story I thought he would never stop
laughing.
“This case,” he said, “is the absolute limit.”
“You’ll come with us to London?”
“I wouldn’t miss it for a fortune.”
We duly met the honeymoon couple at Paddington.
“Where the hell have you been?” Thoyne demanded harshly.
“Where?” Billy echoed. “On my honeymoon. There is Mrs. Billy
Clevedon, and—”
“No,” I interrupted suavely; “Lady Clevedon.”
He swung round facing me.
“Who the hell are you, and what the devil do you mean by that?” he
asked.
“Sir Philip Clevedon is dead,” I replied quietly.
He stood glaring at me for a moment or two, as if he thought I was
mad, then, reading confirmation in the faces around him, he turned
to his wife.
“Do you hear that, Elsie?” he shouted. “Sir Philip is dead, and I am
Sir William, and you are My Lady, and, yes, by gad! I’ve got pots of
money. By Jove! yes. Poor old Philip—he was a bit of a—but there,
he’s dead. What a life it is!”
“The fact is,” I went on, cutting short his excitement, “that Sir Philip
Clevedon was murdered, and”—I paused a moment or two so that I
might get the full effect—“there is a warrant out for your arrest.”
“Murdered!” he echoed. “Arrest!”
“Well,” Pepster interrupted slowly. “I wouldn’t say arrest. The police
are interested—you see, your absence seemed to require—”
“And where the devil do you come into the picture?” the new Sir
William demanded.
“I—oh, I am the police,” Pepster retorted.
“But, surely,” Kitty said haltingly, “Mr. Trevor has proved—Billy was in
London on the night of the 23rd—an alibi—”
“There can be no alibi in a poison case,” I returned gravely. “The
crime is committed, not when the victim dies but when the poison is
placed—wherever it is placed. For example, if I were to put prussic
acid now in some whisky which you were to drink next Sunday, I
might go off to Paris, or be on the high seas far off enough, anyway,
when you drink the whisky, but I should still be guilty of—”
“Is that the story?” Billy broke in. “Did I put prussic acid in Philip’s
whisky? Come, we’ll get back to Cartordale. I am Sir William and
White Towers belongs to me. I’m going to take possession. And if
anyone thinks I killed Sir Philip, well, let them prove it and be
damned to them.”
He broke off with an angry laugh and stood facing us. His lovely little
bride thrust her hand through his arm.
“Yes,” she said, in that musical voice of hers that had charmed huge
crowds on two continents, “let them prove it and—be damned to
them!”
But her laugh was one of real amusement. Lady Clevedon was
looking forward to enjoying life and had no objection to a sensation
or two. Possibly she had found the honeymoon just a trifle slow.
Anyway, she made a charming picture of loyalty and confidence as
she stood arm-in-arm with her husband facing those who were
practically accusing him of murder.
 CHAPTER XXI
WHY TULMIN BLACKMAILED
CLEVEDON

Sir William and Lady Clevedon settled down in Cartordale and very
quickly made themselves popular with their neighbours. Billy himself
was of a buoyant and friendly disposition, and even if he had been
far less genial, Lady Clevedon would have pulled him through. I
never met a sunnier person than she was, and if she had designedly
set out to dissipate any possible suspicion that may have gathered
round her husband, she could not have gone a better way about it.
But if she had any such intent she did not show it. They both acted
as if they took it calmly for granted that any idea of Billy’s
participation in the tragedy was futile nonsense. Nor did they
hesitate to discuss it, and apparently accepted my interposition as a
matter of course. No doubt Thoyne and Kitty had explained to them
my part in the story. As they became more and more immersed in
their plans for refurnishing White Towers and in various social
activities, the mystery dropped more and more into the background.
That was all the better for me. The necessity of consulting other folk
and especially of explaining, or of concealing, because it more
frequently amounts to that, is always something of a nuisance when
one is engaged in delicate investigations.
But I had a little passage with Lady Clevedon the elder that was not
entirely without entertainment. I was passing the big gates of
Hapforth House just as she emerged. I fancy she had seen me from
the windows of the lodge and had come out with the intention of
intercepting me. She stood with both hands on her stick surveying
me with a dry smile.
“So, Mr. Detective, you haven’t yet discovered who killed Philip
Clevedon,” she said.
“I don’t know that I haven’t,” I returned. “But knowledge isn’t proof
and there are libel laws to be watched.”
“That is an easy way of getting out of it,” she cried mockingly. “A
detective ought—”
“But I am not a detective,” I interrupted.
“No, you are not, that’s true enough,” she agreed grimly, as she
turned abruptly and began walking towards Hapforth House.
When I reached Stone Hollow again, I found waiting for me a little
wizened man with indeterminate features and a general air of
dilapidation, though his eyes under shaggy grey brows were bright
and piercing.
“Hullo, Stillman!” I cried, “you at last, is it? I have been expecting
you for some time, but I suppose it wasn’t an easy job. Have you got
it?”
Stillman sat for a few minutes gazing into the fire. I knew his habit
well and did not attempt to hurry him. He was a very methodical
person, with a way of arranging his thoughts and choosing his words
that was sometimes a little irritating to those wanting to hear what he
had to say. I, knowing him well, merely waited until he was ready.
“You told me to find out—” he began and then paused, glancing at
me as if in inquiry.
“Why Tulmin was blackmailing Sir Philip Clevedon,” I replied
promptly. “Tulmin had some hold over Clevedon—what was it?”
“Precisely.”
I had “discovered” Stillman some years before, and had made much
use of him. What his past was I did not know, though I suspected
that it would not bear a too detailed investigation. He was certainly
an expert burglar, as I had more than once put to the test; he could
copy a signature with the fidelity of the camera; he could empty a
man’s pocket with the dexterity of a professional; he knew every
possible trick with the cards; he seemed, in short, to be an expert in
every form of roguery, and yet, as far as I knew, he had never
engaged the attention of the police. If he had been a rogue, he had
covered his tracks with singular skill.
But he may only have been, like myself, a student of roguery. I was
an expert pickpocket, an accomplished burglar, could open a safe by
listening, and would guarantee to copy any man’s signature so as to
deceive even himself; and more than once during my investigations I
had found my accomplishments extremely useful. I should have
made a very dangerous criminal, but I kept within the law, and I was
willing to give Stillman also the full benefit of the doubt. As a sleuth,
I never met his equal; in the patient, persistent, unwearying,
remorseless pursuit of an individual, in turning a person, man or
woman, inside out, in penetrating the most sullen reserve and
uncovering the secrets of the past he was unapproachable.
I had the first taste of his quality in the Strongeley case. He brought
me some information and I happened to remark that I must have
Robert Strongeley shadowed. “Try me,” he said, and as I was just
then too busily occupied to do it myself, and had nobody else whom I
could put on, I agreed. He followed Strongeley half round the world,
and wormed out secrets that even Strongeley himself had forgotten.
Since then I had many times employed him, and he always promptly
answered my call, possibly because I paid well, but even more, I
think, because my cases were nearly always interesting. How he
lived or what he did in the unemployed intervals I cannot say and
never inquired. A lack of curiosity is often a form of wisdom.
I had placed Tulmin in his hands. “This man,” I said, “has been
blackmailing the late Sir Philip Clevedon and I want to know why.”
And there I left it. Stillman, I knew, would sooner or later bring me
the information I required.
“I went down to Ilbay,” Stillman said, “but I could not get on board the
yacht. But chance helped me there. Mr. Thoyne came off the ship
bringing Tulmin with him. The latter went to London and so did I.
Whether Thoyne had given Tulmin an address, or whether Tulmin
went there on his own, I didn’t know, but I followed him and obtained
a room in the same house. Later I learnt that the house was one in
which Tulmin had lodged when he first came over from America and
before he went to Cartordale.”
“America?” I interposed. “Did Thoyne know him in America?”
“That is the story,” Stillman replied, with a quiet grin. “Thoyne—
Clevedon—Tulmin—all from America. Tulmin had some money of
his own, but Thoyne was making him a fairly generous allowance, is
still, for that matter. But to begin at the beginning. When Sir Philip
Clevedon—er—died, Mr. Thoyne offered Tulmin a job as steward on
his yacht.”
“Did Tulmin say why the offer was made?”
“No—no special reason, anyway. He was out of a job and Thoyne
wanted a steward. But it is a little curious that Mr. Thoyne offered
him about twice the usual pay if he would go then and there at once.”
I smiled appreciatively. It was, indeed, a little curious,
“Though, if he hadn’t done that,” Stillman went on, “Tulmin probably
wouldn’t have gone, because he wasn’t short of money. At all
events he went. But hardly had he got to know his way about the
yacht when a telegram came. ‘I want you to go to London and wait
for me there,’ Mr. Thoyne said to him. And that seems to be the
whole story.”
“Did Tulmin see the telegram?”
“No, Mr. Thoyne burnt that when he had read it.”
That, of course, was Kitty Clevedon’s telegram warning Thoyne of
my threatened visit.
“It was lucky Tulmin went to London—what should you have done if
he hadn’t?” I asked, with some little curiosity.
“Oh, I should have found a way,” Stillman replied. “Perhaps an
opportunity of boarding the yacht would have presented itself, or I
might have learnt its destination and met it there. I should have
found Tulmin some way. But that telegram eased matters
considerably. I am much obliged to whoever sent it.”
In all his confidences Thoyne had never told me why he took Tulmin
away, nor had he given me any indication that he knew where he
was.
“As to Tulmin,” Stillman went on, “I had rather a lot of trouble with
him. He wasn’t exactly an easy subject. But I got there in time. He
is too fond of his whisky to keep many secrets. And I have spent a
lot of money in whisky. At to-day’s prices, you know, whisky does
cost money. But I had to drag it out of him almost a word at a time
and piece it together as best I could. But I think I have it straight
now.”
The story was very simple. As Stillman had said, the three men had
all hailed from America where Clevedon, known then as Calcott had
been an object of much attention from the police. Tulmin himself
was a “crook,” though of rather smaller dimensions than the other,
and they had occasionally worked together. Then Calcott
disappeared and it was given out that he was dead.
It was some time after Calcott’s ending that Tulmin, finding the police
in America inconveniently eager to make his acquaintance, crossed
over to England, which offered at once a refuge and a fresh field for
his operations. It was in London that he met Sir Philip Clevedon as
the latter was going from a taxi towards the dignified entrance to his
club. They faced each other at the foot of the stone steps.
“Calcott!” Tulmin cried, with a welcoming grin.
“I beg your pardon,” Sir Philip replied, with the icy composure that
characterised him.
“I said ‘Calcott,’” Tulmin retorted, in no way perturbed.
“Yes, I heard you, but I don’t know what it means,” Sir Philip made
answer.
“It’s a clever bluff,” Tulmin responded. “And I’ve heard of doubles, of
course. But do you know that Felter is in London”—Felter was head
of the Chicago detective bureau, and a man whom the late Calcott
had good reason to fear—“on some stunt or other and looking as
foxy as ever? It gave me a turn of the shivers when I ran up against
him suddenly in Oxford Street. I wonder if you could persuade him
to believe in doubles or whether he might not want to see that scar
on your left knee. He put it there, you know, didn’t he, and could
identify it. Anyway, I am looking for a job as confidential man—valet,
secretary—something soft and clean and well-paid. I am tired of
being a ‘crook.’”
What Tulmin actually would have done, or even could have done
had Clevedon bluffed it out, I don’t know. But apparently the latter
funked the risk and the end of it was that Tulmin was installed at
White Towers as Sir Philip Clevedon’s confidential valet. That, in
brief, was the story Stillman told me, nor was it difficult to supply the
missing lines. Clevedon had never expected to succeed to the title
since there were several lives in front of him, but they disappeared
one by one, and accordingly he shed his Calcott existence like a
discarded hat. He was accepted on this side without question or
demur, and indeed, there seems to have been no doubt regarding
his identity. The whole story was extremely interesting, but I did not
see that so far it helped much in the solution of my own particular
mystery. I was a good deal more concerned with Thoyne’s part in
the play.
“The hold Tulmin had over Clevedon seems clear enough,” I
observed reflectively. “But I don’t quite see how he managed to
hook Thoyne on unless Thoyne was also—”
“No, there is nothing against Mr. Thoyne,” Stillman responded
promptly and decisively. “He is paying Tulmin to keep out of the way,
but I think that is simply so that there may be no scandal—no public
identification of Clevedon with Calcott.”
“Then he knew that Clevedon was Calcott?”
“Yes, Tulmin says so.”
“I wonder how he knew.”
“I am not sure about that, but Tulmin was positive that he did know,
and that he was keeping Tulmin out of the way so as to keep the
name of Clevedon out of the mess. Isn’t Thoyne marrying into the
Clevedon family? Anyway,” Stillman added, with a queer chuckle,
“Tulmin doesn’t expect him to go on paying for ever. ‘As long as it
lasts,’ in his own phrase. The hold isn’t a very strong one; and I
don’t think myself Tulmin will turn nasty when the money stops. His
own record isn’t so clean that he need court publicity.”
“I am not quite clear about it yet,” I remarked. “You said there was
no special reason assigned for Thoyne’s action in making Tulmin his
steward at double pay, but now—”
“Oh, yes, I was not quite clear. Mr. Thoyne did not give Tulmin any
reason when he offered him the job. It was afterwards that he
explained what he had in mind—to make sure that nothing got out
regarding Calcott. Indeed, I am not quite sure that he actually
explained in so many words. But he knew about Calcott—Tulmin is
sure of that—and perhaps Tulmin jumped to the conclusion that that
was his motive.”
“Yes, I dare say it would puzzle Tulmin to know why Thoyne should
appear so friendly.”
I made up my mind at all events that I would interview Tulmin
myself. Not that I had any specific aim in view. But it would at least
be useful to learn all I could regarding Clevedon’s past. Stillman’s
story had opened new possibilities. If Tulmin could recognise
Clevedon as Calcott, others might have done so. It might easily be
that one would have to go back into those dead years to solve the
mystery of the Clevedon tragedy. And among those possibilities was
Thoyne. He may have known Clevedon in America and have had
good reason, quite apart from their rivalry for Kitty Clevedon’s
affections, to desire his death.
At all events I determined that I would have an interview with Ronald
Thoyne before many hours were out. I felt that I had a legitimate
grievance against him. He had known more about Tulmin and
Clevedon than he had ever told me and though he had invited me to
investigate the mystery, he had given me only a half-confidence. I
could at least teach him a lesson on that, I thought rather grimly,
besides which, somewhere at the back of my mind was a queer
suspicion that Thoyne had deliberately thrown me off the scent,
telling me, with every appearance of frankness, much that did not
matter, but remaining stubbornly reticent on several things that did.
 CHAPTER XXII
MORE ANONYMOUS LETTERS

I sent Stillman back to keep an eye on Tulmin until I could myself

interview him and then set myself to arrange a meeting with Thoyne.
He was staying at White Towers and I had no difficulty in finding him.
“Hallo!” he cried. “You look very serious, Holt. What is the matter?
Have you made a fresh discovery?”
“Yes,” I said, “I have.”
“Well, cheer up. I can’t say you look pleased about it.”
“Thoyne,” I responded, looking him straight in the face. “Did you
ever hear the name of Calcott?”
He sent me a quick glance that was partly, I think, surprise but was
not entirely devoid of wrath. The name had evidently no very
pleasant sound in his ears.
“You see,” I went on, interpreting his half-instinctive movement in my
own way, “you have given me a lot of quite unnecessary trouble.
Had you been frank with me—”
“I was frank on everything that mattered,” he said sullenly.
“You thought the fact that Clevedon had been an American crook
known as Calcott whom you had met in Chicago—”
“That’s a lie, anyway.”
“You needn’t get excited about it,” I rejoined equably.
“Excited, the devil!” he cried. “I am not excited. I’m as calm as you
are.”
“Then perhaps you would like to tell me the whole story.”
“What story?”
“The story of Calcott, the crook, and what you knew about him in
Chicago.”
“I did not know him in Chicago.”
He sat himself down and ran his fingers two or three times through
his thick hair.
“You are rather a marvel,” he said, with a smile that was just a little
rueful. “How you get these things sorted out amazes me. First one
and then another, you get them all straightened and leave no loose
ends. No, I never knew Calcott, though I’d heard of him. But I had
known Tulmin in Chicago. I caught him looting my baggage—it was
in the car outside my house and he was just moving off with a bag. I
caught him and thrashed him and let him go. I recognised him when
I met him here, and he knew me also. I didn’t interfere. He seemed
to be living an honest life as far as I could gather and I didn’t want to
rob the poor devil of his chance. It was he who told me about
Calcott. You see, after they quarrelled—”
“Quarrelled!” I repeated. “Did—but I must have the whole story now.
There is more in this than I thought. If there was a quarrel—”
“Yes, what of it?”
Thoyne spoke a little impatiently as if he were tired of the whole
subject and merely wanted to bury it.
“Well, a quarrel—is sometimes a motive for murder—”
“I always thought Tulmin did it,” he responded quietly. “But I’ll tell
you all I know and then perhaps you can leave me alone. Damn
Clevedon and damn Tulmin. Why should I be worried about their
affairs in this fashion? I didn’t ask to be mixed up in it, did I? Of
course, I did it to help Kitty, and would do it all again, and more for
her. And all through the infernal foolery of this secret marriage. Why
couldn’t Clevedon tell his sister he was going to be married? The
whole thing’s been a nightmare to me and I’m dead sick of it. I didn’t
murder Clevedon and I don’t know who did, unless it was Tulmin. If
you would find the assassin and tie him up I might get some peace.”
“But it was you who took Tulmin away and hid him,” I replied.
“Yes, I know it was—what of it?”
“But if you thought he was the murderer—?”
“Of course I thought he was the murderer. You don’t think I should
have involved an innocent man, do you? Yes, I persuaded Tulmin to
go away in order to keep suspicion off Billy Clevedon. Kitty was
terrified and I was a bit anxious myself.”
“And as to this quarrel?” I interposed.
“I don’t know the rights of that, except that Tulmin had wanted more
money than Clevedon was willing to pay. Kitty had told me, you
know, that Clevedon had wanted her to marry him and that she
intended to consent. We were not formally engaged then, though it
was all but fixed up between us. But the word lay with her, of
course, and I was trying to be as philosophical as I could over my
dismissal when one night Tulmin came to me with a queer, mixed
yarn, of which at first I could make nothing. ‘What have you come to
me for?’ I said. ‘I’ve come to sell you a secret,’ he replied. My first
idea was to give the swine a good sound kicking and pack him off. ‘I
could tell you something about Sir Philip that’ll make Miss Kitty
impossible,’ he added, and at that I waited.
“I dare say you’ll blame me, but I don’t pretend to be any better than
anybody else, and besides, he’d stolen her from me. So I listened.
He told me he knew something against Clevedon, who had been
paying him to keep silence. Now he wanted to go back to America—
Tulmin did, I mean—and had asked Clevedon for a lump sum, and
Clevedon had threatened to shoot him. That is the best thing I ever
heard about Clevedon. Tulmin is a little rat, for whom shooting is a
lot too good. But Clevedon had stolen my woman and I didn’t mean
to lose any chance that came. I said he could have the money if I
found the secret worth it. He wanted it in advance, but I told him
he’d have it my way or no way. And then he told me what Clevedon
had been across the water.
“At first I took him to mean that Clevedon was an impostor and had
no right to the title and estates, but it seems I was wrong there. I
went off to Clevedon next day and we had a right royal rumpus about
it—that was the interview described at the inquest. I didn’t mention
Tulmin’s name—the little rat had made that a condition. ‘You can’t
deny it,’ I said to Clevedon. ‘I come from Chicago, you know. I
recognised you months ago.’ He seemed impressed and it was
rather a good lie. ‘But I didn’t interfere,’ I went on, ‘until you tried to
steal my woman, and we Americans are always ready to fight for our
women.’ That housekeeper woman didn’t hear all that, apparently.
Then Clevedon denied the whole story and we began to get angry.”
“I see,” I interposed, “and when you said you’d find a way of making
him give Miss Clevedon up, you meant—”
“I meant I would get the Chicago police on his trail.”
“Did you know that Clevedon gave Tulmin a cheque for £500 the day
before the murder?”
“No, did he? Well, evidently Tulmin didn’t think it enough.”
“What day was it Tulmin came to see you?”
“It was that same morning, February 23rd.”
“Clevedon gave Tulmin £500, which was less than Tulmin wanted, so
Tulmin double-crossed Clevedon and came to you.”
“That seems like it.”
“It opens all sorts of fresh avenues,” I remarked.
“Don’t say that,” Thoyne murmured, with a groan. “I was hoping it
would end the case. I never want to be mixed up in another murder
mystery. It is the very deuce.”
“Suppose Clevedon, having quarrelled with Tulmin, and knowing you
also had penetrated his secret—”
“Do you mean it was suicide?” Thoyne cried, his whole face lighting
up. “If you could prove that I would—I would give you a cheque for
ten thousand pounds. It would settle such a lot, wouldn’t it? Suicide,
yes, I think after all it must be suicide.”
He gazed eagerly at my unresponsive face, then shrugged his
shoulders a little angrily.
“Yes,” I replied slowly, “but then, what of the hatpin?”
His face fell at that.
“Clevedon certainly didn’t stab himself with a hatpin,” I added. “But
you may as well finish the story,” I went on, “and tell me why you
spirited Tulmin away.”
“Oh, that’s quite simple,” he replied. “Kitty was worried about her
brother, whose absence puzzled her, as it did the rest of us. So I
offered Tulmin a job, and he jumped at it.”
“Did you tell him—”
“Of course not, I’m not a fool.”
“And was that why you offered to buy my house?”
He laughed at the recollection of that particular interview.
“I dare say you thought me an awful idiot,” he said.
“And now you’ve told me everything.”
“Yes,” he responded, “everything.”
The truth or otherwise of which will appear in due course.
On my way out old Lady Clevedon met me, grimmer and more
caustic than ever.
“Any discoveries, Mr. Detective?” she cried. “But I suppose I need
not ask. Have you seen the Midlington Courier to-day? It has an
interesting article on the Clevedon Case—I forget how many weeks
gone and nothing done. It wants to know if the police—”
“But I have nothing to do with the police,” I interrupted smilingly.
Pepster, whom I found awaiting me at Stone Hollow, began on the
newspaper article as soon as we met.
“What do you think of that?” he cried, waving the cutting as if it had
been a flag. “Have you read it? ‘Unfortunately, we cannot
congratulate the police, who seem to have been waiting, like the
famous Micawber, for something to turn up.’ What do you think of
it?”
“Oh, newspaper writers are very fond of dragging Mr. Micawber in,” I
replied. “He is overworked.”
“Damn Micawber!”
“Yes,” I rejoined, with a quiet laugh. “I should feel like that if I
belonged to the police.”
“Well, you’re in the case, anyway,” Pepster said tartly. “And that
reminds me. I have some news for you. At least, I think I have. But
with you one never knows. Quite likely you have it all entered up
already. Did you ever hear of Mary Grainger?”
“No, who is she?”
“Thank God, I’ve got a novelty at last. She’s daughter to Grainger,
the Midlington chemist. Did you know he had a daughter?”
“No, does she live at home?”
“She doesn’t live anywhere, she’s dead.”
“Yes?”
“Did you know that?”
I shook my head to express a negative.
“Then it really is one to me,” he said, with an air of great satisfaction.
“Yes,” I agreed, “it is one to you if it means anything. I take it there is
more behind. The decease of a young lady I never met is hardly a
matter for excitement in itself.”
“Yes, there is more behind,” he said slowly, nodding his head.
“There is, for instance, Nora Lepley behind. She and Mary Grainger
both attended the High School in Midlington and have been for years
inseparable friends. Nora frequently spent weeks at a time with the
Graingers at Midlington and apparently had the run of the shop. She
goes frequently to see the old man even now. She was there one
day last week. Now suppose—well, Nora Lepley could have got the
prussic acid that way.”
“It is certainly one to you,” I agreed, slowly and thoughtfully.
“I have something else,” Pepster went on, taking out his wallet.
“More anonymous letters?” I queried.
“Yes, two.”
He handed them across to me. One was a fragment of blue paper,
on which was printed in red ink:

THOYNE IS STILL AT
LIBERTY. WHY?

The other was a picture postcard—a view of the Midlington Parish

Church—and the message, in pencil, ran:

WHY ARE YOU PROTECTING

THOYNE. HAS HE PAID YOU?

“It wasn’t sent open like that,” Pepster explained. “It came in an
envelope. It’s a popular card, printed by the hundred and sold by